PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
12734191-1	2003	The tetrahydrobiopterin (BH4) cofactor is essential for the biosynthesis of catecholamines and serotonin and for nitric-oxide synthase (NOS).	sapropterin	4-23	nitric oxide synthase 1, neuronal	Mus musculus	113-134
12734191-1	2003	The tetrahydrobiopterin (BH4) cofactor is essential for the biosynthesis of catecholamines and serotonin and for nitric-oxide synthase (NOS).	sapropterin	25-28	nitric oxide synthase 1, neuronal	Mus musculus	113-134
12834873-4	2003	Nitric oxide (NO) is an important messenger molecule in the central nervous system, especially in the cerebellum, and it is produced via the enzyme, nitric oxide synthase (NOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	149-170
12623792-5	2003	The rise in BFcrb was attenuated by 73 +/- 3% in nNOS-/- mice (P < 0.05, n = 6).	bfcrb	12-17	nitric oxide synthase 1, neuronal	Mus musculus	49-53
12623792-6	2003	The increases in BFcrb produced by superfusion of Crus II with glutamate or by systemic administration of harmaline were also attenuated in nNOS-/- mice (P < 0.05).	bfcrb	17-22	nitric oxide synthase 1, neuronal	Mus musculus	140-144
12623792-6	2003	The increases in BFcrb produced by superfusion of Crus II with glutamate or by systemic administration of harmaline were also attenuated in nNOS-/- mice (P < 0.05).	Glutamic Acid	63-72	nitric oxide synthase 1, neuronal	Mus musculus	140-144
12623792-6	2003	The increases in BFcrb produced by superfusion of Crus II with glutamate or by systemic administration of harmaline were also attenuated in nNOS-/- mice (P < 0.05).	Harmaline	106-115	nitric oxide synthase 1, neuronal	Mus musculus	140-144
12934649-4	2003	In that study we suggested that EGCG could prevent cytokine-induced beta-cell destruction by down-regulation of nitric oxide synthase (NOS) through inhibition of NF-kappaB activation.	epigallocatechin gallate	32-36	nitric oxide synthase 1, neuronal	Mus musculus	112-133
12864970-3	2003	Baseline corticosterone concentrations were higher in nNOS(-/-) than WT mice.	Corticosterone	9-23	nitric oxide synthase 1, neuronal	Mus musculus	54-58
12764022-4	2003	These responses were markedly attenuated in mice lacking NOS1 (NOS1-/-) (15+/-2% increase in dP/dt-EDV; P<0.001 versus WT; and no change in tau; P<0.01 versus WT).	dp	93-95	nitric oxide synthase 1, neuronal	Mus musculus	57-61
12764022-4	2003	These responses were markedly attenuated in mice lacking NOS1 (NOS1-/-) (15+/-2% increase in dP/dt-EDV; P<0.001 versus WT; and no change in tau; P<0.01 versus WT).	dp	93-95	nitric oxide synthase 1, neuronal	Mus musculus	63-67
12781920-1	2003	Nitric oxide (NO) from endothelial or neuronal NO synthases (eNOS or nNOS) may contribute both to the cerebrovascular responses to oxygen and potentially to the peroxynitrite-mediated toxic effects of hyperbaric oxygen (HBO(2)) on the central nervous system (CNS O(2) toxicity).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	69-73
12781920-1	2003	Nitric oxide (NO) from endothelial or neuronal NO synthases (eNOS or nNOS) may contribute both to the cerebrovascular responses to oxygen and potentially to the peroxynitrite-mediated toxic effects of hyperbaric oxygen (HBO(2)) on the central nervous system (CNS O(2) toxicity).	Oxygen	131-137	nitric oxide synthase 1, neuronal	Mus musculus	69-73
12781920-1	2003	Nitric oxide (NO) from endothelial or neuronal NO synthases (eNOS or nNOS) may contribute both to the cerebrovascular responses to oxygen and potentially to the peroxynitrite-mediated toxic effects of hyperbaric oxygen (HBO(2)) on the central nervous system (CNS O(2) toxicity).	Peroxynitrous Acid	161-174	nitric oxide synthase 1, neuronal	Mus musculus	69-73
12781920-1	2003	Nitric oxide (NO) from endothelial or neuronal NO synthases (eNOS or nNOS) may contribute both to the cerebrovascular responses to oxygen and potentially to the peroxynitrite-mediated toxic effects of hyperbaric oxygen (HBO(2)) on the central nervous system (CNS O(2) toxicity).	Oxygen	212-218	nitric oxide synthase 1, neuronal	Mus musculus	69-73
12781920-1	2003	Nitric oxide (NO) from endothelial or neuronal NO synthases (eNOS or nNOS) may contribute both to the cerebrovascular responses to oxygen and potentially to the peroxynitrite-mediated toxic effects of hyperbaric oxygen (HBO(2)) on the central nervous system (CNS O(2) toxicity).	o(2)	222-226	nitric oxide synthase 1, neuronal	Mus musculus	69-73
12846982-4	2003	The mechanisms of MPTP-induced neurotoxicity are not yet fully understood but involve activation of N-methyl-D-aspartate (NMDA) receptors by glutamate, production of NO by nNOS and iNOS, oxidative injury to DNA, and activation of the DNA damage-sensing enzyme poly (ADP-ribose) polymerase (PARP).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	18-22	nitric oxide synthase 1, neuronal	Mus musculus	172-176
12880486-8	2003	Furthermore, NO fosters dopamine depletion, and the said neurotoxicity is averted by nNOS inhibitors such as 7-nitroindazole working on tyrosine hydroxylase-immunoreactive neurons in substantia nigra pars compacta.	Dopamine	24-32	nitric oxide synthase 1, neuronal	Mus musculus	85-89
12880486-8	2003	Furthermore, NO fosters dopamine depletion, and the said neurotoxicity is averted by nNOS inhibitors such as 7-nitroindazole working on tyrosine hydroxylase-immunoreactive neurons in substantia nigra pars compacta.	7-nitroindazole	109-124	nitric oxide synthase 1, neuronal	Mus musculus	85-89
12880486-9	2003	Moreover, mutant mice lacking the nNOS gene are more resistant to MPTP neurotoxicity when compared with wild-type littermates.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	66-70	nitric oxide synthase 1, neuronal	Mus musculus	34-38
12938735-5	2003	In addition to superoxide, nitric oxide production by nNOS or by microglial iNOS also contributes to the MPTP neurotoxocity.	Nitric Oxide	27-39	nitric oxide synthase 1, neuronal	Mus musculus	54-58
12938735-5	2003	In addition to superoxide, nitric oxide production by nNOS or by microglial iNOS also contributes to the MPTP neurotoxocity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	105-109	nitric oxide synthase 1, neuronal	Mus musculus	54-58
12938735-6	2003	Mice with endowed defences against superoxide or with deficiency in the nNOS and iNOS are protected from MPTP toxicity suggesting that formation of reactive oxygen and nitrogen intermediates both intracellularly and extracellularly contributes to the demise of dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	105-109	nitric oxide synthase 1, neuronal	Mus musculus	72-76
12938735-6	2003	Mice with endowed defences against superoxide or with deficiency in the nNOS and iNOS are protected from MPTP toxicity suggesting that formation of reactive oxygen and nitrogen intermediates both intracellularly and extracellularly contributes to the demise of dopaminergic neurons.	Oxygen	157-163	nitric oxide synthase 1, neuronal	Mus musculus	72-76
12938735-6	2003	Mice with endowed defences against superoxide or with deficiency in the nNOS and iNOS are protected from MPTP toxicity suggesting that formation of reactive oxygen and nitrogen intermediates both intracellularly and extracellularly contributes to the demise of dopaminergic neurons.	Nitrogen	168-176	nitric oxide synthase 1, neuronal	Mus musculus	72-76
12761894-4	2003	NO is generated from L-arginine by the enzyme nitric oxide synthase (NOS).	Arginine	21-31	nitric oxide synthase 1, neuronal	Mus musculus	46-67
12704728-3	2003	NO is produced from l-arginine by the enzyme, nitric oxide synthase (NOS), which has three isoforms: endothelial (NOS3), neural (NOS1), and inducible (NOS2).	Arginine	20-30	nitric oxide synthase 1, neuronal	Mus musculus	46-67
12704728-3	2003	NO is produced from l-arginine by the enzyme, nitric oxide synthase (NOS), which has three isoforms: endothelial (NOS3), neural (NOS1), and inducible (NOS2).	Arginine	20-30	nitric oxide synthase 1, neuronal	Mus musculus	129-133
12817894-0	2003	Gabapentin blocks L-type and P/Q-type Ca2+ channels involved in depolarization-stimulated nitric oxide synthase activity in primary cultures of neurons from mouse cerebral cortex.	Gabapentin	0-10	nitric oxide synthase 1, neuronal	Mus musculus	90-111
12895429-2	2003	Contractions to ET-1 and/or thromboxane may be enhanced during chronic deficiency in expression or activity of NO synthase (NOS).	Thromboxanes	28-39	nitric oxide synthase 1, neuronal	Mus musculus	111-122
12817894-1	2003	PURPOSE: The effect of gabapentin [1-(aminomethyl)cyclohexane acetic acid] on Ca2+ channels involving the activation of nitric oxide synthase (NOS) was investigated in primary neuronal culture of mouse cerebral cortex.	Gabapentin	23-33	nitric oxide synthase 1, neuronal	Mus musculus	120-141
12817894-1	2003	PURPOSE: The effect of gabapentin [1-(aminomethyl)cyclohexane acetic acid] on Ca2+ channels involving the activation of nitric oxide synthase (NOS) was investigated in primary neuronal culture of mouse cerebral cortex.	Gabapentin	35-73	nitric oxide synthase 1, neuronal	Mus musculus	120-141
12799144-6	2003	The mechanism of toxicity involved stimulation of nitric oxide production via activation of the nitric oxide synthases, nNOS and iNOS.	Nitric Oxide	50-62	nitric oxide synthase 1, neuronal	Mus musculus	120-124
12505875-7	2003	Inhibition of nitric oxide synthase (NOS) with nitro-l-arginine augmented HPV in PKC-epsilon +/+ but not -/- mice.	Nitroarginine	47-63	nitric oxide synthase 1, neuronal	Mus musculus	14-35
12677017-1	2003	BACKGROUND AND PURPOSE: The purpose of this study was to test the hypothesis that nitric oxide is required for preconditioning in an intact animal model of focal ischemia using neuronal and endothelial nitric oxide synthase (nNOS and eNOS) knockout mice.	Nitric Oxide	82-94	nitric oxide synthase 1, neuronal	Mus musculus	225-229
12589527-1	2003	RATIONALE: Previous studies have shown the anxiolytic-like effects of nitrous oxide (N(2)O) to be sensitive to antagonism by non-specific inhibitors of nitric oxide synthase (NOS).	Nitrous Oxide	70-83	nitric oxide synthase 1, neuronal	Mus musculus	152-173
12600881-0	2003	Vasomodulation by skeletal muscle-derived nitric oxide requires alpha-syntrophin-mediated sarcolemmal localization of neuronal Nitric oxide synthase.	Nitric Oxide	42-54	nitric oxide synthase 1, neuronal	Mus musculus	118-148
12600881-2	2003	Nitric oxide (NO) produced by skeletal muscle nNOS is proposed to regulate blood flow in exercising muscle by diffusing from the skeletal muscle fibers to the nearby microvessels where it attenuates alpha-adrenergic vasoconstriction.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	46-50
12597993-0	2003	Comparison of the effects of specific and nonspecific inhibition of nitric oxide synthase on morphine analgesia, tolerance and dependence in mice.	Morphine	93-101	nitric oxide synthase 1, neuronal	Mus musculus	68-89
12614381-0	2003	Modulation of cortical nitric oxide synthase, glutamate, and redox state by nifedipine and taurine in PTZ-kindled mice.	Nifedipine	76-86	nitric oxide synthase 1, neuronal	Mus musculus	23-44
12644275-0	2003	Antisense knockdown of neuronal nitric oxide synthase antagonizes nitrous oxide-induced behavior.	Nitrous Oxide	66-79	nitric oxide synthase 1, neuronal	Mus musculus	23-53
12644275-1	2003	The behavioral effects of nitrous oxide (N(2)O) were antagonized by non-specific inhibitors of nitric oxide synthase (NOS).	Nitrous Oxide	26-39	nitric oxide synthase 1, neuronal	Mus musculus	95-116
12644275-1	2003	The behavioral effects of nitrous oxide (N(2)O) were antagonized by non-specific inhibitors of nitric oxide synthase (NOS).	Nitrous Oxide	41-47	nitric oxide synthase 1, neuronal	Mus musculus	95-116
12675928-0	2003	The nNOS inhibitor, AR-R17477AR, prevents the loss of NF68 immunoreactivity induced by methamphetamine in the mouse striatum.	ar-r17477ar	20-31	nitric oxide synthase 1, neuronal	Mus musculus	4-8
12675928-0	2003	The nNOS inhibitor, AR-R17477AR, prevents the loss of NF68 immunoreactivity induced by methamphetamine in the mouse striatum.	Methamphetamine	87-102	nitric oxide synthase 1, neuronal	Mus musculus	4-8
12675928-2	2003	The ability of low ambient temperature, or of the specific neuronal nitric oxide synthase (nNOS) inhibitor AR-R17477AR, to protect against both long-term striatal NF68 and dopamine loss induced by METH (3 mg/kg, i.p.)	ar-r17477ar	107-118	nitric oxide synthase 1, neuronal	Mus musculus	91-95
12614381-0	2003	Modulation of cortical nitric oxide synthase, glutamate, and redox state by nifedipine and taurine in PTZ-kindled mice.	Taurine	91-98	nitric oxide synthase 1, neuronal	Mus musculus	23-44
12614381-1	2003	PURPOSE: Correlation between pentylenetetrazol (PTZ)-induced kindling and the cortical nitric oxide synthase (NOS), intracellular calcium [Ca2+]i, glutamate, and free radicals was studied in mice, as well as the modulatory action of nifedipine and taurine on these parameters.	Pentylenetetrazole	29-46	nitric oxide synthase 1, neuronal	Mus musculus	87-108
12614381-1	2003	PURPOSE: Correlation between pentylenetetrazol (PTZ)-induced kindling and the cortical nitric oxide synthase (NOS), intracellular calcium [Ca2+]i, glutamate, and free radicals was studied in mice, as well as the modulatory action of nifedipine and taurine on these parameters.	Pentylenetetrazole	48-51	nitric oxide synthase 1, neuronal	Mus musculus	87-108
12614381-1	2003	PURPOSE: Correlation between pentylenetetrazol (PTZ)-induced kindling and the cortical nitric oxide synthase (NOS), intracellular calcium [Ca2+]i, glutamate, and free radicals was studied in mice, as well as the modulatory action of nifedipine and taurine on these parameters.	Nifedipine	233-243	nitric oxide synthase 1, neuronal	Mus musculus	87-108
12614381-1	2003	PURPOSE: Correlation between pentylenetetrazol (PTZ)-induced kindling and the cortical nitric oxide synthase (NOS), intracellular calcium [Ca2+]i, glutamate, and free radicals was studied in mice, as well as the modulatory action of nifedipine and taurine on these parameters.	Taurine	248-255	nitric oxide synthase 1, neuronal	Mus musculus	87-108
12529255-0	2003	Reduced inotropic heart response in selenium-deficient mice relates with inducible nitric oxide synthase.	Selenium	36-44	nitric oxide synthase 1, neuronal	Mus musculus	83-104
12911523-2	2003	Nitric oxide synthase (NOS) inhibitors were evaluated for their ability to inhibit the rise in reactive nitrogen intermediates (RNI) induced by bacterial lipopolysaccharide (LPS) in mice.	reactive nitrogen intermediates	95-126	nitric oxide synthase 1, neuronal	Mus musculus	0-21
12911523-2	2003	Nitric oxide synthase (NOS) inhibitors were evaluated for their ability to inhibit the rise in reactive nitrogen intermediates (RNI) induced by bacterial lipopolysaccharide (LPS) in mice.	rni	128-131	nitric oxide synthase 1, neuronal	Mus musculus	0-21
12926546-0	2003	Study on the influence of potent inhibitors of neuronal nitric oxide synthase on the antinociceptive and anticonvulsant activity of benzodiazepines in mice.	Benzodiazepines	132-147	nitric oxide synthase 1, neuronal	Mus musculus	47-77
12529255-2	2003	This diminished response could be reversed by feeding Se(-) mice the Se(+) diet for 1 wk or by pretreatment with nitric oxide synthase (NOS) inhibitors such as N(G)-monomethyl-l-arginine or aminopyridine.	omega-N-Methylarginine	160-186	nitric oxide synthase 1, neuronal	Mus musculus	113-134
14699893-0	2003	Correlation of inbred mouse responsiveness to nitrous oxide (N2O) with brain nitric oxide synthase (NOS) activity.	Nitrous Oxide	46-59	nitric oxide synthase 1, neuronal	Mus musculus	77-98
12580953-0	2003	A nitric oxide synthase inhibitor, N(G)-nitro-l-arginine-methyl-ester, exerts potent antiangiogenic effects on plasmacytoma in a newly established multiple myeloma severe combined immunodeficient mouse model.	NG-Nitroarginine Methyl Ester	35-69	nitric oxide synthase 1, neuronal	Mus musculus	2-23
12580953-2	2003	In the present study, we examined the anticancer potential of an inhibitor of nitric oxide synthase (NOS), NG-nitro-l-arginine methyl ester (L-NAME), in a novel severe combined immunodeficient mouse model (KHM mouse) that harbours the highly sanguineous plasmacytoma cell line KHM-4, derived from a patient with highly chemoresistant MM.	NG-Nitroarginine Methyl Ester	141-147	nitric oxide synthase 1, neuronal	Mus musculus	78-99
12522125-0	2003	Long-term vitamin C treatment increases vascular tetrahydrobiopterin levels and nitric oxide synthase activity.	Ascorbic Acid	10-19	nitric oxide synthase 1, neuronal	Mus musculus	80-101
12522125-1	2003	In cultured endothelial cells, the antioxidant, L-ascorbic acid (vitamin C), increases nitric oxide synthase (NOS) enzyme activity via chemical stabilization of tetrahydrobiopterin.	Ascorbic Acid	48-63	nitric oxide synthase 1, neuronal	Mus musculus	87-108
12522125-1	2003	In cultured endothelial cells, the antioxidant, L-ascorbic acid (vitamin C), increases nitric oxide synthase (NOS) enzyme activity via chemical stabilization of tetrahydrobiopterin.	Ascorbic Acid	65-74	nitric oxide synthase 1, neuronal	Mus musculus	87-108
12522125-1	2003	In cultured endothelial cells, the antioxidant, L-ascorbic acid (vitamin C), increases nitric oxide synthase (NOS) enzyme activity via chemical stabilization of tetrahydrobiopterin.	sapropterin	161-180	nitric oxide synthase 1, neuronal	Mus musculus	87-108
12494944-10	2003	Furthermore, myeloperoxidase and nNOS/eNOS may contribute to nitrotyrosine formation in the absence of iNOS.	3-nitrotyrosine	61-74	nitric oxide synthase 1, neuronal	Mus musculus	33-37
12868590-2	2003	Recently, two isoforms of nitric oxide (NO) synthase (nNOS and eNOS) and NO itself have been identified at the light microscopic level in the vestibulocochlear system of mice using specific antibodies and a new fluorescence indicator.	Nitric Oxide	26-38	nitric oxide synthase 1, neuronal	Mus musculus	54-58
12524231-1	2003	OBJECTIVE: L-arginine serves as a substrate for the formation of NO by the NO synthase (NOS) enzymes.	Arginine	11-21	nitric oxide synthase 1, neuronal	Mus musculus	75-86
12507775-5	2003	The results also show a substantial increase in NO production in cells overexpressing GH that could be blocked by N(G)-monomethyl-L-arginine (L-NMMA), an L-arginine analogue that competitively inhibits all three isoforms of nitric oxide synthase (NOS).	omega-N-Methylarginine	114-140	nitric oxide synthase 1, neuronal	Mus musculus	224-245
12507775-5	2003	The results also show a substantial increase in NO production in cells overexpressing GH that could be blocked by N(G)-monomethyl-L-arginine (L-NMMA), an L-arginine analogue that competitively inhibits all three isoforms of nitric oxide synthase (NOS).	omega-N-Methylarginine	142-148	nitric oxide synthase 1, neuronal	Mus musculus	224-245
12507775-5	2003	The results also show a substantial increase in NO production in cells overexpressing GH that could be blocked by N(G)-monomethyl-L-arginine (L-NMMA), an L-arginine analogue that competitively inhibits all three isoforms of nitric oxide synthase (NOS).	Arginine	130-140	nitric oxide synthase 1, neuronal	Mus musculus	224-245
12831857-6	2003	We observe N-methyl-D-aspartate-dependent citrulline production in pyramidal cells of mouse hippocampus, which is absent in nNOS(Delta/Delta) animals.	N-Methylaspartate	11-31	nitric oxide synthase 1, neuronal	Mus musculus	124-128
12831857-6	2003	We observe N-methyl-D-aspartate-dependent citrulline production in pyramidal cells of mouse hippocampus, which is absent in nNOS(Delta/Delta) animals.	Citrulline	42-52	nitric oxide synthase 1, neuronal	Mus musculus	124-128
14699893-0	2003	Correlation of inbred mouse responsiveness to nitrous oxide (N2O) with brain nitric oxide synthase (NOS) activity.	Nitrous Oxide	61-64	nitric oxide synthase 1, neuronal	Mus musculus	77-98
12477528-6	2002	Nitric oxide studies included the delivery of nitric oxide synthase (NOS) inhibitors, N(G)-nitro-L-arginine methyl ester (L-NAME), or N(G)-nitro-D-arginine methyl ester, by the same method.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	46-67
12468582-5	2002	Inhibition of nNOS with 10 micro mol/L S-methyl-L-thiocitrulline significantly decreased the afferent arteriolar diameter of AT1A receptor-deficient mice, from 15.1+/-1.2 to 5.0+/-0.3 micro m (n=7), and the decrease was significantly greater than that observed in wild-type mice (from 15.9+/-1.2 to 10.6+/-1.3 micro m; n=8).	S-methylthiocitrulline	39-64	nitric oxide synthase 1, neuronal	Mus musculus	14-18
12468582-6	2002	During nNOS inhibition, the initial and sustained afferent arteriolar constrictor responses to acetazolamide in wild-type mice averaged 54.4+/-6.4% and 44.8+/-11.3%; respectively, and were similar to those in AT1A receptor-deficient mice (53.2+/-6.4% and 59.5+/-4.4%, respectively).	Acetazolamide	95-108	nitric oxide synthase 1, neuronal	Mus musculus	7-11
12217856-1	2002	Our laboratory has previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in fluid absorption (J(v)) and HCO absorption (J(HCO3)) in the proximal tubule and develop metabolic acidosis.	7 alpha-hydroxy-4-cholesten-3-one	137-140	nitric oxide synthase 1, neuronal	Mus musculus	54-84
12389206-1	2002	In brain and peripheral tissues, steroid hormones regulate nitric oxide synthase (nNOS).	Steroids	33-40	nitric oxide synthase 1, neuronal	Mus musculus	82-86
12372425-5	2002	In neuronal nitric oxide synthase (nNOS) knockout mice, the VEGF concentration was also elevated after prazosin treatment but remained almost unchanged in endothelial nitric oxide synthase (eNOS) knockout mice.	Prazosin	103-111	nitric oxide synthase 1, neuronal	Mus musculus	3-33
12372425-5	2002	In neuronal nitric oxide synthase (nNOS) knockout mice, the VEGF concentration was also elevated after prazosin treatment but remained almost unchanged in endothelial nitric oxide synthase (eNOS) knockout mice.	Prazosin	103-111	nitric oxide synthase 1, neuronal	Mus musculus	35-39
12217856-1	2002	Our laboratory has previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in fluid absorption (J(v)) and HCO absorption (J(HCO3)) in the proximal tubule and develop metabolic acidosis.	7 alpha-hydroxy-4-cholesten-3-one	137-140	nitric oxide synthase 1, neuronal	Mus musculus	86-90
12217856-1	2002	Our laboratory has previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in fluid absorption (J(v)) and HCO absorption (J(HCO3)) in the proximal tubule and develop metabolic acidosis.	Bicarbonates	155-159	nitric oxide synthase 1, neuronal	Mus musculus	54-84
12217856-1	2002	Our laboratory has previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in fluid absorption (J(v)) and HCO absorption (J(HCO3)) in the proximal tubule and develop metabolic acidosis.	Bicarbonates	155-159	nitric oxide synthase 1, neuronal	Mus musculus	86-90
12356678-3	2002	Neutralization of endogenous IFN-gamma production or treatment with NO synthase (NOS) inhibitor, L-N-monomethyl-arginine, blocked Con A-induced NO production and greatly restored proliferation by SC from infected mice.	l-n-monomethyl-arginine	97-120	nitric oxide synthase 1, neuronal	Mus musculus	68-79
12392201-3	2002	Previous work showed that the inhibitor of neuronal nitric oxide synthase (nNOS) might produce protection against MPTP-induced dopaminergic toxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	114-118	nitric oxide synthase 1, neuronal	Mus musculus	43-73
12351742-0	2002	The neuronal nitric oxide synthase gene is critically involved in neurobehavioral effects of alcohol.	Alcohols	93-100	nitric oxide synthase 1, neuronal	Mus musculus	4-34
12392201-3	2002	Previous work showed that the inhibitor of neuronal nitric oxide synthase (nNOS) might produce protection against MPTP-induced dopaminergic toxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	114-118	nitric oxide synthase 1, neuronal	Mus musculus	75-79
12351742-1	2002	In the present study, we describe a new role of the neuronal nitric oxide synthase (nNOS) gene in the regulation of alcohol drinking behavior.	Alcohols	116-123	nitric oxide synthase 1, neuronal	Mus musculus	52-82
12392201-9	2002	The present study demonstrates that nNOS inhibitor 7-nitroindazole as well as MAO inhibitors clorgyline and pargyline can produce dose-dependent neuroprotection against the dopaminergic neurotoxicity of MPTP.	7-nitroindazole	51-66	nitric oxide synthase 1, neuronal	Mus musculus	36-40
12351742-1	2002	In the present study, we describe a new role of the neuronal nitric oxide synthase (nNOS) gene in the regulation of alcohol drinking behavior.	Alcohols	116-123	nitric oxide synthase 1, neuronal	Mus musculus	84-88
12351742-3	2002	nNOS -/- mice did not differ in consumption and preference for low alcohol concentrations from wild-type animals; however, nNOS -/- mice consumed sixfold more alcohol from highly concentrated alcohol solutions than wild-type mice.	Alcohols	159-166	nitric oxide synthase 1, neuronal	Mus musculus	123-127
12392201-9	2002	The present study demonstrates that nNOS inhibitor 7-nitroindazole as well as MAO inhibitors clorgyline and pargyline can produce dose-dependent neuroprotection against the dopaminergic neurotoxicity of MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	203-207	nitric oxide synthase 1, neuronal	Mus musculus	36-40
12351742-3	2002	nNOS -/- mice did not differ in consumption and preference for low alcohol concentrations from wild-type animals; however, nNOS -/- mice consumed sixfold more alcohol from highly concentrated alcohol solutions than wild-type mice.	Alcohols	159-166	nitric oxide synthase 1, neuronal	Mus musculus	123-127
12351742-4	2002	Taste studies with either sucrose or quinine solutions revealed that alcohol intake in nNOS -/- and wild-type mice is associated, at least in part, with sweet solution intake but not with the taste of bitterness.	Alcohols	69-76	nitric oxide synthase 1, neuronal	Mus musculus	87-91
12437128-4	2002	Furthermore, we investigated the influence of glucose on the activity of nNOS and the expression of PIN and are able to show that both are increased by glucose stimulation in the beta-cell lines but not in the mouse fibroblastic cell line LTK.	Glucose	46-53	nitric oxide synthase 1, neuronal	Mus musculus	73-77
12351742-5	2002	When compared with wild-type mice, the nNOS -/- mice were found to be less sensitive to the sedative effects of ethanol as measured by shorter recovery time from ethanol-induced sleep and did not develop rapid tolerance to ethanol-induced hypothermia, although plasma ethanol concentrations were not significantly different from those of controls.	Ethanol	112-119	nitric oxide synthase 1, neuronal	Mus musculus	39-43
12351742-5	2002	When compared with wild-type mice, the nNOS -/- mice were found to be less sensitive to the sedative effects of ethanol as measured by shorter recovery time from ethanol-induced sleep and did not develop rapid tolerance to ethanol-induced hypothermia, although plasma ethanol concentrations were not significantly different from those of controls.	Ethanol	162-169	nitric oxide synthase 1, neuronal	Mus musculus	39-43
12351742-5	2002	When compared with wild-type mice, the nNOS -/- mice were found to be less sensitive to the sedative effects of ethanol as measured by shorter recovery time from ethanol-induced sleep and did not develop rapid tolerance to ethanol-induced hypothermia, although plasma ethanol concentrations were not significantly different from those of controls.	Ethanol	162-169	nitric oxide synthase 1, neuronal	Mus musculus	39-43
12351742-5	2002	When compared with wild-type mice, the nNOS -/- mice were found to be less sensitive to the sedative effects of ethanol as measured by shorter recovery time from ethanol-induced sleep and did not develop rapid tolerance to ethanol-induced hypothermia, although plasma ethanol concentrations were not significantly different from those of controls.	Ethanol	162-169	nitric oxide synthase 1, neuronal	Mus musculus	39-43
12351742-9	2002	In summary, the nNOS gene is critically involved in the regulation of neurobehavioral effects of alcohol.	Alcohols	97-104	nitric oxide synthase 1, neuronal	Mus musculus	16-20
12234657-0	2002	Deficiency of neuronal nitric oxide synthase (nNOS) worsens alcohol-induced microencephaly and neuronal loss in developing mice.	Alcohols	60-67	nitric oxide synthase 1, neuronal	Mus musculus	14-44
12234657-0	2002	Deficiency of neuronal nitric oxide synthase (nNOS) worsens alcohol-induced microencephaly and neuronal loss in developing mice.	Alcohols	60-67	nitric oxide synthase 1, neuronal	Mus musculus	46-50
12234657-2	2002	We tested the hypothesis that neonatal mice carrying a null mutation for neuronal nitric oxide synthase (nNOS), the enzyme which synthesizes NO in neurons, have increased vulnerability to alcohol-induced microencephaly and neuronal loss.	Alcohols	188-195	nitric oxide synthase 1, neuronal	Mus musculus	73-103
12234657-2	2002	We tested the hypothesis that neonatal mice carrying a null mutation for neuronal nitric oxide synthase (nNOS), the enzyme which synthesizes NO in neurons, have increased vulnerability to alcohol-induced microencephaly and neuronal loss.	Alcohols	188-195	nitric oxide synthase 1, neuronal	Mus musculus	105-109
12234657-7	2002	Quantification of cerebellar neurons revealed that alcohol-induced losses of Purkinje cells and granule cells were both significantly greater in the nNOS(-/-) mice than in wild type.	Alcohols	51-58	nitric oxide synthase 1, neuronal	Mus musculus	149-153
12234657-8	2002	The increased vulnerability of nNOS-deficient neurons to alcohol-induced cell death was confirmed in vitro.	Alcohols	57-64	nitric oxide synthase 1, neuronal	Mus musculus	31-35
12234657-10	2002	At each alcohol concentration, the nNOS(-/-) neurons had a significantly greater cell loss than did the wild-type neurons.	Alcohols	8-15	nitric oxide synthase 1, neuronal	Mus musculus	35-39
12234657-11	2002	The results demonstrate that deficiency of nNOS decreases the ability of developing neurons to survive the toxic effects of alcohol.	Alcohols	124-131	nitric oxide synthase 1, neuronal	Mus musculus	43-47
12181132-6	2002	The anti-inflammatory effects of late EtOH-PC were abolished by treatment with adenosine deaminase, an adenosine A(2) (but not A(1)) receptor antagonist, or a NO synthase (NOS) inhibitor during the period of EtOH-PC.	Ethanol	38-42	nitric oxide synthase 1, neuronal	Mus musculus	159-170
12181132-6	2002	The anti-inflammatory effects of late EtOH-PC were abolished by treatment with adenosine deaminase, an adenosine A(2) (but not A(1)) receptor antagonist, or a NO synthase (NOS) inhibitor during the period of EtOH-PC.	pc	43-45	nitric oxide synthase 1, neuronal	Mus musculus	159-170
12437128-4	2002	Furthermore, we investigated the influence of glucose on the activity of nNOS and the expression of PIN and are able to show that both are increased by glucose stimulation in the beta-cell lines but not in the mouse fibroblastic cell line LTK.	Glucose	152-159	nitric oxide synthase 1, neuronal	Mus musculus	73-77
12135619-3	2002	We also observed that Aroclor 1254 treatment reduced the level of nNOS expression.	Chlorodiphenyl (54% Chlorine)	22-34	nitric oxide synthase 1, neuronal	Mus musculus	66-70
12354305-0	2002	NMDA-induced acetylcholine release in mouse striatum: role of NO synthase isoforms.	N-Methylaspartate	0-4	nitric oxide synthase 1, neuronal	Mus musculus	62-73
12322787-0	2002	Therapeutic effect of neuronal nitric oxide synthase inhibitor (7-nitroindazole) against MPTP neurotoxicity in mice.	7-nitroindazole	64-79	nitric oxide synthase 1, neuronal	Mus musculus	22-52
12322787-0	2002	Therapeutic effect of neuronal nitric oxide synthase inhibitor (7-nitroindazole) against MPTP neurotoxicity in mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	89-93	nitric oxide synthase 1, neuronal	Mus musculus	22-52
12322787-8	2002	These results demonstrate that the protective mechanism by which 7-nitroindazole counteracts MPTP neurotoxicity in mice may be due not only to inhibition of nNOS, but also to MAO-B inhibition.	7-nitroindazole	65-80	nitric oxide synthase 1, neuronal	Mus musculus	157-161
12322787-8	2002	These results demonstrate that the protective mechanism by which 7-nitroindazole counteracts MPTP neurotoxicity in mice may be due not only to inhibition of nNOS, but also to MAO-B inhibition.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	93-97	nitric oxide synthase 1, neuronal	Mus musculus	157-161
12387363-2	2002	Inhibition of NO synthase (NOS) activity in the brain produces a neuroprotective effect against PD induced by MPTP Green tea containing high levels of (-)-epigallocatechin 3-gallate (EGCG) was administered to test whether EGCG attenuates MPTP-induced PD in mice through the inhibition of NOS expression.	mptp green	110-120	nitric oxide synthase 1, neuronal	Mus musculus	14-25
12387363-2	2002	Inhibition of NO synthase (NOS) activity in the brain produces a neuroprotective effect against PD induced by MPTP Green tea containing high levels of (-)-epigallocatechin 3-gallate (EGCG) was administered to test whether EGCG attenuates MPTP-induced PD in mice through the inhibition of NOS expression.	epigallocatechin gallate	183-187	nitric oxide synthase 1, neuronal	Mus musculus	14-25
12387363-2	2002	Inhibition of NO synthase (NOS) activity in the brain produces a neuroprotective effect against PD induced by MPTP Green tea containing high levels of (-)-epigallocatechin 3-gallate (EGCG) was administered to test whether EGCG attenuates MPTP-induced PD in mice through the inhibition of NOS expression.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	110-114	nitric oxide synthase 1, neuronal	Mus musculus	14-25
12387363-5	2002	Both tea and EGCG decreased expressions of nNOS in the substantia nigra.	epigallocatechin gallate	13-17	nitric oxide synthase 1, neuronal	Mus musculus	43-47
12387363-6	2002	Also tea plus MPTP and EGCG plus MPTP treatments decreased expressions of neuronal NO synthase (nNOS) at the similar levels of EGCG treatment group.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	14-18	nitric oxide synthase 1, neuronal	Mus musculus	83-94
12387363-6	2002	Also tea plus MPTP and EGCG plus MPTP treatments decreased expressions of neuronal NO synthase (nNOS) at the similar levels of EGCG treatment group.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	14-18	nitric oxide synthase 1, neuronal	Mus musculus	96-100
12387363-6	2002	Also tea plus MPTP and EGCG plus MPTP treatments decreased expressions of neuronal NO synthase (nNOS) at the similar levels of EGCG treatment group.	epigallocatechin gallate	23-27	nitric oxide synthase 1, neuronal	Mus musculus	83-94
12387363-6	2002	Also tea plus MPTP and EGCG plus MPTP treatments decreased expressions of neuronal NO synthase (nNOS) at the similar levels of EGCG treatment group.	epigallocatechin gallate	23-27	nitric oxide synthase 1, neuronal	Mus musculus	96-100
12387363-6	2002	Also tea plus MPTP and EGCG plus MPTP treatments decreased expressions of neuronal NO synthase (nNOS) at the similar levels of EGCG treatment group.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	33-37	nitric oxide synthase 1, neuronal	Mus musculus	83-94
12387363-6	2002	Also tea plus MPTP and EGCG plus MPTP treatments decreased expressions of neuronal NO synthase (nNOS) at the similar levels of EGCG treatment group.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	33-37	nitric oxide synthase 1, neuronal	Mus musculus	96-100
12387363-7	2002	Therefore, the preventive effects of tea and EGCG may be explained by the inhibition of nNOS in the substantia nigra.	epigallocatechin gallate	45-49	nitric oxide synthase 1, neuronal	Mus musculus	88-92
12201806-8	2002	However, they do support a role for oestrogens, mediated by oestrogen receptor alpha, in regulation and production of neuronal nitric oxide synthase, which in turn may control dopamine agonist release.	Dopamine	176-184	nitric oxide synthase 1, neuronal	Mus musculus	118-148
12165537-5	2002	To determine the role of NO in this process, mice were pretreated with the NO synthase (NOS) inhibitor NG-methyl-L-arginine.	ng-methyl-l-arginine	103-123	nitric oxide synthase 1, neuronal	Mus musculus	75-86
12135619-6	2002	Therefore, these results suggest that PCBs have the potential for dopaminergic neurotoxicity, which may be related with the PCBs-mediated alteration of NO production originating from nNOS at least in part.	Polychlorinated Biphenyls	38-42	nitric oxide synthase 1, neuronal	Mus musculus	183-187
12135619-6	2002	Therefore, these results suggest that PCBs have the potential for dopaminergic neurotoxicity, which may be related with the PCBs-mediated alteration of NO production originating from nNOS at least in part.	Polychlorinated Biphenyls	124-128	nitric oxide synthase 1, neuronal	Mus musculus	183-187
12067851-1	2002	Isotopic techniques were used to test the hypothesis that exercise and nitric oxide synthase (NOS) inhibition have distinct effects on tissue-specific fatty acid and glucose uptakes in a conscious, chronically catheterized mouse model.	Fatty Acids	151-161	nitric oxide synthase 1, neuronal	Mus musculus	71-92
12115690-1	2002	We examined the expression of calcium binding proteins parvalbumin (PV), calretinin (CR), and calbindin D28K (CB), and neuronal nitric oxide synthase (nNOS) in gamma-aminobutyric acid (GABA)ergic neurons of the mouse hippocampus, with particular reference to areal and dorsoventral differences.	gamma-Aminobutyric Acid	160-183	nitric oxide synthase 1, neuronal	Mus musculus	151-155
12067851-1	2002	Isotopic techniques were used to test the hypothesis that exercise and nitric oxide synthase (NOS) inhibition have distinct effects on tissue-specific fatty acid and glucose uptakes in a conscious, chronically catheterized mouse model.	Glucose	166-173	nitric oxide synthase 1, neuronal	Mus musculus	71-92
12081996-4	2002	In addition, we examined the effects of acute specific inhibition of NOS1 with vinyl-L-N-5-(1-imino-3-butenyl)-L-ornithine (L-VNIO, 500 micromol/L).	vinyl-l-n-5-(1-imino-3-butenyl)-l-ornithine	79-122	nitric oxide synthase 1, neuronal	Mus musculus	69-73
12086978-18	2002	These data reveal the relative importance of nNOS, compared to eNOS, as the critical NOS isoform in the control of erectile function and illustrate that the nNOS isoform is required for sildenafil-induced facilitation of erectile responses in vivo in mice.	Sildenafil Citrate	186-196	nitric oxide synthase 1, neuronal	Mus musculus	45-49
12086978-18	2002	These data reveal the relative importance of nNOS, compared to eNOS, as the critical NOS isoform in the control of erectile function and illustrate that the nNOS isoform is required for sildenafil-induced facilitation of erectile responses in vivo in mice.	Sildenafil Citrate	186-196	nitric oxide synthase 1, neuronal	Mus musculus	157-161
12072412-4	2002	We generated a new line of nNOS knockout mice (KN2) lacking exon 6, which codes for the heme-binding domain of nNOS.	Heme	88-92	nitric oxide synthase 1, neuronal	Mus musculus	27-31
12072412-4	2002	We generated a new line of nNOS knockout mice (KN2) lacking exon 6, which codes for the heme-binding domain of nNOS.	Heme	88-92	nitric oxide synthase 1, neuronal	Mus musculus	111-115
12462194-1	2002	Nitric oxide (NO), produced by distinct nitric oxide synthase (NOS) isoforms, and prostaglandins generated by expression of cyclooxygenases are important mediators in tumor progression.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	40-61
12020853-8	2002	These findings indicate that nNOS activity is altered in a complex manner in HD transgenic mice and suggest that these abnormalities occur in the setting of a more global disturbance of calcium-regulated proteins.	Calcium	186-193	nitric oxide synthase 1, neuronal	Mus musculus	29-33
12011984-5	2002	The nitric oxide synthase (NOS) inhibitor, NGmono-methyl-L-arginine (L-NMMA), blunted this effect only in LM3 cells while in LM2 cells the action of CARB was blocked by Nomega hydroxy-L-arginine (L-OH-Arg), which is known to inhibit the arginase pathway.	omega-N-Methylarginine	43-67	nitric oxide synthase 1, neuronal	Mus musculus	4-25
12362417-10	2002	Baseline ECGs and contrary responses to muscarinic blockade by atropine in mice deficient in neuronal nitric oxide synthase (nNOS) suggest that the autonomic dysfunction in mdx mice may be independent of decreased myocardial nNOS.	Atropine	63-71	nitric oxide synthase 1, neuronal	Mus musculus	93-123
12362417-10	2002	Baseline ECGs and contrary responses to muscarinic blockade by atropine in mice deficient in neuronal nitric oxide synthase (nNOS) suggest that the autonomic dysfunction in mdx mice may be independent of decreased myocardial nNOS.	Atropine	63-71	nitric oxide synthase 1, neuronal	Mus musculus	125-129
12769267-3	2002	In different strains of wild type mice and NOS-3 knockouts, urea-resistant (and therefore specific) NOS NADPH diaphorase histochemistry and NOS-1 immunohistochemistry revealed that NOS-1 activity and protein were present in the sarcolemma region of a subpopulation of atrial and ventricular working cardiomyocytes, but not in those of the impulse conducting system.	Urea	60-64	nitric oxide synthase 1, neuronal	Mus musculus	181-186
12011984-5	2002	The nitric oxide synthase (NOS) inhibitor, NGmono-methyl-L-arginine (L-NMMA), blunted this effect only in LM3 cells while in LM2 cells the action of CARB was blocked by Nomega hydroxy-L-arginine (L-OH-Arg), which is known to inhibit the arginase pathway.	omega-N-Methylarginine	69-75	nitric oxide synthase 1, neuronal	Mus musculus	4-25
12011984-5	2002	The nitric oxide synthase (NOS) inhibitor, NGmono-methyl-L-arginine (L-NMMA), blunted this effect only in LM3 cells while in LM2 cells the action of CARB was blocked by Nomega hydroxy-L-arginine (L-OH-Arg), which is known to inhibit the arginase pathway.	Carbachol	149-153	nitric oxide synthase 1, neuronal	Mus musculus	4-25
12011984-5	2002	The nitric oxide synthase (NOS) inhibitor, NGmono-methyl-L-arginine (L-NMMA), blunted this effect only in LM3 cells while in LM2 cells the action of CARB was blocked by Nomega hydroxy-L-arginine (L-OH-Arg), which is known to inhibit the arginase pathway.	hydroxy-l-arginine	176-194	nitric oxide synthase 1, neuronal	Mus musculus	4-25
12011984-5	2002	The nitric oxide synthase (NOS) inhibitor, NGmono-methyl-L-arginine (L-NMMA), blunted this effect only in LM3 cells while in LM2 cells the action of CARB was blocked by Nomega hydroxy-L-arginine (L-OH-Arg), which is known to inhibit the arginase pathway.	l-oh-arg	196-204	nitric oxide synthase 1, neuronal	Mus musculus	4-25
12162457-3	2002	Experiments with nitric oxide synthase (NOS) inhibition and 15N-labeled L-arginine as NOS substrate verify the origin of trapped NO from L-arginine.	Arginine	137-147	nitric oxide synthase 1, neuronal	Mus musculus	17-38
11992469-1	2002	Nitric oxide (NO), a unique biological messenger molecule, is synthesized by three isoforms of the enzyme NO synthase (NOS) and diffuses from the site of production across cellular membranes.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	106-117
12031632-0	2002	Effects of nitric oxide synthase inhibitors 7-NI, L-NAME, and L-NOARG in staircase test.	7-nitroindazole	44-48	nitric oxide synthase 1, neuronal	Mus musculus	11-32
12031632-1	2002	BACKGROUND: The objective of the study was to investigate the effects of the nitric oxide synthase (NOS) inhibitors 7-nitroindazole (7-NI), N(G)-nitro-L-arginine (L-NOARG), and N(G)-nitro-L-arginine methyl ester (L-NAME) on the behavior of mice in the staircase test.	7-nitroindazole	116-131	nitric oxide synthase 1, neuronal	Mus musculus	77-98
12031632-1	2002	BACKGROUND: The objective of the study was to investigate the effects of the nitric oxide synthase (NOS) inhibitors 7-nitroindazole (7-NI), N(G)-nitro-L-arginine (L-NOARG), and N(G)-nitro-L-arginine methyl ester (L-NAME) on the behavior of mice in the staircase test.	7-nitroindazole	133-138	nitric oxide synthase 1, neuronal	Mus musculus	77-98
12031632-1	2002	BACKGROUND: The objective of the study was to investigate the effects of the nitric oxide synthase (NOS) inhibitors 7-nitroindazole (7-NI), N(G)-nitro-L-arginine (L-NOARG), and N(G)-nitro-L-arginine methyl ester (L-NAME) on the behavior of mice in the staircase test.	Nitroarginine	163-170	nitric oxide synthase 1, neuronal	Mus musculus	77-98
12150542-1	2002	Nitric oxide (NO), synthesized by the enzyme nitric oxide synthase (NOS), acts as an intercellular messenger associated with various physiological and pathological events.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	45-66
12105098-5	2002	The METH-induced dopaminergic neurotoxicity may be mediated by the generation of peroxynitrite and can be protected by antioxidants selenium, melatonin, and selective nNOS inhibitor, 7-nitroindazole.	Methamphetamine	4-8	nitric oxide synthase 1, neuronal	Mus musculus	167-171
12105098-5	2002	The METH-induced dopaminergic neurotoxicity may be mediated by the generation of peroxynitrite and can be protected by antioxidants selenium, melatonin, and selective nNOS inhibitor, 7-nitroindazole.	7-nitroindazole	183-198	nitric oxide synthase 1, neuronal	Mus musculus	167-171
11919080-3	2002	We also assessed the contribution of the neuronal (nNOS), the endothelial (eNOS), and the inducible (iNOS) isoforms of nitric oxide synthase (NOS) to tyrosine nitration in skeletal muscles both under normal conditions and in response to severe sepsis.	Tyrosine	150-158	nitric oxide synthase 1, neuronal	Mus musculus	119-140
11900796-1	2002	Cyclosporin A (CsA) and other immunophilin-binding agents are known to inactivate neuronal nitric oxide synthase (nNOS).	Cyclosporine	0-13	nitric oxide synthase 1, neuronal	Mus musculus	82-112
11900796-1	2002	Cyclosporin A (CsA) and other immunophilin-binding agents are known to inactivate neuronal nitric oxide synthase (nNOS).	Cyclosporine	0-13	nitric oxide synthase 1, neuronal	Mus musculus	114-118
11900796-1	2002	Cyclosporin A (CsA) and other immunophilin-binding agents are known to inactivate neuronal nitric oxide synthase (nNOS).	Cyclosporine	15-18	nitric oxide synthase 1, neuronal	Mus musculus	82-112
11900796-1	2002	Cyclosporin A (CsA) and other immunophilin-binding agents are known to inactivate neuronal nitric oxide synthase (nNOS).	Cyclosporine	15-18	nitric oxide synthase 1, neuronal	Mus musculus	114-118
11900796-7	2002	Nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine (LNNA; 10, 40 and 80 mg/kg i.p.)	Nitroarginine	38-59	nitric oxide synthase 1, neuronal	Mus musculus	0-21
11900796-7	2002	Nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine (LNNA; 10, 40 and 80 mg/kg i.p.)	Nitroarginine	61-65	nitric oxide synthase 1, neuronal	Mus musculus	0-21
12009031-12	2002	Nitric oxide (NO), derived from L-argin-ine, is produced by two forms(constitutive and inducible) of nitric oxide synthase (NOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	101-122
12009031-12	2002	Nitric oxide (NO), derived from L-argin-ine, is produced by two forms(constitutive and inducible) of nitric oxide synthase (NOS).	Arginine	32-43	nitric oxide synthase 1, neuronal	Mus musculus	101-122
11967238-8	2002	In mice with genetic deletion of NOS1, low- and high-salt diets caused similar changes of COX-2 immunoreactivity (106% and -52%, P<0.05) than those seen in wild-type mice (43% and -78%, P<0.05).	Salts	53-57	nitric oxide synthase 1, neuronal	Mus musculus	33-37
11867766-1	2002	The specificity of the reactions of nitric oxide (NO) with its neuronal targets is determined in part by the precise localizations of neuronal NO synthase (nNOS) within the cell.	Nitric Oxide	36-48	nitric oxide synthase 1, neuronal	Mus musculus	156-160
11867766-3	2002	Here, we show that the nNOS adapter protein, CAPON, interacts with synapsins I, II, and III through an N-terminal phosphotyrosine-binding domain interaction, which leads to a ternary complex comprising nNOS, CAPON, and synapsin I.	Phosphotyrosine	114-129	nitric oxide synthase 1, neuronal	Mus musculus	23-27
11867766-3	2002	Here, we show that the nNOS adapter protein, CAPON, interacts with synapsins I, II, and III through an N-terminal phosphotyrosine-binding domain interaction, which leads to a ternary complex comprising nNOS, CAPON, and synapsin I.	Phosphotyrosine	114-129	nitric oxide synthase 1, neuronal	Mus musculus	202-206
11901190-1	2002	Nitric oxide (NO) is produced by NO synthase (NOS) in many cells and plays important roles in the neuronal, muscular, cardiovascular, and immune systems.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	33-44
11850347-4	2002	Both NO release and apoptosis could be inhibited by neutralizing anti-IL-1beta antibody or the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine-methyl ester (L-NAME), demonstrating the requirement for IL-1beta-mediated NO release in silica-induced apoptosis.	NG-Nitroarginine Methyl Ester	123-157	nitric oxide synthase 1, neuronal	Mus musculus	95-106
11890736-1	2002	In some neurological disorders, excessive nitric oxide (NO, nitrogen monoxide) produced by inducible and/or neuronal nitric oxide synthases (iNOS and nNOS) is able to combine with superoxide (O(minus sign)(2)) to form peroxynitrite (ONOO(minus sign)), which can then induce p53-dependent neural apoptosis.	Nitric Oxide	42-54	nitric oxide synthase 1, neuronal	Mus musculus	150-154
11890736-1	2002	In some neurological disorders, excessive nitric oxide (NO, nitrogen monoxide) produced by inducible and/or neuronal nitric oxide synthases (iNOS and nNOS) is able to combine with superoxide (O(minus sign)(2)) to form peroxynitrite (ONOO(minus sign)), which can then induce p53-dependent neural apoptosis.	Nitric Oxide	60-77	nitric oxide synthase 1, neuronal	Mus musculus	150-154
11890736-1	2002	In some neurological disorders, excessive nitric oxide (NO, nitrogen monoxide) produced by inducible and/or neuronal nitric oxide synthases (iNOS and nNOS) is able to combine with superoxide (O(minus sign)(2)) to form peroxynitrite (ONOO(minus sign)), which can then induce p53-dependent neural apoptosis.	Superoxides	180-190	nitric oxide synthase 1, neuronal	Mus musculus	150-154
11890736-1	2002	In some neurological disorders, excessive nitric oxide (NO, nitrogen monoxide) produced by inducible and/or neuronal nitric oxide synthases (iNOS and nNOS) is able to combine with superoxide (O(minus sign)(2)) to form peroxynitrite (ONOO(minus sign)), which can then induce p53-dependent neural apoptosis.	Peroxynitrous Acid	218-231	nitric oxide synthase 1, neuronal	Mus musculus	150-154
11890736-1	2002	In some neurological disorders, excessive nitric oxide (NO, nitrogen monoxide) produced by inducible and/or neuronal nitric oxide synthases (iNOS and nNOS) is able to combine with superoxide (O(minus sign)(2)) to form peroxynitrite (ONOO(minus sign)), which can then induce p53-dependent neural apoptosis.	onoo	233-237	nitric oxide synthase 1, neuronal	Mus musculus	150-154
11850347-4	2002	Both NO release and apoptosis could be inhibited by neutralizing anti-IL-1beta antibody or the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine-methyl ester (L-NAME), demonstrating the requirement for IL-1beta-mediated NO release in silica-induced apoptosis.	NG-Nitroarginine Methyl Ester	159-165	nitric oxide synthase 1, neuronal	Mus musculus	95-106
11788389-10	2002	In conclusion, nNOS-derived NO, via activation of cGMP, together with prostaglandins, maintains flow-induced dilation in coronary arteries of male eNOS-KO mice.	Cyclic GMP	50-54	nitric oxide synthase 1, neuronal	Mus musculus	15-19
11850522-2	2002	Experiments were performed in wild-type (WT) and mutant mice deficient in nitric oxide synthase-1 (NOS-1), as well as in WT mice administered the NOS-1 inhibitor 7-nitroindazole (7-NI; 50 mg x kg(-1); I.P.).	7-nitroindazole	162-177	nitric oxide synthase 1, neuronal	Mus musculus	146-151
11990722-0	2002	Effect of the neuronal nitric oxide synthase inhibitor 7-nitroindazole on methylphenidate-induced hyperlocomotion in mice.	7-nitroindazole	55-70	nitric oxide synthase 1, neuronal	Mus musculus	14-44
11990722-0	2002	Effect of the neuronal nitric oxide synthase inhibitor 7-nitroindazole on methylphenidate-induced hyperlocomotion in mice.	Methylphenidate	74-89	nitric oxide synthase 1, neuronal	Mus musculus	14-44
11990722-3	2002	In the first experiment, mice were administered either vehicle or the nNOS inhibitor 7-nitroindazole (7-NI; 25 mg/kg), prior to the administration of MPD (10 or 40 mg/kg), for five consecutive days; injections were paired with the test cage ("novel environment") on days 1 and 5.	7-nitroindazole	85-100	nitric oxide synthase 1, neuronal	Mus musculus	70-74
11934255-1	2002	Nitric oxide (NO) is a potent bioactive molecule produced in the presence of NO synthase (NOS) enzymes, which mediates numerous physiological functions under constitutive conditions.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	77-88
11829530-6	2002	The principal neurons of such nNOS(-/-)-mice, which are equivalent to the nNOS-containing neurons in the LDT of wild-type mice exhibited a decreased nitrotyrosine-IR and an increased phosphotyrosine-IR if compared to those of wild-type mice.	3-nitrotyrosine	149-162	nitric oxide synthase 1, neuronal	Mus musculus	30-34
11829530-6	2002	The principal neurons of such nNOS(-/-)-mice, which are equivalent to the nNOS-containing neurons in the LDT of wild-type mice exhibited a decreased nitrotyrosine-IR and an increased phosphotyrosine-IR if compared to those of wild-type mice.	Phosphotyrosine	183-198	nitric oxide synthase 1, neuronal	Mus musculus	30-34
11829530-8	2002	When the residual nNOS activity in nNOS(-/-)-mice was inhibited by treatment with N-omega-nitro-L-arginine methyl ester (L-NAME) the principal neurons displayed a moderate MAP-2 and NF-staining.	NG-Nitroarginine Methyl Ester	82-119	nitric oxide synthase 1, neuronal	Mus musculus	18-22
11829530-8	2002	When the residual nNOS activity in nNOS(-/-)-mice was inhibited by treatment with N-omega-nitro-L-arginine methyl ester (L-NAME) the principal neurons displayed a moderate MAP-2 and NF-staining.	NG-Nitroarginine Methyl Ester	82-119	nitric oxide synthase 1, neuronal	Mus musculus	35-39
11829530-8	2002	When the residual nNOS activity in nNOS(-/-)-mice was inhibited by treatment with N-omega-nitro-L-arginine methyl ester (L-NAME) the principal neurons displayed a moderate MAP-2 and NF-staining.	NG-Nitroarginine Methyl Ester	121-127	nitric oxide synthase 1, neuronal	Mus musculus	18-22
11829530-8	2002	When the residual nNOS activity in nNOS(-/-)-mice was inhibited by treatment with N-omega-nitro-L-arginine methyl ester (L-NAME) the principal neurons displayed a moderate MAP-2 and NF-staining.	NG-Nitroarginine Methyl Ester	121-127	nitric oxide synthase 1, neuronal	Mus musculus	35-39
11936620-10	2002	Furthermore, mice treated with celecoxib expressed more Nitric Oxide Synthase-1 (NOS-1), a crucial component of the innate immune system in the restriction of VSV propagation.	Celecoxib	31-40	nitric oxide synthase 1, neuronal	Mus musculus	56-79
11936620-10	2002	Furthermore, mice treated with celecoxib expressed more Nitric Oxide Synthase-1 (NOS-1), a crucial component of the innate immune system in the restriction of VSV propagation.	Celecoxib	31-40	nitric oxide synthase 1, neuronal	Mus musculus	81-86
11788389-10	2002	In conclusion, nNOS-derived NO, via activation of cGMP, together with prostaglandins, maintains flow-induced dilation in coronary arteries of male eNOS-KO mice.	Prostaglandins	70-84	nitric oxide synthase 1, neuronal	Mus musculus	15-19
11709397-6	2001	Selective nNOS inhibitors, vinyl-L-niohydrochloride or 1-2-trifluoromethylphenyl imidazole, or the guanylyl cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one significantly (P < 0.05) attenuated the decrease in HR with VNS at 3 Hz in nNOS+/+ atria.	1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one	127-170	nitric oxide synthase 1, neuronal	Mus musculus	249-253
11853122-1	2002	This study was designed to determine the possible potentiation of catalepsy behavior after coadministration of N(G)-nitro-L-arginine (L-NOARG), an inhibitor of nitric oxide synthase (NOS), and tiapride, a specific antagonist for D2 receptors, in male mice.	Nitroarginine	111-132	nitric oxide synthase 1, neuronal	Mus musculus	160-181
11853122-1	2002	This study was designed to determine the possible potentiation of catalepsy behavior after coadministration of N(G)-nitro-L-arginine (L-NOARG), an inhibitor of nitric oxide synthase (NOS), and tiapride, a specific antagonist for D2 receptors, in male mice.	Nitroarginine	134-141	nitric oxide synthase 1, neuronal	Mus musculus	160-181
11999381-5	2002	However, the increase was returned to a normal level by the NOS (nitric oxide synthase) inhibitor, L-NMMA, indicating that the NO was formed via a biosynthetic pathway.	omega-N-Methylarginine	99-105	nitric oxide synthase 1, neuronal	Mus musculus	65-86
11993849-0	2002	The specificity of the histochemical NADPH diaphorase reaction for nitric oxide synthase-1 in skeletal muscles is increased in the presence of urea.	Urea	143-147	nitric oxide synthase 1, neuronal	Mus musculus	67-90
11993849-4	2002	All myofibers of both C57 mice and NOS-1 knockout mice contained significant intrafibrar NADPH diaphorase activity which was inhibited to almost background levels when 2 M urea was added to the incubation medium.	Urea	172-176	nitric oxide synthase 1, neuronal	Mus musculus	35-40
11993849-7	2002	The catalytic activity in tongue and tibialis anterior muscle was reduced in presence of 2 M urea to approximately 27% in C57 mice and to 7-17% in NOS-1 knockout mice, respectively.	Urea	93-97	nitric oxide synthase 1, neuronal	Mus musculus	147-152
11993849-10	2002	In conclusion, we recommend the addition of 2 M urea to the incubation medium to increase the specificity of the NADPH diaphorase reaction to localise NOS-1 with the use of catalytic histochemistry.	Urea	48-52	nitric oxide synthase 1, neuronal	Mus musculus	151-156
12121307-3	2002	It also is known that two isoforms of nitric oxide (NO) synthetase (nNOS and eNOS) are essential for the long-term potentiation (LTP), a plastic response of neurons.	Nitric Oxide	38-50	nitric oxide synthase 1, neuronal	Mus musculus	68-72
11773322-4	2002	In isolated smooth muscle cells from wild-type, eNOS knockout and nNOS knockout mice, the relaxation induced by VIP (10(-9) M) was inhibited by approximately 70-95 % by both the non-selective NOS inhibitor N(G)-nitro-L-arginine (L-NA; 10(-4) M) and the selective inducible NOS inhibitor N-(3-(aminomethyl)-benzyl)acetamidine (1400W; 10(-6) M).	Nitroarginine	206-227	nitric oxide synthase 1, neuronal	Mus musculus	66-70
11744335-4	2001	Nitric oxide synthase activity was measured in isolated brain and liver mitochondria using the arginine to citrulline conversion assay.	Arginine	95-103	nitric oxide synthase 1, neuronal	Mus musculus	0-21
11744335-4	2001	Nitric oxide synthase activity was measured in isolated brain and liver mitochondria using the arginine to citrulline conversion assay.	Citrulline	107-117	nitric oxide synthase 1, neuronal	Mus musculus	0-21
11726818-1	2001	BACKGROUND: Recent studies from our laboratory have demonstrated that in vivo contractile function of rejecting mouse heterotopic abdominal heart allografts 5 days after transplantation is depressed to 40% of that of syngenic controls, and that this depression of function is prevented by the nitric oxide synthase (NOS) inhibitor NG-monomethyl-l-arginine.	omega-N-Methylarginine	331-355	nitric oxide synthase 1, neuronal	Mus musculus	293-314
11739248-14	2001	Pretreatment with the nitric oxide synthase (NOS) inhibitor 7-NI (50 mg kg(-1)x3) produced neuroprotection, but also significant hypothermia.	7-nitroindazole	60-64	nitric oxide synthase 1, neuronal	Mus musculus	22-43
11748861-3	2001	There has been much interest in the role of nitric oxide (NO(*)) in the pathogenesis of these diseases because the enzyme that synthesizes NO(*), nitric oxide synthase (NOS), is associated with the DGC.	Nitric Oxide	44-56	nitric oxide synthase 1, neuronal	Mus musculus	146-167
11689164-2	2001	Both of these findings potentially implicate nitric oxide (NO) and its converting enzyme, nitric oxide synthase (NOS), in HD.	Nitric Oxide	45-57	nitric oxide synthase 1, neuronal	Mus musculus	90-111
11687280-0	2001	Spinal cord nitric oxide synthase and heme oxygenase limit morphine induced analgesia.	Morphine	59-67	nitric oxide synthase 1, neuronal	Mus musculus	12-33
11695891-0	2001	Crystal structure of nitric oxide synthase bound to nitro indazole reveals a novel inactivation mechanism.	3-NITRO-1H-INDAZOLE	52-66	nitric oxide synthase 1, neuronal	Mus musculus	21-42
11695891-1	2001	Nitric oxide is generated under normal and pathophysiological conditions by three distinct isoforms of nitric oxide synthase (NOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	103-124
11687280-1	2001	Spinal cord tissue contains two enzyme systems capable of producing monoxide gases which in turn are linked to the stimulation of soluble guanylate cyclase, nitric oxide synthase (NOS) which produces NO and heme oxygenase (HO) which produces CO.	Carbon Monoxide	68-76	nitric oxide synthase 1, neuronal	Mus musculus	157-178
11687280-1	2001	Spinal cord tissue contains two enzyme systems capable of producing monoxide gases which in turn are linked to the stimulation of soluble guanylate cyclase, nitric oxide synthase (NOS) which produces NO and heme oxygenase (HO) which produces CO.	Carbon Monoxide	242-244	nitric oxide synthase 1, neuronal	Mus musculus	157-178
11708847-10	2001	Diazoxide pretreatment significantly increased nuclear translocation of p65 which was blocked by protein kinase C (PKC) or nitric oxide synthase (NOS) inhibition.	Diazoxide	0-9	nitric oxide synthase 1, neuronal	Mus musculus	123-144
11703584-10	2001	However, in nNOS +/+ mice, 7-nitroindazole (7-NI) perfused into the macula densa significantly potentiated the TGF response (P = 0.001), while in nNOS -/- mice, this potentiation was absent.	7-nitroindazole	27-42	nitric oxide synthase 1, neuronal	Mus musculus	12-16
11703584-10	2001	However, in nNOS +/+ mice, 7-nitroindazole (7-NI) perfused into the macula densa significantly potentiated the TGF response (P = 0.001), while in nNOS -/- mice, this potentiation was absent.	7-nitroindazole	44-48	nitric oxide synthase 1, neuronal	Mus musculus	12-16
11703584-17	2001	Third, the results obtained in the +/+ and -/- mice also confirm that the effect of 7-NI is due to inhibition of macula densa nNOS.	7-nitroindazole	84-88	nitric oxide synthase 1, neuronal	Mus musculus	126-130
11703584-18	2001	Finally, during low sodium intake (without induction of TGF), the regulation of basal Af-Art resistance by macula densa nNOS suggests that NO in the macula densa helps maintain renal blood flow during the high renin secretion caused by low sodium intake.	Sodium	240-246	nitric oxide synthase 1, neuronal	Mus musculus	120-124
11703587-1	2001	BACKGROUND: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS) that accumulates in renal insufficiency and may be a uremic toxin.	dimethylarginine	23-39	nitric oxide synthase 1, neuronal	Mus musculus	77-98
11703587-1	2001	BACKGROUND: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS) that accumulates in renal insufficiency and may be a uremic toxin.	N,N-dimethylarginine	41-45	nitric oxide synthase 1, neuronal	Mus musculus	77-98
11745948-1	2001	In skeletal muscle fibers, nitric oxide is synthesized by neuronal nitric oxide synthase (nNOS), which normally associates with the dystrophin complex in close proximity to the sarcolemma.	Nitric Oxide	27-39	nitric oxide synthase 1, neuronal	Mus musculus	58-88
11745948-1	2001	In skeletal muscle fibers, nitric oxide is synthesized by neuronal nitric oxide synthase (nNOS), which normally associates with the dystrophin complex in close proximity to the sarcolemma.	Nitric Oxide	27-39	nitric oxide synthase 1, neuronal	Mus musculus	90-94
11597776-6	2001	Pre-administration of the selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), which suppressed the delayed neuronal death as well as astrogliosis in hippocampus of seizure-experienced animals, dramatically repressed the delayed induction of p38beta MAPK in astrocytes.	7-nitroindazole	85-100	nitric oxide synthase 1, neuronal	Mus musculus	36-66
11720083-1	2001	Genetically obese (ob/ob) mice were employed for the study of the effect of metformin on activity and expression of nitric oxide synthase (NOS ) in vitro and in vivo.	Metformin	76-85	nitric oxide synthase 1, neuronal	Mus musculus	116-137
11597776-6	2001	Pre-administration of the selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), which suppressed the delayed neuronal death as well as astrogliosis in hippocampus of seizure-experienced animals, dramatically repressed the delayed induction of p38beta MAPK in astrocytes.	7-nitroindazole	85-100	nitric oxide synthase 1, neuronal	Mus musculus	68-72
11597776-6	2001	Pre-administration of the selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), which suppressed the delayed neuronal death as well as astrogliosis in hippocampus of seizure-experienced animals, dramatically repressed the delayed induction of p38beta MAPK in astrocytes.	7-nitroindazole	102-106	nitric oxide synthase 1, neuronal	Mus musculus	36-66
11597776-6	2001	Pre-administration of the selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), which suppressed the delayed neuronal death as well as astrogliosis in hippocampus of seizure-experienced animals, dramatically repressed the delayed induction of p38beta MAPK in astrocytes.	7-nitroindazole	102-106	nitric oxide synthase 1, neuronal	Mus musculus	68-72
11591728-32	2001	Elucidation of PMCA as an interaction partner and major regulator of NOS-I provides evidence for a new dimension of integration between calcium and NO signaling pathways.	Calcium	136-143	nitric oxide synthase 1, neuronal	Mus musculus	69-74
11602186-6	2001	Further studies revealed that the NO synthase (NOS) inhibitor, 7-nitroindazole (7-NI), reduced significantly thapsigargin-induced Ca(2+) release and capacitative Ca(2+) entry and reversed thapsigargin inhibition of the AC Type 5/6 isoform (AC5/6).	7-nitroindazole	63-78	nitric oxide synthase 1, neuronal	Mus musculus	34-45
11602186-6	2001	Further studies revealed that the NO synthase (NOS) inhibitor, 7-nitroindazole (7-NI), reduced significantly thapsigargin-induced Ca(2+) release and capacitative Ca(2+) entry and reversed thapsigargin inhibition of the AC Type 5/6 isoform (AC5/6).	7-nitroindazole	80-84	nitric oxide synthase 1, neuronal	Mus musculus	34-45
11602186-6	2001	Further studies revealed that the NO synthase (NOS) inhibitor, 7-nitroindazole (7-NI), reduced significantly thapsigargin-induced Ca(2+) release and capacitative Ca(2+) entry and reversed thapsigargin inhibition of the AC Type 5/6 isoform (AC5/6).	Thapsigargin	109-121	nitric oxide synthase 1, neuronal	Mus musculus	34-45
11602186-6	2001	Further studies revealed that the NO synthase (NOS) inhibitor, 7-nitroindazole (7-NI), reduced significantly thapsigargin-induced Ca(2+) release and capacitative Ca(2+) entry and reversed thapsigargin inhibition of the AC Type 5/6 isoform (AC5/6).	Thapsigargin	188-200	nitric oxide synthase 1, neuronal	Mus musculus	34-45
11461780-1	2001	Crocidolite fibers stimulated nitric oxide synthase (NOS) activity and expression in glial and alveolar murine macrophages: this effect was inhibited by iron supplementation and enhanced by iron chelation.	Asbestos, Crocidolite	0-11	nitric oxide synthase 1, neuronal	Mus musculus	30-51
11590196-7	2001	Inhibition of nitric oxide synthase (NOS) isoforms with L-NAME or aminoguanidine blocked time-dependent increases in HIV gene expression in activated macrophages cultured ex vivo.	NG-Nitroarginine Methyl Ester	56-62	nitric oxide synthase 1, neuronal	Mus musculus	14-35
11590196-7	2001	Inhibition of nitric oxide synthase (NOS) isoforms with L-NAME or aminoguanidine blocked time-dependent increases in HIV gene expression in activated macrophages cultured ex vivo.	pimagedine	66-80	nitric oxide synthase 1, neuronal	Mus musculus	14-35
11585554-2	2001	Production of nitric oxide in the nNOS-containing neurons is sensitive to dopamine stimulation.	Nitric Oxide	14-26	nitric oxide synthase 1, neuronal	Mus musculus	34-38
11585554-2	2001	Production of nitric oxide in the nNOS-containing neurons is sensitive to dopamine stimulation.	Dopamine	74-82	nitric oxide synthase 1, neuronal	Mus musculus	34-38
11585554-3	2001	Using quantitative in situ hybridization, the present study investigated the alteration in basal nNOS mRNA expression in striatal nNOS-containing neurons of mice treated with the psychostimulant amphetamine or a full D1 dopamine receptor agonist, SKF-82958.	Amphetamine	195-206	nitric oxide synthase 1, neuronal	Mus musculus	97-101
11585554-3	2001	Using quantitative in situ hybridization, the present study investigated the alteration in basal nNOS mRNA expression in striatal nNOS-containing neurons of mice treated with the psychostimulant amphetamine or a full D1 dopamine receptor agonist, SKF-82958.	Amphetamine	195-206	nitric oxide synthase 1, neuronal	Mus musculus	130-134
11585554-4	2001	A single systemic injection of amphetamine induced a dose-related change in striatal nNOS mRNA expression.	Amphetamine	31-42	nitric oxide synthase 1, neuronal	Mus musculus	85-89
11585554-5	2001	Whereas amphetamine at 4 mg/kg decreased basal levels of nNOS mRNA in both the dorsal (caudoputamen) and ventral (nucleus accumbens) striatum, the drug at a higher dose (12 mg/kg) increased nNOS expression in the two regions.	Amphetamine	8-19	nitric oxide synthase 1, neuronal	Mus musculus	57-61
11585554-7	2001	These data indicate that constitutive nNOS expression in nitric oxide-producing neurons of the mouse striatum is regulated by dopaminergic transmission.	Nitric Oxide	57-69	nitric oxide synthase 1, neuronal	Mus musculus	38-42
11585554-8	2001	Altered nNOS expression may result in changes in nitric oxide synthesis and thus contribute to biological actions of dopamine stimulants.	Nitric Oxide	49-61	nitric oxide synthase 1, neuronal	Mus musculus	8-12
11585554-8	2001	Altered nNOS expression may result in changes in nitric oxide synthesis and thus contribute to biological actions of dopamine stimulants.	Dopamine	117-125	nitric oxide synthase 1, neuronal	Mus musculus	8-12
11564648-8	2001	Superfusion with 7-nitroindazole (100 microM), a selective inhibitor of nNOS, had no effect on leukocyte adhesion in wild-type animals.	7-nitroindazole	17-32	nitric oxide synthase 1, neuronal	Mus musculus	72-76
11564662-2	2001	Our previous results showed that the non-selective nitric oxide synthase (NOS) inhibitor L-N(G)-nitroarginine (L-NOARG) and the selective inducible NOS (iNOS) inhibitor N-(3-(acetaminomethyl)-benzyl)acetamidine (1400W) inhibited the relaxant effect of vasoactive intestinal polypeptide (VIP) in isolated smooth muscle cells of the mouse gastric fundus, suggesting the involvement of iNOS.	l-n(g)-nitroarginine	89-109	nitric oxide synthase 1, neuronal	Mus musculus	51-72
11536326-5	2001	We also demonstrated that the delayed induction of alpha B-crystallin and HSP27 immunoreactivities in the hippocampus of epileptic animals was repressed to the levels seen in control animals with preadministration of the selective nNOS inhibitor 7-nitroindazole (7-NI).	7-nitroindazole	246-261	nitric oxide synthase 1, neuronal	Mus musculus	231-235
11536326-5	2001	We also demonstrated that the delayed induction of alpha B-crystallin and HSP27 immunoreactivities in the hippocampus of epileptic animals was repressed to the levels seen in control animals with preadministration of the selective nNOS inhibitor 7-nitroindazole (7-NI).	7-nitroindazole	263-267	nitric oxide synthase 1, neuronal	Mus musculus	231-235
11676198-1	2001	The aim of the present study was to characterize the increase in tetrahydrobiopterin (BH4), which is a cofactor for nitric oxide synthase (NOS), by carboxy-PTIO, a scavenger of nitric oxide (NO), in vascular endothelial cells.	sapropterin	65-84	nitric oxide synthase 1, neuronal	Mus musculus	116-137
11676198-1	2001	The aim of the present study was to characterize the increase in tetrahydrobiopterin (BH4), which is a cofactor for nitric oxide synthase (NOS), by carboxy-PTIO, a scavenger of nitric oxide (NO), in vascular endothelial cells.	sapropterin	86-89	nitric oxide synthase 1, neuronal	Mus musculus	116-137
11461780-1	2001	Crocidolite fibers stimulated nitric oxide synthase (NOS) activity and expression in glial and alveolar murine macrophages: this effect was inhibited by iron supplementation and enhanced by iron chelation.	Iron	153-157	nitric oxide synthase 1, neuronal	Mus musculus	30-51
11461931-4	2001	Luminal application of the nonselective NOS inhibitor nitro-L-arginine (10(-3) and 10(-2) M) enhanced the perfusion-dependent fall in stop-flow pressure in nNOS +/+ (7 +/- 1 to 13 +/- 2 mmHg; P < 0.05) but not in nNOS -/- (7 +/- 1 to 8 +/- 1 mmHg; not significant) mice.	Nitroarginine	54-70	nitric oxide synthase 1, neuronal	Mus musculus	156-160
11461931-4	2001	Luminal application of the nonselective NOS inhibitor nitro-L-arginine (10(-3) and 10(-2) M) enhanced the perfusion-dependent fall in stop-flow pressure in nNOS +/+ (7 +/- 1 to 13 +/- 2 mmHg; P < 0.05) but not in nNOS -/- (7 +/- 1 to 8 +/- 1 mmHg; not significant) mice.	Nitroarginine	54-70	nitric oxide synthase 1, neuronal	Mus musculus	216-220
11461931-7	2001	The data indicate that nNOS in MD tonically attenuates the GFR-lowering influence of ambient luminal NaCl, which may serve to increase the fluid and electrolyte load to the distal tubule, consistent with a role of MD nNOS in tubuloglomerular feedback resetting.	Sodium Chloride	101-105	nitric oxide synthase 1, neuronal	Mus musculus	23-27
11278285-6	2001	Furthermore, we show that inhibition of neuronal nitric-oxide synthase (nNOS) by 7-nitroindazole is sufficient to prevent retinal degeneration implicating a key role for neuronal nitric oxide (NO) in this model.	7-nitroindazole	81-96	nitric oxide synthase 1, neuronal	Mus musculus	40-70
11511520-4	2001	Following sst2 activation by the somatostatin analog RC-160, SHP-1 rapidly recruits nNOS tyrosine dephosphorylates and activates it.	Tyrosine	89-97	nitric oxide synthase 1, neuronal	Mus musculus	84-88
11511520-7	2001	In mouse pancreatic acini, RC-160 treatment reduces nNOS tyrosine phosphorylation accompanied by an increase of its activity.	Tyrosine	57-65	nitric oxide synthase 1, neuronal	Mus musculus	52-56
11278285-6	2001	Furthermore, we show that inhibition of neuronal nitric-oxide synthase (nNOS) by 7-nitroindazole is sufficient to prevent retinal degeneration implicating a key role for neuronal nitric oxide (NO) in this model.	7-nitroindazole	81-96	nitric oxide synthase 1, neuronal	Mus musculus	72-76
11278285-6	2001	Furthermore, we show that inhibition of neuronal nitric-oxide synthase (nNOS) by 7-nitroindazole is sufficient to prevent retinal degeneration implicating a key role for neuronal nitric oxide (NO) in this model.	Nitric Oxide	179-191	nitric oxide synthase 1, neuronal	Mus musculus	40-70
11278285-6	2001	Furthermore, we show that inhibition of neuronal nitric-oxide synthase (nNOS) by 7-nitroindazole is sufficient to prevent retinal degeneration implicating a key role for neuronal nitric oxide (NO) in this model.	Nitric Oxide	179-191	nitric oxide synthase 1, neuronal	Mus musculus	72-76
11337272-4	2001	Overexpression of mutant p53 protein, a p53 point mutation at codon 248 with transition from CGG to TGG, and amplification of the erbB-1 oncogene/epidermal growth factor receptor gene were also observed in NOS-1 cells.	GAMMA-GLUTAMYL-S-(1,2-DICARBOXYETHYL)CYSTEINYLGLYCINE	100-103	nitric oxide synthase 1, neuronal	Mus musculus	206-211
11406294-2	2001	Cellular NO production depends absolutely on the availability of arginine, a substrate of NO synthase (NOS).	Arginine	65-73	nitric oxide synthase 1, neuronal	Mus musculus	90-101
11462792-10	2001	We show that a selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), significantly protect against the formation of 3-NT as well as striatal dopamine depletion.	7-nitroindazole	74-89	nitric oxide synthase 1, neuronal	Mus musculus	25-55
11462792-10	2001	We show that a selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), significantly protect against the formation of 3-NT as well as striatal dopamine depletion.	7-nitroindazole	74-89	nitric oxide synthase 1, neuronal	Mus musculus	57-61
11462792-10	2001	We show that a selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), significantly protect against the formation of 3-NT as well as striatal dopamine depletion.	7-nitroindazole	91-95	nitric oxide synthase 1, neuronal	Mus musculus	25-55
11462792-10	2001	We show that a selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), significantly protect against the formation of 3-NT as well as striatal dopamine depletion.	7-nitroindazole	91-95	nitric oxide synthase 1, neuronal	Mus musculus	57-61
11462792-10	2001	We show that a selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), significantly protect against the formation of 3-NT as well as striatal dopamine depletion.	3-nitrotyrosine	145-149	nitric oxide synthase 1, neuronal	Mus musculus	25-55
11462792-10	2001	We show that a selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), significantly protect against the formation of 3-NT as well as striatal dopamine depletion.	3-nitrotyrosine	145-149	nitric oxide synthase 1, neuronal	Mus musculus	57-61
11462792-10	2001	We show that a selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), significantly protect against the formation of 3-NT as well as striatal dopamine depletion.	Dopamine	170-178	nitric oxide synthase 1, neuronal	Mus musculus	25-55
11462792-10	2001	We show that a selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), significantly protect against the formation of 3-NT as well as striatal dopamine depletion.	Dopamine	170-178	nitric oxide synthase 1, neuronal	Mus musculus	57-61
11398148-8	2001	NO synthase (NOS) activity was shown in alpha Tc6 cells by l-citrulline formation assay.	Citrulline	59-71	nitric oxide synthase 1, neuronal	Mus musculus	0-11
11437984-2	2001	The interval between CMMCs was decreased from approximately 3 min in control solution, by approximately 55% in a nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine (L-NNA; 100 micromol L-1).	Nitroarginine	152-170	nitric oxide synthase 1, neuronal	Mus musculus	113-134
11437984-2	2001	The interval between CMMCs was decreased from approximately 3 min in control solution, by approximately 55% in a nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine (L-NNA; 100 micromol L-1).	Nitroarginine	172-177	nitric oxide synthase 1, neuronal	Mus musculus	113-134
11373254-0	2001	The effects of the nitric oxide synthase inhibitor 7-nitroindazole on the behaviour of mice after chronic ethanol administration.	7-nitroindazole	51-66	nitric oxide synthase 1, neuronal	Mus musculus	19-40
11158630-0	2001	Brain serotonin dysfunction accounts for aggression in male mice lacking neuronal nitric oxide synthase.	Serotonin	6-15	nitric oxide synthase 1, neuronal	Mus musculus	73-103
11379045-4	2001	NG-monomethyl-L-arginine (L-NMMA) and EGTA inhibited the cytokine effect on amylase secretion, involving the participation of a calcium-dependent isoform of nitric oxide synthase (NOS).	omega-N-Methylarginine	0-24	nitric oxide synthase 1, neuronal	Mus musculus	157-178
11379045-4	2001	NG-monomethyl-L-arginine (L-NMMA) and EGTA inhibited the cytokine effect on amylase secretion, involving the participation of a calcium-dependent isoform of nitric oxide synthase (NOS).	omega-N-Methylarginine	26-32	nitric oxide synthase 1, neuronal	Mus musculus	157-178
11379045-4	2001	NG-monomethyl-L-arginine (L-NMMA) and EGTA inhibited the cytokine effect on amylase secretion, involving the participation of a calcium-dependent isoform of nitric oxide synthase (NOS).	Egtazic Acid	38-42	nitric oxide synthase 1, neuronal	Mus musculus	157-178
11379045-4	2001	NG-monomethyl-L-arginine (L-NMMA) and EGTA inhibited the cytokine effect on amylase secretion, involving the participation of a calcium-dependent isoform of nitric oxide synthase (NOS).	Calcium	128-135	nitric oxide synthase 1, neuronal	Mus musculus	157-178
11432693-3	2001	OBJECTIVE AND METHODS: The primary objective was to determine whether neuronal NO synthase (nNOS) is involved in PCP-induced behaviours and neuronal activation, as measured by the expression of c-Fos.	Phencyclidine	113-116	nitric oxide synthase 1, neuronal	Mus musculus	92-96
11432693-4	2001	After characterizing a PCP mouse model (dose-response study, Experiment 1), we measured PCP-induced effects in mice treated with nNOS antisense oligodeoxynucleotides (AS-ODNs) (Experiment 2), and in nNOS knockout (nNOS-/-) mice (Experiment 3).	Phencyclidine	88-91	nitric oxide synthase 1, neuronal	Mus musculus	129-133
11432693-8	2001	In the nNOS-/- mice, PCP induced less behaviour and a decrease in Fos-LIR in the frontal cortex and midline limbic areas, when compared to wild-type littermate controls.	Phencyclidine	21-24	nitric oxide synthase 1, neuronal	Mus musculus	7-11
11432693-10	2001	Furthermore, we show that an intact nNOS system is necessary to obtain PCP-induced effects.	Phencyclidine	71-74	nitric oxide synthase 1, neuronal	Mus musculus	36-40
11312647-7	2001	Inhibitors of inducible nitric oxide synthase (NOS) abrogated PCP-potentiated CMH, although repetitive PCP treatment alone did not increase nitric oxide synthesis systemically or locally in hepatic tissue nor did lipopolysaccharide induction of NOS (without PCP) directly potentiate CMH.	Phencyclidine	62-65	nitric oxide synthase 1, neuronal	Mus musculus	24-45
11312647-7	2001	Inhibitors of inducible nitric oxide synthase (NOS) abrogated PCP-potentiated CMH, although repetitive PCP treatment alone did not increase nitric oxide synthesis systemically or locally in hepatic tissue nor did lipopolysaccharide induction of NOS (without PCP) directly potentiate CMH.	4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide	78-81	nitric oxide synthase 1, neuronal	Mus musculus	24-45
11526978-4	2001	Pretreatment with BZ receptor antagonist flumazenil (FLU), the GABA(A) receptor antagonist SR-95531 or the selective neuronal nitric oxide (NO) synthase (nNOS) inhibitor 7-nitroindazole (7-NI) all antagonized anxiolytic effects of N20 and CP.	7-nitroindazole	170-185	nitric oxide synthase 1, neuronal	Mus musculus	154-158
11238274-1	2001	BACKGROUND: Altered endothelial cell nitric oxide (NO(*)) production in atherosclerosis may be due to a reduction of intracellular tetrahydrobiopterin, which is a critical cofactor for NO synthase (NOS).	Nitric Oxide	37-49	nitric oxide synthase 1, neuronal	Mus musculus	185-196
11238274-1	2001	BACKGROUND: Altered endothelial cell nitric oxide (NO(*)) production in atherosclerosis may be due to a reduction of intracellular tetrahydrobiopterin, which is a critical cofactor for NO synthase (NOS).	sapropterin	131-150	nitric oxide synthase 1, neuronal	Mus musculus	185-196
11238274-12	2001	Peroxynitrite oxidation of tetrahydrobiopterin may represent a pathogenic cause of "uncoupling" of NO synthase.	Peroxynitrous Acid	0-13	nitric oxide synthase 1, neuronal	Mus musculus	99-110
11238274-12	2001	Peroxynitrite oxidation of tetrahydrobiopterin may represent a pathogenic cause of "uncoupling" of NO synthase.	sapropterin	27-46	nitric oxide synthase 1, neuronal	Mus musculus	99-110
11168564-5	2001	We found that an intraperitoneal injection of 10 mg/kg Delta(9)-THC led to the same increase in the hot plate latencies in both genotypes, suggesting that Delta(9)-THC-mediated antinociception does not involve nNOS.	Dronabinol	64-67	nitric oxide synthase 1, neuronal	Mus musculus	210-214
11168564-6	2001	In contrast, a significant Delta(9)-THC-induced decrease of body temperature and locomotor activity was only observed in WT, but not in nNOS-KO mice.	Dronabinol	27-39	nitric oxide synthase 1, neuronal	Mus musculus	136-140
11158245-6	2001	The dopaminergic damage induced by METH treatment was also attenuated in nNOS-/- or SOD-Tg mice.	Methamphetamine	35-39	nitric oxide synthase 1, neuronal	Mus musculus	73-77
11565190-4	2001	Also, NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine is reported to induce a dose-dependent inhibitory effect on the proliferation of osteoblast-like cell lines MG63 and ROS 17/2.8, which indicate that NO may stimulate cell proliferation.	omega-N-Methylarginine	35-59	nitric oxide synthase 1, neuronal	Mus musculus	6-17
11565190-4	2001	Also, NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine is reported to induce a dose-dependent inhibitory effect on the proliferation of osteoblast-like cell lines MG63 and ROS 17/2.8, which indicate that NO may stimulate cell proliferation.	ros	177-180	nitric oxide synthase 1, neuronal	Mus musculus	6-17
11549221-0	2001	The nitric oxide synthase inhibitor, L-NAME, block phencyclidine-induced disruption of prepulse inhibition in mice.	NG-Nitroarginine Methyl Ester	37-43	nitric oxide synthase 1, neuronal	Mus musculus	4-25
11549221-0	2001	The nitric oxide synthase inhibitor, L-NAME, block phencyclidine-induced disruption of prepulse inhibition in mice.	Phencyclidine	51-64	nitric oxide synthase 1, neuronal	Mus musculus	4-25
11549221-3	2001	Recent studies show that the behavioural and biochemical effects of PCP in rats are blocked by nitric oxide synthase (NOS) inhibitors, suggesting that NO plays an important role in the pharmacological effects of PCP.	Phencyclidine	68-71	nitric oxide synthase 1, neuronal	Mus musculus	95-116
11549221-3	2001	Recent studies show that the behavioural and biochemical effects of PCP in rats are blocked by nitric oxide synthase (NOS) inhibitors, suggesting that NO plays an important role in the pharmacological effects of PCP.	Phencyclidine	212-215	nitric oxide synthase 1, neuronal	Mus musculus	95-116
11292369-0	2001	Modulation of cerebellar and hepatic nitric oxide synthase by exogenous arginine and endotoxin.	Arginine	72-80	nitric oxide synthase 1, neuronal	Mus musculus	37-58
11165371-11	2001	We found that the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801, the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) and the heme oxygenase (HO) inhibitor tin protoporphyrin (Sn-P) dose-dependently reduced OIH in this model while the NSAID indomethacin had no effect.	NG-Nitroarginine Methyl Ester	116-150	nitric oxide synthase 1, neuronal	Mus musculus	78-99
11165371-11	2001	We found that the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801, the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) and the heme oxygenase (HO) inhibitor tin protoporphyrin (Sn-P) dose-dependently reduced OIH in this model while the NSAID indomethacin had no effect.	NG-Nitroarginine Methyl Ester	152-158	nitric oxide synthase 1, neuronal	Mus musculus	78-99
11158630-1	2001	Genetically engineered mice with targeted disruption of the neuronal nitric oxide synthase (nNOS) gene established the inhibitory role of nitric oxide (NO) in male impulsive aggressive behavior.	Nitric Oxide	69-81	nitric oxide synthase 1, neuronal	Mus musculus	92-96
11158630-6	2001	We now demonstrate that the excessive aggressiveness and impulsiveness of nNOS knockout mice is caused by selective decrements in serotonin (5-HT) turnover and deficient 5-HT(1A) and 5-HT(1B) receptor function in brain regions regulating emotion.	Serotonin	130-139	nitric oxide synthase 1, neuronal	Mus musculus	74-78
11483302-0	2001	Nitric oxide is involved in ischemia-induced apoptosis in brain: a study in neuronal nitric oxide synthase null mice.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	76-106
11180409-5	2001	As judged by NADPH-diaphorase staining, nitric oxide synthase (NOS) activity is increased in TRK1 cells upon exposure to NGF.	NADP	13-18	nitric oxide synthase 1, neuronal	Mus musculus	40-61
11483302-2	2001	We examined the impact of nitric oxide on development of apoptosis 6, 24, and 72 h after permanent middle cerebral artery occlusion in mutant mice that lack the ability to generate nitric oxide from neuronal nitric oxide synthase.	Nitric Oxide	181-193	nitric oxide synthase 1, neuronal	Mus musculus	199-229
11686901-1	2001	BACKGROUND: The importance of nitric oxide (NO) in hypoxic pulmonary hypertension has been demonstrated using nitric oxide synthase (NOS) knockout mice.	Nitric Oxide	30-42	nitric oxide synthase 1, neuronal	Mus musculus	110-131
11416252-1	2001	BACKGROUND: Nitric oxide (NO) and an essential cofactor for both constitutive and inducible NO synthase (NOS) activity, tetrahydrobiopterin (6R-L-erythro-1",2"-dihydroxypropyl-2-amino-4-hydroxy-5,6,7,8-tetrahydropteridine; BH4), are thought to be important modulators of function in normal and inflamed airways.	Nitric Oxide	12-24	nitric oxide synthase 1, neuronal	Mus musculus	92-103
11146102-1	2000	Recent data suggest that the neuronal isoform of nitric oxide synthase (nNOS) and glutamate receptors of the N-methyl-D-aspartate (NMDA) type are physically coupled and, hence, functionally interrelated.	N-Methylaspartate	109-129	nitric oxide synthase 1, neuronal	Mus musculus	72-76
11146102-1	2000	Recent data suggest that the neuronal isoform of nitric oxide synthase (nNOS) and glutamate receptors of the N-methyl-D-aspartate (NMDA) type are physically coupled and, hence, functionally interrelated.	N-Methylaspartate	131-135	nitric oxide synthase 1, neuronal	Mus musculus	72-76
11146102-9	2000	Otherwise, the observed diminution of NMDAR1-1 splice variant mRNA and protein levels may, at least partially, explain the decreased vulnerability of nNOS alpha(Delta/Delta) mice to glutamate-mediated neurotoxicity.	Glutamic Acid	182-191	nitric oxide synthase 1, neuronal	Mus musculus	150-154
11080550-2	2000	PCP-induced place aversion in naive mice was dose-dependently attenuated by administration of N(G)-nitro-L-arginine methyl ester (L-NAME), a NO synthase (NOS) inhibitor, during the conditioning.	Phencyclidine	0-3	nitric oxide synthase 1, neuronal	Mus musculus	141-152
11080550-2	2000	PCP-induced place aversion in naive mice was dose-dependently attenuated by administration of N(G)-nitro-L-arginine methyl ester (L-NAME), a NO synthase (NOS) inhibitor, during the conditioning.	NG-Nitroarginine Methyl Ester	94-128	nitric oxide synthase 1, neuronal	Mus musculus	141-152
11080550-2	2000	PCP-induced place aversion in naive mice was dose-dependently attenuated by administration of N(G)-nitro-L-arginine methyl ester (L-NAME), a NO synthase (NOS) inhibitor, during the conditioning.	NG-Nitroarginine Methyl Ester	130-136	nitric oxide synthase 1, neuronal	Mus musculus	141-152
11156478-3	2000	The origin of NO from the L-arginine-NO synthase (NOS) pathway was confirmed using the NOS inhibitor N(G)-monomethyl-L-arginine (NMMA) and isotopic tracing experiments with 15N-labelled L-arginine.	omega-N-Methylarginine	101-127	nitric oxide synthase 1, neuronal	Mus musculus	26-48
11108822-10	2000	Overall, the present observations suggest that the melatonin-induced reversal of morphine tolerance and dependence may involve its ability to suppress nitric oxide synthase (NOS) activity.	Melatonin	51-60	nitric oxide synthase 1, neuronal	Mus musculus	151-172
11108822-10	2000	Overall, the present observations suggest that the melatonin-induced reversal of morphine tolerance and dependence may involve its ability to suppress nitric oxide synthase (NOS) activity.	Morphine	81-89	nitric oxide synthase 1, neuronal	Mus musculus	151-172
11077049-2	2000	In this study, we investigated the inhibitory effects of curcumin and its metabolites, tetrahydrocurcumin, hexahydrocurcumin, and octahydrocurcumin, on the induction of NO synthase (NOS) in RAW 264.7 cells activated with lipopolysaccharide (LPS).	Curcumin	57-65	nitric oxide synthase 1, neuronal	Mus musculus	169-180
11077049-2	2000	In this study, we investigated the inhibitory effects of curcumin and its metabolites, tetrahydrocurcumin, hexahydrocurcumin, and octahydrocurcumin, on the induction of NO synthase (NOS) in RAW 264.7 cells activated with lipopolysaccharide (LPS).	tetrahydrocurcumin	87-105	nitric oxide synthase 1, neuronal	Mus musculus	169-180
11077049-2	2000	In this study, we investigated the inhibitory effects of curcumin and its metabolites, tetrahydrocurcumin, hexahydrocurcumin, and octahydrocurcumin, on the induction of NO synthase (NOS) in RAW 264.7 cells activated with lipopolysaccharide (LPS).	hexahydrocurcumin	107-124	nitric oxide synthase 1, neuronal	Mus musculus	169-180
11077049-2	2000	In this study, we investigated the inhibitory effects of curcumin and its metabolites, tetrahydrocurcumin, hexahydrocurcumin, and octahydrocurcumin, on the induction of NO synthase (NOS) in RAW 264.7 cells activated with lipopolysaccharide (LPS).	Octahydrocurcumin	130-147	nitric oxide synthase 1, neuronal	Mus musculus	169-180
11099109-1	2000	Nitric oxide (NO), which has several physiological functions in skin, is generated by NO synthase (NOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	86-97
11058547-4	2000	The present study was undertaken to examine if nitric oxide (NO) production by nitric oxide synthase (NOS) isoforms mediates the inhibitory action of CGRP on uterine contractions as has been suggested earlier.	Nitric Oxide	47-59	nitric oxide synthase 1, neuronal	Mus musculus	79-100
11106424-8	2000	Other heme proteins, namely neuronal nitric oxide synthase and soluble guanylate cyclase, function normally in mice with limited heme.	Heme	6-10	nitric oxide synthase 1, neuronal	Mus musculus	28-58
11056465-9	2000	The onset of nNOS expression in the different laminae is earlier than has been reported in studies using NADPHd as a marker for nNOS.	nadphd	105-111	nitric oxide synthase 1, neuronal	Mus musculus	13-17
11056465-10	2000	The temporal and spatial patterns of nNOS expression reported here match more closely the time course of pathway refinement in the SC, providing additional evidence for the involvement of nitric oxide in this process.	Nitric Oxide	188-200	nitric oxide synthase 1, neuronal	Mus musculus	37-41
11085350-5	2000	Macrophages have many unique functions, and nitric oxide (NO) produced by NO synthase (NOS) which is induced in response to some cytokines and bacterial products such as lipopolysaccharide (LPS) is responsible for the bactericidal, tumoricidal and immune regulatory activities.	Nitric Oxide	44-56	nitric oxide synthase 1, neuronal	Mus musculus	74-85
11092532-3	2000	NO is produced from arginine by nitric oxide synthase (NOS), an enzyme that exists in both constitutive and inducible (iNOS) forms.	Arginine	20-28	nitric oxide synthase 1, neuronal	Mus musculus	32-53
11156478-3	2000	The origin of NO from the L-arginine-NO synthase (NOS) pathway was confirmed using the NOS inhibitor N(G)-monomethyl-L-arginine (NMMA) and isotopic tracing experiments with 15N-labelled L-arginine.	omega-N-Methylarginine	129-133	nitric oxide synthase 1, neuronal	Mus musculus	26-48
11156478-3	2000	The origin of NO from the L-arginine-NO synthase (NOS) pathway was confirmed using the NOS inhibitor N(G)-monomethyl-L-arginine (NMMA) and isotopic tracing experiments with 15N-labelled L-arginine.	15n	173-176	nitric oxide synthase 1, neuronal	Mus musculus	26-48
11085313-9	2000	The intensity of METH-induced locomotion in nNOS(-/-) mice on day 1 and 4 was similar, suggesting that locomotor sensitization did not develop.	Methamphetamine	17-21	nitric oxide synthase 1, neuronal	Mus musculus	44-48
11009479-8	2000	In contrast, trifluoromethylphenylimidazole, an inhibitor of neuronal NOS (nNOS), decreased ACh-induced dilation in arteries from eNOS-deficient mice but had no effect on responses in wild-type mice.	2-Phenyl-4-(trifluoromethyl)-1H-imidazole	13-43	nitric oxide synthase 1, neuronal	Mus musculus	61-73
11009479-8	2000	In contrast, trifluoromethylphenylimidazole, an inhibitor of neuronal NOS (nNOS), decreased ACh-induced dilation in arteries from eNOS-deficient mice but had no effect on responses in wild-type mice.	2-Phenyl-4-(trifluoromethyl)-1H-imidazole	13-43	nitric oxide synthase 1, neuronal	Mus musculus	75-79
11009479-8	2000	In contrast, trifluoromethylphenylimidazole, an inhibitor of neuronal NOS (nNOS), decreased ACh-induced dilation in arteries from eNOS-deficient mice but had no effect on responses in wild-type mice.	Acetylcholine	92-95	nitric oxide synthase 1, neuronal	Mus musculus	61-73
11009479-8	2000	In contrast, trifluoromethylphenylimidazole, an inhibitor of neuronal NOS (nNOS), decreased ACh-induced dilation in arteries from eNOS-deficient mice but had no effect on responses in wild-type mice.	Acetylcholine	92-95	nitric oxide synthase 1, neuronal	Mus musculus	75-79
11014214-0	2000	Cytological characterization of a pituitary folliculo-stellate-like cell line, Tpit/F1, with special reference to adenosine triphosphate-mediated neuronal nitric oxide synthase expression and nitric oxide secretion.	Adenosine Triphosphate	114-136	nitric oxide synthase 1, neuronal	Mus musculus	146-176
11014214-11	2000	Interestingly, both neuronal nitric oxide synthase messenger RNA and NO secretion were increased by ATP administration (10 and 100 microM).	Adenosine Triphosphate	100-103	nitric oxide synthase 1, neuronal	Mus musculus	20-50
11006970-0	2000	nNOS inhibitors attenuate methamphetamine-induced dopaminergic neurotoxicity but not hyperthermia in mice.	Methamphetamine	26-41	nitric oxide synthase 1, neuronal	Mus musculus	0-4
11006970-2	2000	We investigated the effect of several neuronal nitric oxide synthase (nNOS) inhibitors on METH-induced hyperthermia and striatal dopaminergic neurotoxicity.	Methamphetamine	90-94	nitric oxide synthase 1, neuronal	Mus musculus	38-68
11006970-2	2000	We investigated the effect of several neuronal nitric oxide synthase (nNOS) inhibitors on METH-induced hyperthermia and striatal dopaminergic neurotoxicity.	Methamphetamine	90-94	nitric oxide synthase 1, neuronal	Mus musculus	70-74
11006970-5	2000	Pretreatment with the nNOS inhibitors S-methylthiocitrulline (SMTC; 10 mg/kg) or 3-bromo-7-nitroindazole (3-Br-7-NI; 20 mg/kg) before each METH injection did not affect the persistent hyperthermia produced by METH, but afforded protection against the depletion of dopaminergic markers.	S-methylthiocitrulline	38-60	nitric oxide synthase 1, neuronal	Mus musculus	22-26
11006970-5	2000	Pretreatment with the nNOS inhibitors S-methylthiocitrulline (SMTC; 10 mg/kg) or 3-bromo-7-nitroindazole (3-Br-7-NI; 20 mg/kg) before each METH injection did not affect the persistent hyperthermia produced by METH, but afforded protection against the depletion of dopaminergic markers.	S-methylthiocitrulline	62-66	nitric oxide synthase 1, neuronal	Mus musculus	22-26
11006970-6	2000	A low dose (25 mg/kg) of the nNOS inhibitor 7-nitroindazole (7-NI) did not affect METH-induced hyperthermia, but a high dose (50 mg/kg) produced significant hypothermia.	7-nitroindazole	44-59	nitric oxide synthase 1, neuronal	Mus musculus	29-33
11006970-6	2000	A low dose (25 mg/kg) of the nNOS inhibitor 7-nitroindazole (7-NI) did not affect METH-induced hyperthermia, but a high dose (50 mg/kg) produced significant hypothermia.	7-nitroindazole	61-65	nitric oxide synthase 1, neuronal	Mus musculus	29-33
11006970-7	2000	These findings indicate that low dose of selective nNOS inhibitors protect against METH-induced neurotoxicity with no effect on body temperature and support the hypothesis that nitric oxide (NO) and peroxynitrite have a major role in METH-induced dopaminergic neurotoxicity.	Methamphetamine	83-87	nitric oxide synthase 1, neuronal	Mus musculus	51-55
11006970-7	2000	These findings indicate that low dose of selective nNOS inhibitors protect against METH-induced neurotoxicity with no effect on body temperature and support the hypothesis that nitric oxide (NO) and peroxynitrite have a major role in METH-induced dopaminergic neurotoxicity.	Nitric Oxide	177-189	nitric oxide synthase 1, neuronal	Mus musculus	51-55
11006970-7	2000	These findings indicate that low dose of selective nNOS inhibitors protect against METH-induced neurotoxicity with no effect on body temperature and support the hypothesis that nitric oxide (NO) and peroxynitrite have a major role in METH-induced dopaminergic neurotoxicity.	Peroxynitrous Acid	199-212	nitric oxide synthase 1, neuronal	Mus musculus	51-55
11006970-7	2000	These findings indicate that low dose of selective nNOS inhibitors protect against METH-induced neurotoxicity with no effect on body temperature and support the hypothesis that nitric oxide (NO) and peroxynitrite have a major role in METH-induced dopaminergic neurotoxicity.	Methamphetamine	234-238	nitric oxide synthase 1, neuronal	Mus musculus	51-55
11085313-1	2000	The involvement of the neuronal and inducible nitric oxide synthase (nNOS and iNOS, respectively) in methamphetamine (METH)-induced dopaminergic neurotoxicity and behavioral sensitization was investigated.	Methamphetamine	101-116	nitric oxide synthase 1, neuronal	Mus musculus	69-73
10927028-0	2000	Inhibition of neuronal nitric oxide synthase activity by 3-[2-[4-(3-chloro-2-methylphenyl)- 1-piperazinyl]ethyl]-5, 6-dimethoxy-1-(4-imidazolylmethyl)-1H-indazole dihydrochloride 3.5 hydrate (DY-9760e), a novel neuroprotective agent, in vitro and in cultured neuroblastoma cells in situ.	3-(2-(4-(3-chloro-2-methylphenyl)1-piperazinyl)ethyl)5,6-dimethoxy-1-(4-imidazolylmethyl)-1H-indazol dihydrochloride 3.5 hydrate	192-200	nitric oxide synthase 1, neuronal	Mus musculus	23-44
10925177-2	2000	Both, nNOS and iNOS were upregulated in the dorsal horns of the spinal cord in response to the zymosan challenge.	Zymosan	95-102	nitric oxide synthase 1, neuronal	Mus musculus	6-10
11042340-3	2000	We have previously shown that elimination of nNOS neurons, either by targeted disruption of the gene or by pharmacological depletion with intraparenchymal quisqualate, can decrease injury after hypoxia-ischemia.	Quisqualic Acid	155-166	nitric oxide synthase 1, neuronal	Mus musculus	45-49
11042340-4	2000	Using a simpler pharmacological approach, we studied the efficacy of a systemically administered NOS inhibitor, 7-nitroindazole, a relatively selective inhibitor of nNOS activity.	7-nitroindazole	112-127	nitric oxide synthase 1, neuronal	Mus musculus	165-169
11021993-9	2000	VSV-infected mice treated with celecoxib expressed more NOS-1 and produced more NO in their CNS compared to the controls.	Celecoxib	31-40	nitric oxide synthase 1, neuronal	Mus musculus	56-61
10874031-1	2000	We have previously demonstrated that phosphorylation of neuronal nitric-oxide synthase (nNOS) at Ser(847) by Ca(2+)/calmodulin-dependent protein kinases (CaM kinases) attenuates the catalytic activity of the enzyme in vitro (Hayashi Y., Nishio M., Naito Y., Yokokura H., Nimura Y., Hidaka H., and Watanabe Y.	Serine	97-100	nitric oxide synthase 1, neuronal	Mus musculus	56-86
10874031-1	2000	We have previously demonstrated that phosphorylation of neuronal nitric-oxide synthase (nNOS) at Ser(847) by Ca(2+)/calmodulin-dependent protein kinases (CaM kinases) attenuates the catalytic activity of the enzyme in vitro (Hayashi Y., Nishio M., Naito Y., Yokokura H., Nimura Y., Hidaka H., and Watanabe Y.	Serine	97-100	nitric oxide synthase 1, neuronal	Mus musculus	88-92
10874031-5	2000	In the present study we determined that CaM kinase IIalpha (CaM-K IIalpha) can directly phosphorylate nNOS on Ser(847), leading to a reduction of nNOS activity in cells.	Serine	110-113	nitric oxide synthase 1, neuronal	Mus musculus	102-106
10874031-5	2000	In the present study we determined that CaM kinase IIalpha (CaM-K IIalpha) can directly phosphorylate nNOS on Ser(847), leading to a reduction of nNOS activity in cells.	Serine	110-113	nitric oxide synthase 1, neuronal	Mus musculus	146-150
10874031-11	2000	Thus, our results indicate that Ca(2+) triggers cross-talk signal transduction between CaM kinase and NO and CaM-K IIalpha phosphorylating nNOS on Ser(847), which in turn decreases the gaseous second messenger NO in neuronal cells.	Serine	147-150	nitric oxide synthase 1, neuronal	Mus musculus	139-143
11085313-11	2000	The present findings indicate that nNOS(-/-) mice are more resistant to METH-induced neurotoxicity and behavioral sensitization than iNOS(-/-) mice.	Methamphetamine	72-76	nitric oxide synthase 1, neuronal	Mus musculus	35-39
11085313-12	2000	These results suggest a major role for nNOS rather than iNOS in the effects of METH.	Methamphetamine	79-83	nitric oxide synthase 1, neuronal	Mus musculus	39-43
10924282-2	2000	Mice lacking the neuronal nitric oxide synthase gene (nNOS-/-) exhibit significantly impaired maternal aggression, but increased male aggression, suggesting that nitric oxide (NO) produced by nNOS has opposite actions in maternal and male aggression.	Nitric Oxide	26-38	nitric oxide synthase 1, neuronal	Mus musculus	54-58
11019368-5	2000	In a previous work, we studied the effect of L-arginine, the substrate of nitric oxide synthetase (NOS), on utrophin expression at the muscle membrane.	Arginine	45-55	nitric oxide synthase 1, neuronal	Mus musculus	74-97
10930440-2	2000	In genetic (nonobese diabetic) and toxin-elicited (streptozotocin) models of diabetes in mice, we demonstrate defects in gastric emptying and nonadrenergic, noncholinergic relaxation of pyloric muscle, which resemble defects in mice harboring a deletion of the neuronal nitric oxide synthase gene (nNOS).	Streptozocin	51-65	nitric oxide synthase 1, neuronal	Mus musculus	298-302
10945536-7	2000	Attempts to block tracer uptake by pretreatment with the NOS-I-selective inhibitor 7-nitroindazole or the corresponding unlabeled inhibitor (or desmethyl precursor to AR-R 17443 of similar potency) were unsuccessful.	7-nitroindazole	83-98	nitric oxide synthase 1, neuronal	Mus musculus	57-62
10944418-1	2000	Nitric oxide (NO), a biomolecule with major cytotoxic potency, is generated by NO synthases (NOS) utilizing l-arginine as substrate and citrulline is formed as a "side product."	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	79-91
10944418-1	2000	Nitric oxide (NO), a biomolecule with major cytotoxic potency, is generated by NO synthases (NOS) utilizing l-arginine as substrate and citrulline is formed as a "side product."	Arginine	108-118	nitric oxide synthase 1, neuronal	Mus musculus	79-91
10926966-7	2000	RESULTS: Infarct volume was significantly decreased (47%) in animals treated with the nonselective nitric oxide synthase (NOS) inhibitor N(omega)-nitro-L-arginine (L-NA) at reperfusion.	Nitroarginine	137-162	nitric oxide synthase 1, neuronal	Mus musculus	99-120
10924282-2	2000	Mice lacking the neuronal nitric oxide synthase gene (nNOS-/-) exhibit significantly impaired maternal aggression, but increased male aggression, suggesting that nitric oxide (NO) produced by nNOS has opposite actions in maternal and male aggression.	Nitric Oxide	26-38	nitric oxide synthase 1, neuronal	Mus musculus	192-196
10781602-0	2000	The C terminus of mouse macrophage inducible nitric-oxide synthase attenuates electron flow through the flavin domain.	4,6-dinitro-o-cresol	104-110	nitric oxide synthase 1, neuronal	Mus musculus	45-66
10876072-1	2000	Neurons that express neuronal nitric oxide synthase (nNOS) are selectively spared from nitric oxide (NO)-induced cytotoxicity in acute cerebral ischemia and neurodegenerative conditions but the mechanism of this resistance is unknown.	Nitric Oxide	30-42	nitric oxide synthase 1, neuronal	Mus musculus	53-57
20575850-7	2000	In follow-up experiments nNOS KO mice along with appropriate control (C57BL/6N, SV129 and B6JSV129) mice were treated with METH (5 mg/kg,ip, q 3h x 3) and were sacrificed 72 h after dosing.	Methamphetamine	123-127	nitric oxide synthase 1, neuronal	Mus musculus	25-29
20575850-12	2000	Therefore, these studies strongly suggest the role of peroxynitrite, nNOS and DA system in METH-induced neurotoxicity and behavioral sensitization.	Methamphetamine	91-95	nitric oxide synthase 1, neuronal	Mus musculus	69-73
10893328-1	2000	Islet production of nitric oxide (NO) and CO in relation to islet hormone secretion was investigated in mice given the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) in their drinking water.	NG-Nitroarginine Methyl Ester	147-181	nitric oxide synthase 1, neuronal	Mus musculus	119-130
11051593-0	2000	Zinc and nitric oxide synthase inhibitor L-NAME attenuate NPY-induced feeding in mice.	NG-Nitroarginine Methyl Ester	41-47	nitric oxide synthase 1, neuronal	Mus musculus	9-30
10966931-0	2000	Defective fluid and HCO(3)(-) absorption in proximal tubule of neuronal nitric oxide synthase-knockout mice.	Bicarbonates	20-26	nitric oxide synthase 1, neuronal	Mus musculus	63-93
10966931-4	2000	In nNOS-knockout mice, the urinary excretion of HCO(3)(-) was significantly higher than in the wild-type mice (3.12 +/- 0.52 vs. 1.	Bicarbonates	48-54	nitric oxide synthase 1, neuronal	Mus musculus	3-7
10966931-6	2000	Both arterial blood HCO(3)(-) concentration (20.7 vs. 25.7 mM) and blood pH (7.27 vs. 7.34) were lower, indicating a significant metabolic acidosis in nNOS-knockout mice.	Bicarbonates	20-26	nitric oxide synthase 1, neuronal	Mus musculus	151-155
10966931-7	2000	Blood pressure was lower in nNOS-knockout mice (76.2 +/- 4.6 mmHg) than in wild-type control animals (102.9 +/- 8.4 mmHg); however, it increased in response to L-NAME (125.5 +/- 5.07 mmHg).	NG-Nitroarginine Methyl Ester	160-166	nitric oxide synthase 1, neuronal	Mus musculus	28-32
10966931-9	2000	Our data show that a large component of HCO(3)(-) and fluid absorption in the proximal tubule is controlled by nNOS.	7 alpha-hydroxy-4-cholesten-3-one	40-43	nitric oxide synthase 1, neuronal	Mus musculus	111-115
10966931-10	2000	Mice without this isozyme are defective in absorption of fluid and HCO(3)(-) in the proximal tubule and develop metabolic acidosis, suggesting that nNOS plays an important role in the regulation of acid-base balance.	Bicarbonates	67-73	nitric oxide synthase 1, neuronal	Mus musculus	148-152
10823926-6	2000	IRP1 expression decreased time-dependently to about 40% of control levels after 16 h. Down-regulation of IRP1 protein levels was correlated with the amount of NO produced and was partially abolished by the NO synthase (NOS) inhibitor N-monomethyl-l-arginine.	omega-N-Methylarginine	234-257	nitric oxide synthase 1, neuronal	Mus musculus	206-217
10820202-0	2000	Retinoic acid-mediated enhancement of the cholinergic/neuronal nitric oxide synthase phenotype of the medial septal SN56 clone: establishment of a nitric oxide-sensitive proapoptotic state.	Tretinoin	0-13	nitric oxide synthase 1, neuronal	Mus musculus	54-84
10775149-2	2000	Mice were treated with N(omega)-nitro-L-arginine methyl ester (L-NAME) an inhibitor of nitric oxide synthase (NOS) or with the NOS substrate L-arginine for 8 wk.	NG-Nitroarginine Methyl Ester	63-69	nitric oxide synthase 1, neuronal	Mus musculus	87-108
10780996-0	2000	Central injection of nitric oxide synthase inhibitors increases peripheral interleukin-6 and serum amyloid A: involvement of adrenaline from adrenal medulla.	Epinephrine	125-135	nitric oxide synthase 1, neuronal	Mus musculus	21-42
10905473-1	2000	Studies from our laboratory using acute pharmacologic blockade of nitric oxide synthase (NOS) activity have suggested that nitric oxide (NO) has an important role in regulating carbohydrate metabolism.	Carbohydrates	177-189	nitric oxide synthase 1, neuronal	Mus musculus	66-87
10904848-3	2000	NO is synthesized from L-arginine by the enzyme nitric oxide synthase (NOS).	Arginine	23-33	nitric oxide synthase 1, neuronal	Mus musculus	48-69
10779667-10	2000	of 7-NI (30 min), a selective inhibitor of neuronal NOS (nNOS), inhibited NOS activity in the spinal cord and produced anti-nociception, confirming that writhing is sensitive to inhibition of nNOS.	7-nitroindazole	3-7	nitric oxide synthase 1, neuronal	Mus musculus	43-55
10779667-10	2000	of 7-NI (30 min), a selective inhibitor of neuronal NOS (nNOS), inhibited NOS activity in the spinal cord and produced anti-nociception, confirming that writhing is sensitive to inhibition of nNOS.	7-nitroindazole	3-7	nitric oxide synthase 1, neuronal	Mus musculus	57-61
10779667-10	2000	of 7-NI (30 min), a selective inhibitor of neuronal NOS (nNOS), inhibited NOS activity in the spinal cord and produced anti-nociception, confirming that writhing is sensitive to inhibition of nNOS.	7-nitroindazole	3-7	nitric oxide synthase 1, neuronal	Mus musculus	192-196
10779667-12	2000	This novel effect appears to be initiated by the transient inhibition of nNOS as delayed anti-nociception was mimicked by 7-NI at doses (10-100 nmol) that no longer inhibited spinal nNOS (25 nmol) at 24 h. Co-administration with L-arginine prevented the delayed (24 h) anti-nociceptive effects of L-NAME (30 nmol).	7-nitroindazole	122-126	nitric oxide synthase 1, neuronal	Mus musculus	73-77
10779667-12	2000	This novel effect appears to be initiated by the transient inhibition of nNOS as delayed anti-nociception was mimicked by 7-NI at doses (10-100 nmol) that no longer inhibited spinal nNOS (25 nmol) at 24 h. Co-administration with L-arginine prevented the delayed (24 h) anti-nociceptive effects of L-NAME (30 nmol).	Arginine	229-239	nitric oxide synthase 1, neuronal	Mus musculus	73-77
10779667-12	2000	This novel effect appears to be initiated by the transient inhibition of nNOS as delayed anti-nociception was mimicked by 7-NI at doses (10-100 nmol) that no longer inhibited spinal nNOS (25 nmol) at 24 h. Co-administration with L-arginine prevented the delayed (24 h) anti-nociceptive effects of L-NAME (30 nmol).	NG-Nitroarginine Methyl Ester	297-303	nitric oxide synthase 1, neuronal	Mus musculus	73-77
10790861-1	2000	We have shown previously that the neuronal nitric oxide synthase (nNOS) is involved in the rewarding effect of cocaine as determined by the conditioned place preference (CPP) paradigm.	Cocaine	111-118	nitric oxide synthase 1, neuronal	Mus musculus	34-64
10790861-1	2000	We have shown previously that the neuronal nitric oxide synthase (nNOS) is involved in the rewarding effect of cocaine as determined by the conditioned place preference (CPP) paradigm.	Cocaine	111-118	nitric oxide synthase 1, neuronal	Mus musculus	66-70
10727711-9	2000	of 7-nitroindazole (7-NI), a non-selective non hypertensive inhibitor of nitric oxide synthase (NOS), significantly decreased MPP(+) levels.	7-nitroindazole	3-18	nitric oxide synthase 1, neuronal	Mus musculus	73-94
10762349-7	2000	Methyl bromide inhalation induced a degeneration of olfactory axons in both strains, but had different effects on the expression of nNOS/ND and tyrosine hydroxylase.	methyl bromide	0-14	nitric oxide synthase 1, neuronal	Mus musculus	132-136
10809176-5	2000	However, the degree of enhancement by inosine on NO production and nitric oxide synthase (NOS) activity in LPS-treated RAW 264.7 was weaker than the effect of adenosine.	Inosine	38-45	nitric oxide synthase 1, neuronal	Mus musculus	67-88
10749148-0	2000	Effect of cyclooxygenase and nitric oxide synthase inhibitors on tumor growth in mouse tumor models with and without cancer cachexia related to prostanoids.	Prostaglandins	144-155	nitric oxide synthase 1, neuronal	Mus musculus	29-50
10749148-6	2000	Nitric oxide synthase (NOS) inhibitors (N(omega)-nitro-L-arginine methyl ester and N(omega)-nitro-L-arginine) reduced tumor growth in vivo by approximately 50% in both tumor models.	NG-Nitroarginine Methyl Ester	40-78	nitric oxide synthase 1, neuronal	Mus musculus	0-21
10749148-6	2000	Nitric oxide synthase (NOS) inhibitors (N(omega)-nitro-L-arginine methyl ester and N(omega)-nitro-L-arginine) reduced tumor growth in vivo by approximately 50% in both tumor models.	Nitroarginine	40-65	nitric oxide synthase 1, neuronal	Mus musculus	0-21
10683266-0	2000	Cellular and enzymatic studies of N(omega)-propyl-l-arginine and S-ethyl-N-[4-(trifluoromethyl)phenyl]isothiourea as reversible, slowly dissociating inhibitors selective for the neuronal nitric oxide synthase isoform.	N(omega)-propylarginine	34-60	nitric oxide synthase 1, neuronal	Mus musculus	178-208
10683266-0	2000	Cellular and enzymatic studies of N(omega)-propyl-l-arginine and S-ethyl-N-[4-(trifluoromethyl)phenyl]isothiourea as reversible, slowly dissociating inhibitors selective for the neuronal nitric oxide synthase isoform.	S-ethyl N-(4-(trifluoromethyl)phenyl)isothiourea	65-113	nitric oxide synthase 1, neuronal	Mus musculus	178-208
10683266-1	2000	N(omega)propyl-l-arginine (NPA) and S-ethyl-N-[4-(trifluoromethyl)phenyl]isothiourea (TFMPITU) inhibit selectively the neuronal nitric oxide (NO) synthase (nNOS) isoform.	N(omega)-propylarginine	0-25	nitric oxide synthase 1, neuronal	Mus musculus	156-160
10683266-1	2000	N(omega)propyl-l-arginine (NPA) and S-ethyl-N-[4-(trifluoromethyl)phenyl]isothiourea (TFMPITU) inhibit selectively the neuronal nitric oxide (NO) synthase (nNOS) isoform.	N(omega)-propylarginine	27-30	nitric oxide synthase 1, neuronal	Mus musculus	156-160
10683266-1	2000	N(omega)propyl-l-arginine (NPA) and S-ethyl-N-[4-(trifluoromethyl)phenyl]isothiourea (TFMPITU) inhibit selectively the neuronal nitric oxide (NO) synthase (nNOS) isoform.	S-ethyl N-(4-(trifluoromethyl)phenyl)isothiourea	36-84	nitric oxide synthase 1, neuronal	Mus musculus	156-160
10683266-1	2000	N(omega)propyl-l-arginine (NPA) and S-ethyl-N-[4-(trifluoromethyl)phenyl]isothiourea (TFMPITU) inhibit selectively the neuronal nitric oxide (NO) synthase (nNOS) isoform.	S-ethyl N-(4-(trifluoromethyl)phenyl)isothiourea	86-93	nitric oxide synthase 1, neuronal	Mus musculus	156-160
10683266-6	2000	NPA and TFMPITU bind to nNOS rapidly producing a heme-substrate interaction as revealed by difference spectrophotometry.	Heme	49-53	nitric oxide synthase 1, neuronal	Mus musculus	24-28
12404337-1	2000	Due to the claim that chronic administration of lithium or L-N(G)-nitroarginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor reduces morphine withdrawal syndrome, the effects of chronic administration of lithium, L-NAME, or L-arginine (L-Arg), a precursor of NO, alone or co-administration of lithium with L-Arg or L-NAME, on naloxone-precipitated withdrawal syndrome and physical dependence development to morphine in mice chronically treated with morphine, were evaluated.	Lithium	48-55	nitric oxide synthase 1, neuronal	Mus musculus	105-126
12404337-1	2000	Due to the claim that chronic administration of lithium or L-N(G)-nitroarginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor reduces morphine withdrawal syndrome, the effects of chronic administration of lithium, L-NAME, or L-arginine (L-Arg), a precursor of NO, alone or co-administration of lithium with L-Arg or L-NAME, on naloxone-precipitated withdrawal syndrome and physical dependence development to morphine in mice chronically treated with morphine, were evaluated.	l-n(g)-nitroarginine methyl ester	59-92	nitric oxide synthase 1, neuronal	Mus musculus	105-126
12404337-1	2000	Due to the claim that chronic administration of lithium or L-N(G)-nitroarginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor reduces morphine withdrawal syndrome, the effects of chronic administration of lithium, L-NAME, or L-arginine (L-Arg), a precursor of NO, alone or co-administration of lithium with L-Arg or L-NAME, on naloxone-precipitated withdrawal syndrome and physical dependence development to morphine in mice chronically treated with morphine, were evaluated.	NG-Nitroarginine Methyl Ester	94-100	nitric oxide synthase 1, neuronal	Mus musculus	105-126
10723268-6	2000	In RAW 264.7 cells, auranofin (0.3-3 microM) inhibited lipopolysaccharide-induced NO synthesis by inhibiting the induction of NO synthase (NOS) protein expression.	Auranofin	20-29	nitric oxide synthase 1, neuronal	Mus musculus	126-137
10820202-5	2000	Treatment of SN56 cells with retinoic acid (RA; 1 microM) for 48 h increased ChAT mRNA (+126%), protein (+88%), and activity (+215%) and increased nNOS mRNA (+98%), protein (+400%), and activity (+15%).	Tretinoin	29-42	nitric oxide synthase 1, neuronal	Mus musculus	147-151
10820202-5	2000	Treatment of SN56 cells with retinoic acid (RA; 1 microM) for 48 h increased ChAT mRNA (+126%), protein (+88%), and activity (+215%) and increased nNOS mRNA (+98%), protein (+400%), and activity (+15%).	Tretinoin	44-46	nitric oxide synthase 1, neuronal	Mus musculus	147-151
10820202-7	2000	Treatment with dexamethasone, which largely blocked the RA-mediated increase in nNOS expression, or inhibition of nNOS activity with methylthiocitrulline strongly potentiated the apoptotic response to SNAP in RA-treated SN56 cells.	Dexamethasone	15-28	nitric oxide synthase 1, neuronal	Mus musculus	80-84
10820202-7	2000	Treatment with dexamethasone, which largely blocked the RA-mediated increase in nNOS expression, or inhibition of nNOS activity with methylthiocitrulline strongly potentiated the apoptotic response to SNAP in RA-treated SN56 cells.	Tretinoin	56-58	nitric oxide synthase 1, neuronal	Mus musculus	80-84
10820202-7	2000	Treatment with dexamethasone, which largely blocked the RA-mediated increase in nNOS expression, or inhibition of nNOS activity with methylthiocitrulline strongly potentiated the apoptotic response to SNAP in RA-treated SN56 cells.	S-methylthiocitrulline	133-153	nitric oxide synthase 1, neuronal	Mus musculus	114-118
10727738-9	2000	These results show that refinement of the IRP is delayed when expression of eNOS and nNOS is disrupted, presumably to axons with uncorrelated activity because nitric oxide serves as a repellant molecule during normal development.	Nitric Oxide	159-171	nitric oxide synthase 1, neuronal	Mus musculus	85-89
10708693-1	2000	Our previous studies indicated that inhibition or ablation of the neuronal nitric oxide synthase (nNOS) prevents the development of sensitization to the locomotor-stimulating effect of cocaine and cocaine-induced conditioned place preference (CPP).	Cocaine	185-192	nitric oxide synthase 1, neuronal	Mus musculus	66-96
10708693-1	2000	Our previous studies indicated that inhibition or ablation of the neuronal nitric oxide synthase (nNOS) prevents the development of sensitization to the locomotor-stimulating effect of cocaine and cocaine-induced conditioned place preference (CPP).	Cocaine	185-192	nitric oxide synthase 1, neuronal	Mus musculus	98-102
10708693-1	2000	Our previous studies indicated that inhibition or ablation of the neuronal nitric oxide synthase (nNOS) prevents the development of sensitization to the locomotor-stimulating effect of cocaine and cocaine-induced conditioned place preference (CPP).	Cocaine	197-204	nitric oxide synthase 1, neuronal	Mus musculus	66-96
10708693-1	2000	Our previous studies indicated that inhibition or ablation of the neuronal nitric oxide synthase (nNOS) prevents the development of sensitization to the locomotor-stimulating effect of cocaine and cocaine-induced conditioned place preference (CPP).	Cocaine	197-204	nitric oxide synthase 1, neuronal	Mus musculus	98-102
10708693-2	2000	The present study was undertaken to investigate the effect of the nNOS inhibitor, 7-nitroindazole (7-NI), on ethanol-induced locomotor sensitization and CPP in DBA/2J mice.	7-nitroindazole	82-97	nitric oxide synthase 1, neuronal	Mus musculus	66-70
10708693-2	2000	The present study was undertaken to investigate the effect of the nNOS inhibitor, 7-nitroindazole (7-NI), on ethanol-induced locomotor sensitization and CPP in DBA/2J mice.	7-nitroindazole	99-103	nitric oxide synthase 1, neuronal	Mus musculus	66-70
10708693-2	2000	The present study was undertaken to investigate the effect of the nNOS inhibitor, 7-nitroindazole (7-NI), on ethanol-induced locomotor sensitization and CPP in DBA/2J mice.	Ethanol	109-116	nitric oxide synthase 1, neuronal	Mus musculus	66-70
10708693-10	2000	Taken together, results of the present study indicate that blockade of nNOS by 7-NI-attenuated ethanol-induced behavioral sensitization and completely blocked the rewarding effect of ethanol.	7-nitroindazole	79-83	nitric oxide synthase 1, neuronal	Mus musculus	71-75
10708693-10	2000	Taken together, results of the present study indicate that blockade of nNOS by 7-NI-attenuated ethanol-induced behavioral sensitization and completely blocked the rewarding effect of ethanol.	Ethanol	95-102	nitric oxide synthase 1, neuronal	Mus musculus	71-75
10708693-10	2000	Taken together, results of the present study indicate that blockade of nNOS by 7-NI-attenuated ethanol-induced behavioral sensitization and completely blocked the rewarding effect of ethanol.	Ethanol	183-190	nitric oxide synthase 1, neuronal	Mus musculus	71-75
10708693-11	2000	These findings support the role of NO in ethanol actions and further suggest that the nNOS system is relevant to the rewarding effects of various drugs of abuse.	Ethanol	41-48	nitric oxide synthase 1, neuronal	Mus musculus	86-90
10764216-5	2000	Administration of the general NO-synthase inhibitor nitro-L-arginine methyl ester (L-NAME, 50 mg kg(-1) day(-1)) to mice kept on the low-salt/ramipril regimen caused a decrease of renal renin mRNA levels in wt and nNOS-/- mice, but not in eNOS-/- mice.	nitro-l-arginine methyl ester	52-81	nitric oxide synthase 1, neuronal	Mus musculus	214-218
10764216-5	2000	Administration of the general NO-synthase inhibitor nitro-L-arginine methyl ester (L-NAME, 50 mg kg(-1) day(-1)) to mice kept on the low-salt/ramipril regimen caused a decrease of renal renin mRNA levels in wt and nNOS-/- mice, but not in eNOS-/- mice.	NG-Nitroarginine Methyl Ester	83-89	nitric oxide synthase 1, neuronal	Mus musculus	214-218
10686338-4	2000	The expression of nitric oxide synthase (NOS) which catalyzes the formation of a similar neurotransmitter nitric oxide (NO) from arginine is increased in the spinal cords of animals chronically exposed to morphine and other opioids.	Arginine	129-137	nitric oxide synthase 1, neuronal	Mus musculus	18-39
10686338-4	2000	The expression of nitric oxide synthase (NOS) which catalyzes the formation of a similar neurotransmitter nitric oxide (NO) from arginine is increased in the spinal cords of animals chronically exposed to morphine and other opioids.	Morphine	205-213	nitric oxide synthase 1, neuronal	Mus musculus	18-39
10677544-6	2000	Glutamate neurotransmission involving N-methyl-d-aspartate (NMDA) receptors and neuronal nitric oxide synthase (nNOS) activity in part mediates neuronal DNA strand breaks and PARP activity, which are diminished by NMDA antagonists and NOS inhibitors and also diminished in mice with targeted deletion of nNOS gene (nNOS(-/-)).	Glutamic Acid	0-9	nitric oxide synthase 1, neuronal	Mus musculus	80-110
10677544-6	2000	Glutamate neurotransmission involving N-methyl-d-aspartate (NMDA) receptors and neuronal nitric oxide synthase (nNOS) activity in part mediates neuronal DNA strand breaks and PARP activity, which are diminished by NMDA antagonists and NOS inhibitors and also diminished in mice with targeted deletion of nNOS gene (nNOS(-/-)).	Glutamic Acid	0-9	nitric oxide synthase 1, neuronal	Mus musculus	112-116
10677544-6	2000	Glutamate neurotransmission involving N-methyl-d-aspartate (NMDA) receptors and neuronal nitric oxide synthase (nNOS) activity in part mediates neuronal DNA strand breaks and PARP activity, which are diminished by NMDA antagonists and NOS inhibitors and also diminished in mice with targeted deletion of nNOS gene (nNOS(-/-)).	Glutamic Acid	0-9	nitric oxide synthase 1, neuronal	Mus musculus	304-308
10677544-6	2000	Glutamate neurotransmission involving N-methyl-d-aspartate (NMDA) receptors and neuronal nitric oxide synthase (nNOS) activity in part mediates neuronal DNA strand breaks and PARP activity, which are diminished by NMDA antagonists and NOS inhibitors and also diminished in mice with targeted deletion of nNOS gene (nNOS(-/-)).	Glutamic Acid	0-9	nitric oxide synthase 1, neuronal	Mus musculus	304-308
10677544-6	2000	Glutamate neurotransmission involving N-methyl-d-aspartate (NMDA) receptors and neuronal nitric oxide synthase (nNOS) activity in part mediates neuronal DNA strand breaks and PARP activity, which are diminished by NMDA antagonists and NOS inhibitors and also diminished in mice with targeted deletion of nNOS gene (nNOS(-/-)).	N-Methylaspartate	60-64	nitric oxide synthase 1, neuronal	Mus musculus	304-308
10677544-6	2000	Glutamate neurotransmission involving N-methyl-d-aspartate (NMDA) receptors and neuronal nitric oxide synthase (nNOS) activity in part mediates neuronal DNA strand breaks and PARP activity, which are diminished by NMDA antagonists and NOS inhibitors and also diminished in mice with targeted deletion of nNOS gene (nNOS(-/-)).	N-Methylaspartate	60-64	nitric oxide synthase 1, neuronal	Mus musculus	304-308
10657997-8	2000	Both DNA damage and cell death in the cerebral cortical neurons were abolished by treatment with 3-bromo-7-nitroindazole (30 mg/kg, intraperitoneal), which specifically inhibited nNOS.	3-bromo-7-nitroindazole	97-120	nitric oxide synthase 1, neuronal	Mus musculus	179-183
10657997-9	2000	Our results suggest that nNOS, its activator (calcium), and peroxynitrite exacerbate oxidative DNA damage after brain ischemia.-Huang, D., Shenoy, A., Cui, J., Huang, W., Liu, P. In situ detection of AP sites and DNA strand breaks bearing 3"-phosphate termini in ischemic mouse brain.	Calcium	46-53	nitric oxide synthase 1, neuronal	Mus musculus	25-29
10657997-9	2000	Our results suggest that nNOS, its activator (calcium), and peroxynitrite exacerbate oxidative DNA damage after brain ischemia.-Huang, D., Shenoy, A., Cui, J., Huang, W., Liu, P. In situ detection of AP sites and DNA strand breaks bearing 3"-phosphate termini in ischemic mouse brain.	Phosphates	242-251	nitric oxide synthase 1, neuronal	Mus musculus	25-29
10727711-9	2000	of 7-nitroindazole (7-NI), a non-selective non hypertensive inhibitor of nitric oxide synthase (NOS), significantly decreased MPP(+) levels.	7-nitroindazole	20-24	nitric oxide synthase 1, neuronal	Mus musculus	73-94
10516139-4	1999	The specific action of nitric oxide depends on its enzymatic sources, namely neuronal nitric oxide synthase (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS), each having distinct tissue localization.	Nitric Oxide	23-35	nitric oxide synthase 1, neuronal	Mus musculus	77-107
10849697-1	2000	Nitric oxide (NO) is endogenously generated from two constitutively expressed nitric oxide synthase (NOS) isoforms, i.e., neuronal (NOS-1) and endothelial (NOS-3).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	78-99
10849697-10	2000	In NOS-1 mutant mice, the ventilatory response to hypoxia (12% O2) were significantly augmented, compared to wild-type (WT) mice.	Oxygen	63-65	nitric oxide synthase 1, neuronal	Mus musculus	3-8
10849697-12	2000	The responses to cyanide were augmented in NOS-1; whereas they were blunted in NOS-3 mutant mice.	Cyanides	17-24	nitric oxide synthase 1, neuronal	Mus musculus	43-48
10642318-14	2000	We next evaluated the role of iNOS and nNOS in the response to L-Arg.	Arginine	63-68	nitric oxide synthase 1, neuronal	Mus musculus	39-43
10642318-15	2000	Addition of 0.5 mmol/L L-Arg to the bath decreased J(Cl) in THALs from iNOS and nNOS knockout mice by 37.7+/-6.4% (P<0.05) and 31.8+/-8.3% (P<0.01), respectively.	Arginine	23-28	nitric oxide synthase 1, neuronal	Mus musculus	80-84
11129101-0	2000	7-Nitroindazole, a nitric oxide synthase inhibitor, enhances the anticonvulsive action of ethosuximide and clonazepam against pentylenetetrazol-induced convulsions.	7-nitroindazole	0-15	nitric oxide synthase 1, neuronal	Mus musculus	19-40
11129101-0	2000	7-Nitroindazole, a nitric oxide synthase inhibitor, enhances the anticonvulsive action of ethosuximide and clonazepam against pentylenetetrazol-induced convulsions.	Ethosuximide	90-102	nitric oxide synthase 1, neuronal	Mus musculus	19-40
11129101-0	2000	7-Nitroindazole, a nitric oxide synthase inhibitor, enhances the anticonvulsive action of ethosuximide and clonazepam against pentylenetetrazol-induced convulsions.	Clonazepam	107-117	nitric oxide synthase 1, neuronal	Mus musculus	19-40
11129101-0	2000	7-Nitroindazole, a nitric oxide synthase inhibitor, enhances the anticonvulsive action of ethosuximide and clonazepam against pentylenetetrazol-induced convulsions.	Pentylenetetrazole	126-143	nitric oxide synthase 1, neuronal	Mus musculus	19-40
11129101-1	2000	The interaction of 7-nitroindazole (7-NI), a nitric oxide synthase (NOS) inhibitor, with the protective activity of conventional antiepileptics against pentylenetetrazol (PTZ)-induced seizures was tested in mice.	7-nitroindazole	19-34	nitric oxide synthase 1, neuronal	Mus musculus	45-66
11129101-1	2000	The interaction of 7-nitroindazole (7-NI), a nitric oxide synthase (NOS) inhibitor, with the protective activity of conventional antiepileptics against pentylenetetrazol (PTZ)-induced seizures was tested in mice.	7-nitroindazole	36-40	nitric oxide synthase 1, neuronal	Mus musculus	45-66
10954047-4	2000	The NO synthase (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) (18.7515 mg/kg), possessed antinociceptive activity.	NG-Nitroarginine Methyl Ester	33-65	nitric oxide synthase 1, neuronal	Mus musculus	4-15
10954047-4	2000	The NO synthase (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) (18.7515 mg/kg), possessed antinociceptive activity.	NG-Nitroarginine Methyl Ester	67-73	nitric oxide synthase 1, neuronal	Mus musculus	4-15
10590407-1	2000	Autoradiography with the nitric oxide synthase (NOS) inhibitor ((3)H)nitro-L-arginine ([(3)H]L-NNA) was used to quantify NOS in cervical and lumbar spinal cord in normal and dystrophic mice.	(3)h)nitro-l-arginine	64-85	nitric oxide synthase 1, neuronal	Mus musculus	25-46
10590407-6	2000	The higher affinity ((3)H)L-NNA binding site colocalized with nNOS and the lower affinity site with iNOS.	Nitroarginine	26-31	nitric oxide synthase 1, neuronal	Mus musculus	62-66
10663419-2	2000	OBJECTIVE: The present study was undertaken to determine the effect of chronic morphine treatment and abstinence on the expression of neuronal NO synthase (neuronal NOS, nNOS) in several brain regions of mice.	Morphine	79-87	nitric oxide synthase 1, neuronal	Mus musculus	156-168
10663419-2	2000	OBJECTIVE: The present study was undertaken to determine the effect of chronic morphine treatment and abstinence on the expression of neuronal NO synthase (neuronal NOS, nNOS) in several brain regions of mice.	Morphine	79-87	nitric oxide synthase 1, neuronal	Mus musculus	170-174
10663419-5	2000	RESULTS: Morphine-dependence produced an increase in the number of nNOS-positive cells in the main and accessory olfactory bulb, olfactory nuclei, cerebellum, locus coeruleus, medulla oblongata (nucleus of the solitary tract and prepositus hypoglossal nucleus), and a decrease in nNOS immunoreactivity in hypothalamus.	Morphine	9-17	nitric oxide synthase 1, neuronal	Mus musculus	67-71
10663419-5	2000	RESULTS: Morphine-dependence produced an increase in the number of nNOS-positive cells in the main and accessory olfactory bulb, olfactory nuclei, cerebellum, locus coeruleus, medulla oblongata (nucleus of the solitary tract and prepositus hypoglossal nucleus), and a decrease in nNOS immunoreactivity in hypothalamus.	Morphine	9-17	nitric oxide synthase 1, neuronal	Mus musculus	280-284
10663419-6	2000	The administration of naloxone to morphine-dependent mice to induce abstinence increased nNOS immunoreactivity in the hypothalamus and locus coeruleus.	Naloxone	22-30	nitric oxide synthase 1, neuronal	Mus musculus	89-93
10663419-6	2000	The administration of naloxone to morphine-dependent mice to induce abstinence increased nNOS immunoreactivity in the hypothalamus and locus coeruleus.	Morphine	34-42	nitric oxide synthase 1, neuronal	Mus musculus	89-93
10663419-7	2000	CONCLUSIONS: These results indicate that the chronic treatment with morphine leads to alterations in nNOS expression in important regions implicated in the physical tolerance and dependence to opiates and suggest the use of specific inhibitors of this isoform in these conditions.	Morphine	68-76	nitric oxide synthase 1, neuronal	Mus musculus	101-105
10672628-1	2000	RATIONALE: NG-nitro-L-arginine (L-NOARG), an inhibitor of nitric-oxide synthase (NOS), induces catalepsy in mice.	Nitroarginine	11-30	nitric oxide synthase 1, neuronal	Mus musculus	58-79
10672628-1	2000	RATIONALE: NG-nitro-L-arginine (L-NOARG), an inhibitor of nitric-oxide synthase (NOS), induces catalepsy in mice.	Nitroarginine	32-39	nitric oxide synthase 1, neuronal	Mus musculus	58-79
10642852-0	1999	Methamphetamine administration causes overexpression of nNOS in the mouse striatum.	Methamphetamine	0-15	nitric oxide synthase 1, neuronal	Mus musculus	56-60
10642852-5	1999	In contrast, METH caused marked increases in nNOS in the striatum and hippocampus at 1 and 24 h post-treatment.	Methamphetamine	13-17	nitric oxide synthase 1, neuronal	Mus musculus	45-49
10637120-1	1999	In stimulated murine macrophage, arginase and nitric oxide synthase (NOS) compete for their common substrate, l-arginine.	Arginine	110-120	nitric oxide synthase 1, neuronal	Mus musculus	46-67
10514420-0	1999	Nitric oxide synthase inhibition by N(G)-nitro-L-arginine methyl ester inhibits tumor-induced angiogenesis in mammary tumors.	NG-Nitroarginine Methyl Ester	36-70	nitric oxide synthase 1, neuronal	Mus musculus	0-21
10514420-1	1999	Using a murine breast cancer model, we earlier found a positive correlation between the expression of nitric oxide synthase (NOS) and tumor progression; treatment with inhibitors of NOS, N(G)-methyl-L-arginine (NMMA) and N(G)-nitro-L-arginine methyl ester (L-NAME), had antitumor and antimetastatic effects that were partly attributed to reduced tumor cell invasiveness.	Nitroarginine	187-209	nitric oxide synthase 1, neuronal	Mus musculus	102-123
10514420-1	1999	Using a murine breast cancer model, we earlier found a positive correlation between the expression of nitric oxide synthase (NOS) and tumor progression; treatment with inhibitors of NOS, N(G)-methyl-L-arginine (NMMA) and N(G)-nitro-L-arginine methyl ester (L-NAME), had antitumor and antimetastatic effects that were partly attributed to reduced tumor cell invasiveness.	N-methylmalonamic acid	211-215	nitric oxide synthase 1, neuronal	Mus musculus	102-123
10514420-1	1999	Using a murine breast cancer model, we earlier found a positive correlation between the expression of nitric oxide synthase (NOS) and tumor progression; treatment with inhibitors of NOS, N(G)-methyl-L-arginine (NMMA) and N(G)-nitro-L-arginine methyl ester (L-NAME), had antitumor and antimetastatic effects that were partly attributed to reduced tumor cell invasiveness.	NG-Nitroarginine Methyl Ester	221-255	nitric oxide synthase 1, neuronal	Mus musculus	102-123
10514420-1	1999	Using a murine breast cancer model, we earlier found a positive correlation between the expression of nitric oxide synthase (NOS) and tumor progression; treatment with inhibitors of NOS, N(G)-methyl-L-arginine (NMMA) and N(G)-nitro-L-arginine methyl ester (L-NAME), had antitumor and antimetastatic effects that were partly attributed to reduced tumor cell invasiveness.	NG-Nitroarginine Methyl Ester	257-263	nitric oxide synthase 1, neuronal	Mus musculus	102-123
10709868-1	2000	Nitric oxide (NO) is generated by 3 major isoforms of nitric oxide synthase (NOS) with complex and overlapping patterns of expression.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	54-75
10583370-7	1999	Fe-DTCS suppressed cytochrome c and ferricyanide reductase activities of nNOS, and markedly increased nNOS-mediated NADPH oxidation.	(N-dithiocarboxysarcosine)iron(III)	0-7	nitric oxide synthase 1, neuronal	Mus musculus	73-77
10583370-7	1999	Fe-DTCS suppressed cytochrome c and ferricyanide reductase activities of nNOS, and markedly increased nNOS-mediated NADPH oxidation.	(N-dithiocarboxysarcosine)iron(III)	0-7	nitric oxide synthase 1, neuronal	Mus musculus	102-106
10583370-7	1999	Fe-DTCS suppressed cytochrome c and ferricyanide reductase activities of nNOS, and markedly increased nNOS-mediated NADPH oxidation.	NADP	116-121	nitric oxide synthase 1, neuronal	Mus musculus	102-106
10583370-8	1999	Concomitantly, it accelerated oxygen consumption caused by activated nNOS.	Oxygen	30-36	nitric oxide synthase 1, neuronal	Mus musculus	69-73
10583370-9	1999	These results suggest that the ESR spin-trapping agent Fe-DTCS inhibits NO synthesis by interfering with the physiological electron flow from NADPH to nNOS heme iron.	(N-dithiocarboxysarcosine)iron(III)	55-62	nitric oxide synthase 1, neuronal	Mus musculus	151-155
10583370-9	1999	These results suggest that the ESR spin-trapping agent Fe-DTCS inhibits NO synthesis by interfering with the physiological electron flow from NADPH to nNOS heme iron.	NADP	142-147	nitric oxide synthase 1, neuronal	Mus musculus	151-155
10583370-9	1999	These results suggest that the ESR spin-trapping agent Fe-DTCS inhibits NO synthesis by interfering with the physiological electron flow from NADPH to nNOS heme iron.	Iron	161-165	nitric oxide synthase 1, neuronal	Mus musculus	151-155
10569751-4	1999	Treatment of the mice with S-methylisothiourea sulfate (SMT), a potent inhibitor of inducible NO synthase (NOS), prevented the elevation of serum NO levels and concomitantly reduced the enhanced response to PTZ.	S-methylisothiopseudouronium	27-54	nitric oxide synthase 1, neuronal	Mus musculus	94-105
10569751-4	1999	Treatment of the mice with S-methylisothiourea sulfate (SMT), a potent inhibitor of inducible NO synthase (NOS), prevented the elevation of serum NO levels and concomitantly reduced the enhanced response to PTZ.	S-methylisothiopseudouronium	56-59	nitric oxide synthase 1, neuronal	Mus musculus	94-105
10569751-4	1999	Treatment of the mice with S-methylisothiourea sulfate (SMT), a potent inhibitor of inducible NO synthase (NOS), prevented the elevation of serum NO levels and concomitantly reduced the enhanced response to PTZ.	Pentylenetetrazole	207-210	nitric oxide synthase 1, neuronal	Mus musculus	94-105
10600405-5	1999	We show that in adult normal and mdx mice (an animal model of Duchenne myopathy) treated with l-arginine, the substrate of nitric oxide synthase (NOS), a pool of utrophin localized at the membrane appeared and increased, respectively.	Arginine	94-104	nitric oxide synthase 1, neuronal	Mus musculus	123-144
10516139-4	1999	The specific action of nitric oxide depends on its enzymatic sources, namely neuronal nitric oxide synthase (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS), each having distinct tissue localization.	Nitric Oxide	23-35	nitric oxide synthase 1, neuronal	Mus musculus	109-113
10498610-4	1999	Addition of the NO synthase (NOS) inhibitor N-monomethyl arginine (NMMA) partially restored Fe uptake but either had no effect on or downregulated TfR expression, which suggests that NO by itself is able to affect iron availability.	n-monomethyl arginine	44-65	nitric oxide synthase 1, neuronal	Mus musculus	16-27
10498610-4	1999	Addition of the NO synthase (NOS) inhibitor N-monomethyl arginine (NMMA) partially restored Fe uptake but either had no effect on or downregulated TfR expression, which suggests that NO by itself is able to affect iron availability.	nmma	67-71	nitric oxide synthase 1, neuronal	Mus musculus	16-27
10498610-4	1999	Addition of the NO synthase (NOS) inhibitor N-monomethyl arginine (NMMA) partially restored Fe uptake but either had no effect on or downregulated TfR expression, which suggests that NO by itself is able to affect iron availability.	Iron	92-94	nitric oxide synthase 1, neuronal	Mus musculus	16-27
10498610-4	1999	Addition of the NO synthase (NOS) inhibitor N-monomethyl arginine (NMMA) partially restored Fe uptake but either had no effect on or downregulated TfR expression, which suggests that NO by itself is able to affect iron availability.	Iron	214-218	nitric oxide synthase 1, neuronal	Mus musculus	16-27
10495405-1	1999	We have studied, by a combined in vitro and in vivo approach, the relation between the inhibitory action of N(G)-nitro-l-arginine methyl ester (L-NAME), a selective inhibitor of nitric oxide synthase (NOS), on the activity of islet constitutive NOS (cNOS) and glucose regulation of islet hormone release in mice.	NG-Nitroarginine Methyl Ester	108-142	nitric oxide synthase 1, neuronal	Mus musculus	178-199
10495405-1	1999	We have studied, by a combined in vitro and in vivo approach, the relation between the inhibitory action of N(G)-nitro-l-arginine methyl ester (L-NAME), a selective inhibitor of nitric oxide synthase (NOS), on the activity of islet constitutive NOS (cNOS) and glucose regulation of islet hormone release in mice.	NG-Nitroarginine Methyl Ester	144-150	nitric oxide synthase 1, neuronal	Mus musculus	178-199
10482797-2	1999	Protection against MPTP neurotoxicity has been shown by treating mice with 7-nitroindazole (7-NI), a reversible inhibitor of both MAO-B and neuronal nitric oxide synthase (nNOS) activity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	19-23	nitric oxide synthase 1, neuronal	Mus musculus	140-170
10493775-2	1999	Specific pharmacological inhibition of nNOS with 7-nitroindazole also augments aggressive behavior.	7-nitroindazole	49-64	nitric oxide synthase 1, neuronal	Mus musculus	39-43
10534440-2	1999	Pharmacological inhibition of nitric oxide synthase (NOS) with the nonspecific NOS inhibitor, l-N(G)-nitro-Arg-methyl ester (l-NAME), induced deficits in both the number of ovarian rupture sites and the number of oocytes recovered in the oviducts of mice.	l-n(g)-nitro-arg-methyl ester	94-123	nitric oxide synthase 1, neuronal	Mus musculus	30-51
10534440-2	1999	Pharmacological inhibition of nitric oxide synthase (NOS) with the nonspecific NOS inhibitor, l-N(G)-nitro-Arg-methyl ester (l-NAME), induced deficits in both the number of ovarian rupture sites and the number of oocytes recovered in the oviducts of mice.	NG-Nitroarginine Methyl Ester	125-131	nitric oxide synthase 1, neuronal	Mus musculus	30-51
10534440-3	1999	Female neuronal NOS knockout (nNOS-/-) mice have normal numbers of rupture sites, but reduced numbers of oocytes recovered following systemic injections of gonadotropins, suggesting that NO produced by nNOS accounts, in part, for deficits in ovulatory efficiency observed after l-NAME administration.	NG-Nitroarginine Methyl Ester	278-284	nitric oxide synthase 1, neuronal	Mus musculus	202-206
10512307-2	1999	ETOH also inhibits PMN recruitment into the lung and enhances NOS I-mediated production of NO.	Ethanol	0-4	nitric oxide synthase 1, neuronal	Mus musculus	62-67
10512307-11	1999	of 7-NI to nNOS-KO mice resulted in death of all the animals within 10 min.	7-nitroindazole	3-7	nitric oxide synthase 1, neuronal	Mus musculus	11-15
10512307-12	1999	Pretreatment of nNOS-KO with 7-NI (10 mg/kg) did not affect LPS-stimulated PMN recruitment.	7-nitroindazole	29-33	nitric oxide synthase 1, neuronal	Mus musculus	16-20
10512307-15	1999	In contrast, pretreatment of nNOS-KO with ETOH produced little inhibition of LPS-stimulated lung recruitment of PMNs when compared with that measured in WT mice.	Ethanol	42-46	nitric oxide synthase 1, neuronal	Mus musculus	29-33
10512307-19	1999	Finally, inhibition of NOS I and NOS I deletion inhibited the in vivo metabolism of ETOH.	Ethanol	84-88	nitric oxide synthase 1, neuronal	Mus musculus	23-28
10512307-19	1999	Finally, inhibition of NOS I and NOS I deletion inhibited the in vivo metabolism of ETOH.	Ethanol	84-88	nitric oxide synthase 1, neuronal	Mus musculus	33-38
10482797-2	1999	Protection against MPTP neurotoxicity has been shown by treating mice with 7-nitroindazole (7-NI), a reversible inhibitor of both MAO-B and neuronal nitric oxide synthase (nNOS) activity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	19-23	nitric oxide synthase 1, neuronal	Mus musculus	172-176
10482797-2	1999	Protection against MPTP neurotoxicity has been shown by treating mice with 7-nitroindazole (7-NI), a reversible inhibitor of both MAO-B and neuronal nitric oxide synthase (nNOS) activity.	7-nitroindazole	75-90	nitric oxide synthase 1, neuronal	Mus musculus	140-170
10482797-2	1999	Protection against MPTP neurotoxicity has been shown by treating mice with 7-nitroindazole (7-NI), a reversible inhibitor of both MAO-B and neuronal nitric oxide synthase (nNOS) activity.	7-nitroindazole	75-90	nitric oxide synthase 1, neuronal	Mus musculus	172-176
10482797-2	1999	Protection against MPTP neurotoxicity has been shown by treating mice with 7-nitroindazole (7-NI), a reversible inhibitor of both MAO-B and neuronal nitric oxide synthase (nNOS) activity.	7-nitroindazole	92-96	nitric oxide synthase 1, neuronal	Mus musculus	140-170
10482797-2	1999	Protection against MPTP neurotoxicity has been shown by treating mice with 7-nitroindazole (7-NI), a reversible inhibitor of both MAO-B and neuronal nitric oxide synthase (nNOS) activity.	7-nitroindazole	92-96	nitric oxide synthase 1, neuronal	Mus musculus	172-176
10404408-9	1999	These results indicate that nNOS-IR neurons in the mouse hippocampus represent a subpopulation of gamma-aminobutyric acid (GABA)ergic neurons and suggest that the laminar distributions of nNOS-IR neurons related to possible functional heterogeneity of GABAergic neurons in each hippocampal layer.	gamma-Aminobutyric Acid	98-121	nitric oxide synthase 1, neuronal	Mus musculus	28-32
10404408-9	1999	These results indicate that nNOS-IR neurons in the mouse hippocampus represent a subpopulation of gamma-aminobutyric acid (GABA)ergic neurons and suggest that the laminar distributions of nNOS-IR neurons related to possible functional heterogeneity of GABAergic neurons in each hippocampal layer.	gamma-Aminobutyric Acid	123-127	nitric oxide synthase 1, neuronal	Mus musculus	28-32
10444402-2	1999	Inhibition of nitric oxide synthase (NOS) and soluble guanylate cyclase (sGC) resulted in complete inhibition of agonist-induced cGMP levels.	Cyclic GMP	129-133	nitric oxide synthase 1, neuronal	Mus musculus	14-35
10478861-0	1999	Lead acetate exposure inhibits nitric oxide synthase activity in capillary and synaptosomal fractions of mouse brain.	lead acetate	0-12	nitric oxide synthase 1, neuronal	Mus musculus	31-52
10407030-9	1999	Our findings provide a cellular localization for nNOS activation in association with ischemic stroke and establish that NO is not likely a direct neurotoxin, whereas its conversion to peroxynitrite is associated with cell death.	Peroxynitrous Acid	184-197	nitric oxide synthase 1, neuronal	Mus musculus	49-53
10442086-2	1999	Nitric oxide (NO) alone or in cooperation with superoxide anion and peroxynitrite is emerging as a predominant effector of neurodegeneration The use of NO synthase (NOS) inhibitors and mutant mice lacking each NOS isoform have provided evidence for the injurious effects of NO derived from neuronal or inducible isoforms.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	152-163
10086391-1	1999	Nitric oxide (NO) is an ubiquitous signaling molecule produced from L-arginine by NO synthase (NOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	82-93
10400091-1	1999	The purpose of this study was to evaluate the role of neuronal nitric oxide synthase (nNOS) in nitrotyrosine (NO2-Tyr) formation in the early phase of ischemia-reperfusion in mouse brain.	3-nitrotyrosine	95-108	nitric oxide synthase 1, neuronal	Mus musculus	54-84
10400091-1	1999	The purpose of this study was to evaluate the role of neuronal nitric oxide synthase (nNOS) in nitrotyrosine (NO2-Tyr) formation in the early phase of ischemia-reperfusion in mouse brain.	3-nitrotyrosine	95-108	nitric oxide synthase 1, neuronal	Mus musculus	86-90
10400091-3	1999	At 25 mg/kg, 7-NI reduced NO2-Tyr formation to about a half of that in the vehicle-treated group (0.10 +/- 0.07 vs. 0.18 +/- 0.05%), while 50 mg/kg suppressed NO2-Tyr formation to below the limit of detection, indicating that nNOS is responsible for most of the NO2-Tyr formation in the early phase after reperfusion.	7-nitroindazole	13-17	nitric oxide synthase 1, neuronal	Mus musculus	226-230
10452129-0	1999	Correlation between inhibitions of morphine withdrawal and nitric-oxide synthase by agmatine.	Morphine	35-43	nitric oxide synthase 1, neuronal	Mus musculus	59-80
10452129-0	1999	Correlation between inhibitions of morphine withdrawal and nitric-oxide synthase by agmatine.	Agmatine	84-92	nitric oxide synthase 1, neuronal	Mus musculus	59-80
10452129-1	1999	AIM: To study correlation between inhibitions of naloxone-precipitated withdrawal jumps and nitric-oxide synthase (NOS) activity by agmatine.	Naloxone	49-57	nitric oxide synthase 1, neuronal	Mus musculus	92-113
10452129-1	1999	AIM: To study correlation between inhibitions of naloxone-precipitated withdrawal jumps and nitric-oxide synthase (NOS) activity by agmatine.	Agmatine	132-140	nitric oxide synthase 1, neuronal	Mus musculus	92-113
10075660-0	1999	Modulation of the remote heme site geometry of recombinant mouse neuronal nitric-oxide synthase by the N-terminal hook region.	Heme	25-29	nitric oxide synthase 1, neuronal	Mus musculus	65-95
10075660-6	1999	These results suggest that Asp-314 and Thr-315 both play critical structural roles in stabilizing the heme domain and subunit interactions in mouse nNOS.	Aspartic Acid	27-30	nitric oxide synthase 1, neuronal	Mus musculus	148-152
10075660-6	1999	These results suggest that Asp-314 and Thr-315 both play critical structural roles in stabilizing the heme domain and subunit interactions in mouse nNOS.	Threonine	39-42	nitric oxide synthase 1, neuronal	Mus musculus	148-152
10075660-6	1999	These results suggest that Asp-314 and Thr-315 both play critical structural roles in stabilizing the heme domain and subunit interactions in mouse nNOS.	Heme	102-106	nitric oxide synthase 1, neuronal	Mus musculus	148-152
10364190-1	1999	Mouse neuronal nitric-oxide synthase 2 (nNOS2) is a unique natural variant of constitutive neuronal nitric-oxide synthase (nNOS) specifically expressed in the central nervous system having a 105-amino acid deletion in the heme-binding domain as a result of in-frame mutation by specific alternative splicing.	Heme	222-226	nitric oxide synthase 1, neuronal	Mus musculus	6-36
10364190-1	1999	Mouse neuronal nitric-oxide synthase 2 (nNOS2) is a unique natural variant of constitutive neuronal nitric-oxide synthase (nNOS) specifically expressed in the central nervous system having a 105-amino acid deletion in the heme-binding domain as a result of in-frame mutation by specific alternative splicing.	Heme	222-226	nitric oxide synthase 1, neuronal	Mus musculus	91-121
10364190-1	1999	Mouse neuronal nitric-oxide synthase 2 (nNOS2) is a unique natural variant of constitutive neuronal nitric-oxide synthase (nNOS) specifically expressed in the central nervous system having a 105-amino acid deletion in the heme-binding domain as a result of in-frame mutation by specific alternative splicing.	Heme	222-226	nitric oxide synthase 1, neuronal	Mus musculus	40-44
10362674-9	1999	Transmigration of neutrophils into the peritoneum following thioglycollate injection was also significantly augmented in nNOS -/- and ecNOS -/- mice.	Thioglycolates	60-74	nitric oxide synthase 1, neuronal	Mus musculus	121-125
10370135-2	1999	It is generated from l-arginine by nitric oxide synthases (NOS), which come in three isoforms depending on the tissue of origin, namely inducible-NOS (iNOS in macrophages), endothelial-NOS (eNOS in endothelial cells) and neural-NOS (nNOS in neural cells).	Arginine	21-31	nitric oxide synthase 1, neuronal	Mus musculus	233-237
10220303-1	1999	It is now known that overproduction of nitric oxide (NO) by nitric oxide synthase (NOS) is an important contributing factor for the development of cardiovascular collapse and subsequent death in endotoxic shock.	Nitric Oxide	39-51	nitric oxide synthase 1, neuronal	Mus musculus	60-81
10086391-1	1999	Nitric oxide (NO) is an ubiquitous signaling molecule produced from L-arginine by NO synthase (NOS).	Arginine	68-78	nitric oxide synthase 1, neuronal	Mus musculus	82-93
9971738-2	1999	As NO is synthesized by NO synthase (NOS) from arginine, a common substrate of arginase, these two enzymes compete for arginine.	Arginine	47-55	nitric oxide synthase 1, neuronal	Mus musculus	24-35
10077313-1	1999	Nitric oxide is formed in the brain primarily by neurons containing neuronal nitric oxide synthase (nNOS), though some neurons may express endothelial NOS (eNOS), and inducible NOS (iNOS) only occurs in neurons following toxic stimuli.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	68-98
10077313-1	1999	Nitric oxide is formed in the brain primarily by neurons containing neuronal nitric oxide synthase (nNOS), though some neurons may express endothelial NOS (eNOS), and inducible NOS (iNOS) only occurs in neurons following toxic stimuli.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	100-104
10077313-3	1999	nNOS- animals resist brain damage following middle cerebral artery occlusions consistent with evidence that excess release of nitric oxide mediates neurotoxicity in ischemic stroke.	Nitric Oxide	126-138	nitric oxide synthase 1, neuronal	Mus musculus	0-4
9971738-2	1999	As NO is synthesized by NO synthase (NOS) from arginine, a common substrate of arginase, these two enzymes compete for arginine.	Arginine	119-127	nitric oxide synthase 1, neuronal	Mus musculus	24-35
10036989-0	1999	Circadian locomotor analysis of male mice lacking the gene for neuronal nitric oxide synthase (nNOS-/-) Nitric oxide (NO) is an endogenous gas that functions as a neurotransmitter.	Nitric Oxide	104-116	nitric oxide synthase 1, neuronal	Mus musculus	63-93
10036989-0	1999	Circadian locomotor analysis of male mice lacking the gene for neuronal nitric oxide synthase (nNOS-/-) Nitric oxide (NO) is an endogenous gas that functions as a neurotransmitter.	Nitric Oxide	104-116	nitric oxide synthase 1, neuronal	Mus musculus	95-102
9892689-13	1999	produced endogenously from cardiac SR NOS, and 7-nitroindazole, a selective nNOS inhibitor, completely prevented this inhibition.	7-nitroindazole	47-62	nitric oxide synthase 1, neuronal	Mus musculus	76-80
9890982-5	1999	In the sarcolemma, nNOS regulates the homeostasis of reactive free radical species and may contribute to the oxidative damage to muscle protein in muscle disease such as Duchenne muscular dystrophy.	reactive free radical species	53-82	nitric oxide synthase 1, neuronal	Mus musculus	19-23
10591048-2	1999	7-Nitroindazole (7-NI) both a reversible MAO-B inhibitor and a neuronal nitric oxide synthase (nNOS) inhibitor, and (R)-deprenyl a potent MAO-B inactivator, provide neuroprotection in the C57BL/6 mouse model of MPTP neurotoxicity.	7-nitroindazole	0-15	nitric oxide synthase 1, neuronal	Mus musculus	63-93
9892224-10	1999	Islets stimulated by glucose or L-arginine displayed a marked increase in their NO-synthase (NOS) activity.	Glucose	21-28	nitric oxide synthase 1, neuronal	Mus musculus	80-91
9892224-10	1999	Islets stimulated by glucose or L-arginine displayed a marked increase in their NO-synthase (NOS) activity.	Arginine	32-42	nitric oxide synthase 1, neuronal	Mus musculus	80-91
10338314-9	1999	The transgenic mice expressing a familial amyotrophic lateral sclerosis-linked mutant human copper/zinc superoxide dismutase type 1 on neuronal nitric oxide synthase null background do not live significantly longer than transgenic mice expressing a familial amyotrophic lateral sclerosis-linked mutant human copper/zinc superoxide dismutase type 1.	Copper	92-98	nitric oxide synthase 1, neuronal	Mus musculus	135-165
10613509-1	1999	The cellular and subcellular distribution of neuronal nitric oxide synthase and its related reduced beta-nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase activity was compared in wild-type and homozygous knockout mice, in which the gene for neuronal nitric oxide synthase has been disrupted, resulting in a lack of the predominant splice isoform alpha.	NADP	100-148	nitric oxide synthase 1, neuronal	Mus musculus	45-75
10613509-1	1999	The cellular and subcellular distribution of neuronal nitric oxide synthase and its related reduced beta-nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase activity was compared in wild-type and homozygous knockout mice, in which the gene for neuronal nitric oxide synthase has been disrupted, resulting in a lack of the predominant splice isoform alpha.	NADP	150-155	nitric oxide synthase 1, neuronal	Mus musculus	45-75
10613509-3	1999	Using the tetrazolium salt 2-(2-benzothiazolyl)-5-styryl-3-(4"-phthalhydrazidyl)-tetrazo++ +-lium chloride (BSPT), these neurons were filled with NADPH-diaphorase reaction product, whereas the equivalent neurons of knockout mice showed, if at all, only traces of neuronal nitric oxide synthase immunoreactivity in parallel to a diminished NADPH-diaphorase labelling.	3-(1,3-BENZOTHIAZOL-2-YL)-2-(1,4-DIOXO-1,2,3,4-TETRAHYDROPHTHALAZIN-6-YL)-5-[(E)-2-PHENYLVINYL]-3H-TETRAAZOL-2-IUM	108-112	nitric oxide synthase 1, neuronal	Mus musculus	263-293
10613509-4	1999	Subcellularly, the neuronal nitric oxide synthase-related diaminobenzidine product was, apparently owing to diffusion artifact, more or less evenly distributed in the cytosol of the neuronal perikarya and dendrites of wild-type mice.	4,4'-Dihydrazino-biphenyl	58-74	nitric oxide synthase 1, neuronal	Mus musculus	19-49
10037495-5	1999	We now report that whereas in wild-type mice, nNOS, like PrPc, is associated with detergent-insoluble cholesterol-rich membranous microdomains (rafts), this is not the case in brains of scrapie-infected or in those of adult PrP(0/0) mice.	Cholesterol	102-113	nitric oxide synthase 1, neuronal	Mus musculus	46-50
9852587-3	1998	Compared to saline-treated wild-type animals the number of dendritic bifurcations was significantly reduced in nNOS knock-out animals and MK-801-treated wild-type animals.	Sodium Chloride	12-18	nitric oxide synthase 1, neuronal	Mus musculus	111-115
9852587-4	1998	There was no significant difference in dendritic bifurcation between MK-801-treated wild-type, MK-801-treated nNOS knock-out, and saline-treated nNOS knock-out animals, suggesting that nNOS knock-out and NMDA receptor block had similar effects.	Dizocilpine Maleate	95-101	nitric oxide synthase 1, neuronal	Mus musculus	110-114
10591048-2	1999	7-Nitroindazole (7-NI) both a reversible MAO-B inhibitor and a neuronal nitric oxide synthase (nNOS) inhibitor, and (R)-deprenyl a potent MAO-B inactivator, provide neuroprotection in the C57BL/6 mouse model of MPTP neurotoxicity.	7-nitroindazole	17-21	nitric oxide synthase 1, neuronal	Mus musculus	63-93
10591048-2	1999	7-Nitroindazole (7-NI) both a reversible MAO-B inhibitor and a neuronal nitric oxide synthase (nNOS) inhibitor, and (R)-deprenyl a potent MAO-B inactivator, provide neuroprotection in the C57BL/6 mouse model of MPTP neurotoxicity.	7-nitroindazole	17-21	nitric oxide synthase 1, neuronal	Mus musculus	95-99
9877018-0	1998	Resistance of neuronal nitric oxide synthase-deficient mice to cocaine-induced locomotor sensitization.	Cocaine	63-70	nitric oxide synthase 1, neuronal	Mus musculus	14-44
10098725-2	1998	Previous experiments indicated that the increase in brain tryptophan and 5-hydroxyindoleacetic acid (5-HIAA) observed in response to administration of endotoxin (lipopolysaccharide, LPS) and interleukin-1 (IL-1) were largely prevented by pretreatment with N-nitro-L-arginine methylester (L-NAME), an inhibitor of NO synthase (NOS).	Tryptophan	58-68	nitric oxide synthase 1, neuronal	Mus musculus	313-324
9877018-2	1998	The present study was undertaken to investigate whether mice lacking the neuronal nitric oxide synthase (nNOS) gene are protected from cocaine-induced behavioral sensitization.	Cocaine	135-142	nitric oxide synthase 1, neuronal	Mus musculus	73-103
9877018-2	1998	The present study was undertaken to investigate whether mice lacking the neuronal nitric oxide synthase (nNOS) gene are protected from cocaine-induced behavioral sensitization.	Cocaine	135-142	nitric oxide synthase 1, neuronal	Mus musculus	105-109
9877018-7	1998	Male homozygote nNOS(-/-) mice were sensitive to the acute effect of cocaine (15 mg/kg) on day 1; however, they developed neither a sensitized response to cocaine (on day 5 and 15) nor a conditioned locomotion.	Cocaine	69-76	nitric oxide synthase 1, neuronal	Mus musculus	16-20
10098725-2	1998	Previous experiments indicated that the increase in brain tryptophan and 5-hydroxyindoleacetic acid (5-HIAA) observed in response to administration of endotoxin (lipopolysaccharide, LPS) and interleukin-1 (IL-1) were largely prevented by pretreatment with N-nitro-L-arginine methylester (L-NAME), an inhibitor of NO synthase (NOS).	Hydroxyindoleacetic Acid	73-99	nitric oxide synthase 1, neuronal	Mus musculus	313-324
9877018-13	1998	Taken together, our results suggest that the resistance of homozygote nNOS(-/-) mice to cocaine-induced behavioral sensitization is primarily due to the deletion of the nNOS gene.	Cocaine	88-95	nitric oxide synthase 1, neuronal	Mus musculus	70-74
10098725-2	1998	Previous experiments indicated that the increase in brain tryptophan and 5-hydroxyindoleacetic acid (5-HIAA) observed in response to administration of endotoxin (lipopolysaccharide, LPS) and interleukin-1 (IL-1) were largely prevented by pretreatment with N-nitro-L-arginine methylester (L-NAME), an inhibitor of NO synthase (NOS).	Hydroxyindoleacetic Acid	101-107	nitric oxide synthase 1, neuronal	Mus musculus	313-324
9877018-13	1998	Taken together, our results suggest that the resistance of homozygote nNOS(-/-) mice to cocaine-induced behavioral sensitization is primarily due to the deletion of the nNOS gene.	Cocaine	88-95	nitric oxide synthase 1, neuronal	Mus musculus	169-173
9679181-2	1998	The role of endogenous nitric oxide (NO) generated by neuronal nitric oxide synthase (NOS-1) in the control of respiration during hypoxia and hypercapnia was assessed using mutant mice deficient in NOS-1.	Nitric Oxide	23-35	nitric oxide synthase 1, neuronal	Mus musculus	54-84
28921181-0	1998	7-Nitroindazole, a selective inhibitor of neuronal nitric oxide synthase: effect on sevoflurane MAC and cerebellar cyclic GMP in mice.	7-nitroindazole	0-15	nitric oxide synthase 1, neuronal	Mus musculus	42-72
28921181-3	1998	We examined the effects of 7-nitroindazole (7-NI), a selective inhibitor of neuronal NOS (nNOS), on the MAC of sevoflurane and cerebellar cyclic guanosine monophosphate (cGMP) levels in mice.	7-nitroindazole	44-48	nitric oxide synthase 1, neuronal	Mus musculus	76-88
28921181-3	1998	We examined the effects of 7-nitroindazole (7-NI), a selective inhibitor of neuronal NOS (nNOS), on the MAC of sevoflurane and cerebellar cyclic guanosine monophosphate (cGMP) levels in mice.	Sevoflurane	111-122	nitric oxide synthase 1, neuronal	Mus musculus	76-88
28921181-3	1998	We examined the effects of 7-nitroindazole (7-NI), a selective inhibitor of neuronal NOS (nNOS), on the MAC of sevoflurane and cerebellar cyclic guanosine monophosphate (cGMP) levels in mice.	Sevoflurane	111-122	nitric oxide synthase 1, neuronal	Mus musculus	90-94
28921181-8	1998	CONCLUSION: Acute or chronic selective inhibition of neuronal NOS decreases the sevoflurane MAC and cerebellar cGMP levels in mice.	Sevoflurane	80-91	nitric oxide synthase 1, neuronal	Mus musculus	53-65
28921181-8	1998	CONCLUSION: Acute or chronic selective inhibition of neuronal NOS decreases the sevoflurane MAC and cerebellar cGMP levels in mice.	Cyclic GMP	111-115	nitric oxide synthase 1, neuronal	Mus musculus	53-65
9715804-1	1998	The effect of acute treatment with L-arginine, a substrate for nitric oxide synthase (NOS) that forms NO, an important second messenger, on morphine antinociception and distribution of morphine in central and peripheral tissues of male Swiss-Webster mice was determined.	Arginine	35-45	nitric oxide synthase 1, neuronal	Mus musculus	63-84
9879728-6	1998	Nitric oxide synthase (NOS) inhibitors, NG-nitro-L-arginine methyl ester and 7-nitroindazole (a selective neuronal NOS inhibitor) markedly inhibited the enhancing effect by either Mn2+ or Ni2+ on the neurogenic detrusor contractions.	Manganese(2+)	180-184	nitric oxide synthase 1, neuronal	Mus musculus	0-21
9879728-6	1998	Nitric oxide synthase (NOS) inhibitors, NG-nitro-L-arginine methyl ester and 7-nitroindazole (a selective neuronal NOS inhibitor) markedly inhibited the enhancing effect by either Mn2+ or Ni2+ on the neurogenic detrusor contractions.	Nickel(2+)	188-192	nitric oxide synthase 1, neuronal	Mus musculus	0-21
9801393-11	1998	However, in the central zone of ischemia, elevations in glutamate and GABA were significantly lower in the nNOS mutants.	Glutamic Acid	56-65	nitric oxide synthase 1, neuronal	Mus musculus	107-111
9801393-11	1998	However, in the central zone of ischemia, elevations in glutamate and GABA were significantly lower in the nNOS mutants.	gamma-Aminobutyric Acid	70-74	nitric oxide synthase 1, neuronal	Mus musculus	107-111
9801393-14	1998	These results suggest that NO derived from the nNOS isoform contributes to tissue damage after focal ischemia by amplifying excitotoxic amino acid release in the core and deleterious waves of SD-like depolarizations in the periphery.	SD 0006	192-194	nitric oxide synthase 1, neuronal	Mus musculus	47-51
9799513-0	1998	Reactions catalyzed by tetrahydrobiopterin-free nitric oxide synthase.	sapropterin	23-42	nitric oxide synthase 1, neuronal	Mus musculus	48-69
9799513-1	1998	Murine macrophage nitric oxide synthase (NOS) was expressed in E. coli and purified in the presence (holoNOS) or absence (H4B-free NOS) of (6R)-tetrahydro-L-biopterin (H4B).	sapropterin	122-125	nitric oxide synthase 1, neuronal	Mus musculus	18-39
9799513-1	1998	Murine macrophage nitric oxide synthase (NOS) was expressed in E. coli and purified in the presence (holoNOS) or absence (H4B-free NOS) of (6R)-tetrahydro-L-biopterin (H4B).	sapropterin	139-166	nitric oxide synthase 1, neuronal	Mus musculus	18-39
9799513-1	1998	Murine macrophage nitric oxide synthase (NOS) was expressed in E. coli and purified in the presence (holoNOS) or absence (H4B-free NOS) of (6R)-tetrahydro-L-biopterin (H4B).	sapropterin	168-171	nitric oxide synthase 1, neuronal	Mus musculus	18-39
9822444-6	1998	eNOS (-/-) mice had higher BP than +/+ or +/-mice, and acute administration of the selective nNOS inhibitor 7-nitroindazole (7-NI) decreased their mean BP from 137+/-13 to 124+/-12 mm Hg (P<0.01).	7-nitroindazole	108-123	nitric oxide synthase 1, neuronal	Mus musculus	93-97
9822444-6	1998	eNOS (-/-) mice had higher BP than +/+ or +/-mice, and acute administration of the selective nNOS inhibitor 7-nitroindazole (7-NI) decreased their mean BP from 137+/-13 to 124+/-12 mm Hg (P<0.01).	7-nitroindazole	125-129	nitric oxide synthase 1, neuronal	Mus musculus	93-97
9769319-11	1998	In nNOS-/- mice, atropine administration led to a much smaller change in mean HR (-2+/-9 vs. 49+/-5 bpm, P = 0.0008) and in HR variance (64+/-24 vs. -903+/-295 bpm2, P = 0.02) than in WT mice.	Atropine	17-25	nitric oxide synthase 1, neuronal	Mus musculus	3-7
9769319-15	1998	However, PTX-treated nNOS-/- mice had a dramatically attenuated response to phenylephrine.	Phenylephrine	76-89	nitric oxide synthase 1, neuronal	Mus musculus	21-25
9679181-2	1998	The role of endogenous nitric oxide (NO) generated by neuronal nitric oxide synthase (NOS-1) in the control of respiration during hypoxia and hypercapnia was assessed using mutant mice deficient in NOS-1.	Nitric Oxide	23-35	nitric oxide synthase 1, neuronal	Mus musculus	86-91
9679181-28	1998	These results support the idea that nitric oxide generated by NOS-1 is an important physiological modulator of respiration during hypoxia.	Nitric Oxide	36-48	nitric oxide synthase 1, neuronal	Mus musculus	62-67
9721919-0	1998	The role of neuronal nitric oxide synthase in cocaine-induced conditioned place preference.	Cocaine	46-53	nitric oxide synthase 1, neuronal	Mus musculus	12-42
9804111-0	1998	Neuronal nitric oxide synthase inhibitor, 7-nitroindazole, delays motor dysfunction and spinal motoneuron degeneration in the wobbler mouse.	7-nitroindazole	42-57	nitric oxide synthase 1, neuronal	Mus musculus	0-30
9721919-2	1998	In the present study we investigated the role of nNOS in the rewarding properties of cocaine.	Cocaine	85-92	nitric oxide synthase 1, neuronal	Mus musculus	49-53
9721919-4	1998	Pretreatment with the nNOS inhibitor, 7-nitroindazole (7-NI; 25 mg/kg), completely blocked cocaine-induced CPP.	7-nitroindazole	38-53	nitric oxide synthase 1, neuronal	Mus musculus	22-26
9721919-4	1998	Pretreatment with the nNOS inhibitor, 7-nitroindazole (7-NI; 25 mg/kg), completely blocked cocaine-induced CPP.	7-nitroindazole	55-59	nitric oxide synthase 1, neuronal	Mus musculus	22-26
9721919-4	1998	Pretreatment with the nNOS inhibitor, 7-nitroindazole (7-NI; 25 mg/kg), completely blocked cocaine-induced CPP.	Cocaine	91-98	nitric oxide synthase 1, neuronal	Mus musculus	22-26
9721919-5	1998	Mice deficient for the nNOS gene (homozygote nNOS(-/-) mice) were resistant to cocaine-induced CPP, while wild-type nNOS(+/+) mice developed a marked CPP following cocaine administration.	Cocaine	79-86	nitric oxide synthase 1, neuronal	Mus musculus	23-27
9721919-5	1998	Mice deficient for the nNOS gene (homozygote nNOS(-/-) mice) were resistant to cocaine-induced CPP, while wild-type nNOS(+/+) mice developed a marked CPP following cocaine administration.	Cocaine	164-171	nitric oxide synthase 1, neuronal	Mus musculus	23-27
9721919-6	1998	Both, the pharmacological and genetic manipulations of nNOS suggest that nitric oxide (NO) is involved in the rewarding properties of cocaine.	Nitric Oxide	73-85	nitric oxide synthase 1, neuronal	Mus musculus	55-59
9721919-6	1998	Both, the pharmacological and genetic manipulations of nNOS suggest that nitric oxide (NO) is involved in the rewarding properties of cocaine.	Cocaine	134-141	nitric oxide synthase 1, neuronal	Mus musculus	55-59
9888514-2	1998	NO is synthesised from arginine, by a family of Nitric Oxide Synthase (NOS).	Arginine	23-31	nitric oxide synthase 1, neuronal	Mus musculus	48-69
9691096-2	1998	We have found that the antimalarial and antiinflammatory drug, chloroquine, is able to stimulate NO synthase (NOS) activity in murine, porcine, and human endothelial cells in vitro: the increase of enzyme activity is dependent on a de novo synthesis of some regulatory protein, as it is inhibited by cycloheximide but is not accompanied by an increased expression of inducible or constitutive NOS isoforms.	Chloroquine	63-74	nitric oxide synthase 1, neuronal	Mus musculus	97-108
9681438-1	1998	This study shows that activation of M1 muscarinic receptors, when coexpressed in Chinese hamster ovary (CHO)-K1 cells with neuronal nitric oxide (NO) synthase (nNOS), produces early and late phases of elevation of both intracellular Ca2+ concentration and nNOS activity.	nitric	132-138	nitric oxide synthase 1, neuronal	Mus musculus	160-164
9681438-4	1998	Two single point mutations in the M1 muscarinic receptor that have previously been shown to uncouple differentially the receptor from phosphoinositide hydrolysis produced parallel attenuation of the rapid phase of nNOS activation.	Phosphatidylinositols	134-150	nitric oxide synthase 1, neuronal	Mus musculus	214-218
9681438-5	1998	Characterization of the prolonged phase of nNOS activation was done using the conversion of L-[3H]arginine to L-[3H]citrulline as well as cGMP formation following stimulation of M1 muscarinic receptors for 60 min.	l-[3h]arginine	92-106	nitric oxide synthase 1, neuronal	Mus musculus	43-47
9681438-5	1998	Characterization of the prolonged phase of nNOS activation was done using the conversion of L-[3H]arginine to L-[3H]citrulline as well as cGMP formation following stimulation of M1 muscarinic receptors for 60 min.	l-[3h]citrulline	110-126	nitric oxide synthase 1, neuronal	Mus musculus	43-47
9681438-5	1998	Characterization of the prolonged phase of nNOS activation was done using the conversion of L-[3H]arginine to L-[3H]citrulline as well as cGMP formation following stimulation of M1 muscarinic receptors for 60 min.	Cyclic GMP	138-142	nitric oxide synthase 1, neuronal	Mus musculus	43-47
9681447-1	1998	It is generally believed that the neuronal form of nitric oxide synthase (nNOS) is constitutively expressed and that regulation of this enzyme"s activity is mediated solely by changes in cytosolic calcium concentration.	Calcium	197-204	nitric oxide synthase 1, neuronal	Mus musculus	74-78
9681447-2	1998	Serendipitously, however, we observed that pretreatment of Chinese hamster ovary (CHO) cells, which coexpress muscarinic M1 receptors and nNOS, with 3.3 microM or 1 mM carbachol (CCh) for 48 h resulted in marked enhancement of maximal muscarinic receptor-stimulated nNOS activity as determined by L-[3H]citrulline and cyclic [3H]GMP production.	Carbachol	168-177	nitric oxide synthase 1, neuronal	Mus musculus	138-142
9681447-2	1998	Serendipitously, however, we observed that pretreatment of Chinese hamster ovary (CHO) cells, which coexpress muscarinic M1 receptors and nNOS, with 3.3 microM or 1 mM carbachol (CCh) for 48 h resulted in marked enhancement of maximal muscarinic receptor-stimulated nNOS activity as determined by L-[3H]citrulline and cyclic [3H]GMP production.	Carbachol	168-177	nitric oxide synthase 1, neuronal	Mus musculus	266-270
9681447-6	1998	It is interesting that ionomycin-stimulated nNOS activity was greater in CCh-pretreated cells.	Ionomycin	23-32	nitric oxide synthase 1, neuronal	Mus musculus	44-48
9681447-6	1998	It is interesting that ionomycin-stimulated nNOS activity was greater in CCh-pretreated cells.	Carbachol	73-76	nitric oxide synthase 1, neuronal	Mus musculus	44-48
9691096-2	1998	We have found that the antimalarial and antiinflammatory drug, chloroquine, is able to stimulate NO synthase (NOS) activity in murine, porcine, and human endothelial cells in vitro: the increase of enzyme activity is dependent on a de novo synthesis of some regulatory protein, as it is inhibited by cycloheximide but is not accompanied by an increased expression of inducible or constitutive NOS isoforms.	Cycloheximide	300-313	nitric oxide synthase 1, neuronal	Mus musculus	97-108
9687566-7	1998	In time-course experiments with 100 nM dexamethasone, maximum down-regulation of NOS I mRNA was seen after 24 hr (55.6 +/- 6.3% of control).	Dexamethasone	39-52	nitric oxide synthase 1, neuronal	Mus musculus	81-86
9687566-10	1998	In experiments with actinomycin D (10 microg/ml), the half-life of the NOS I mRNA was determined to be approximately 12 hr and remained unchanged after glucocorticoid incubation.	Dactinomycin	20-33	nitric oxide synthase 1, neuronal	Mus musculus	71-76
9687566-12	1998	In Western blots, the 160-kDa NOS I protein band was down-regulated to 68.5 +/- 8.4% of control after an incubation of the N1E-115 cells with 100 nM dexamethasone for 26 hr.	Dexamethasone	149-162	nitric oxide synthase 1, neuronal	Mus musculus	30-35
9648894-0	1998	Norepinephrine increases cyclic GMP levels in cerebellar cells from neuronal nitric oxide synthase knockout mice.	Norepinephrine	0-14	nitric oxide synthase 1, neuronal	Mus musculus	77-98
9620931-9	1998	As expected, in murine peritoneal macrophages (MPM) IFN-gamma (2,500 U/ml) enhanced growth inhibition of BCG; the effect was abolished by the nitric oxide synthase (NOS) inhibitor NMMA.	N-methylmalonamic acid	180-184	nitric oxide synthase 1, neuronal	Mus musculus	142-163
9684868-1	1998	Nitric oxide generated by neuronal nitric oxide synthase in contracting skeletal muscle fibers may regulate vascular relaxation via a cGMP-mediated pathway.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	26-56
9684868-1	1998	Nitric oxide generated by neuronal nitric oxide synthase in contracting skeletal muscle fibers may regulate vascular relaxation via a cGMP-mediated pathway.	Cyclic GMP	134-138	nitric oxide synthase 1, neuronal	Mus musculus	26-56
9608580-0	1998	Nitric oxide synthase inhibitors attenuate phencyclidine-induced disruption of prepulse inhibition.	Phencyclidine	43-56	nitric oxide synthase 1, neuronal	Mus musculus	0-21
9608580-2	1998	Results of a previous study showed that nitric oxide synthase (NOS) inhibitors blocked dizocilpine-induced behavior in mice.	Dizocilpine Maleate	87-98	nitric oxide synthase 1, neuronal	Mus musculus	40-61
9678642-2	1998	One pair of experiments demonstrated dose-related reductions in 2-deoxy-D-glucose (2DG)- and insulin-induced solid food intake with increasing dose (10, 25, and 50 mg/kg s.c.) of the NO-synthase (NOS) inhibitor, NG-nitro-L-arginine (L-NOARG), reaching statistical significance at 10 mg/kg L-NOARG when compared to vehicle controls.	Deoxyglucose	64-81	nitric oxide synthase 1, neuronal	Mus musculus	183-194
9678642-2	1998	One pair of experiments demonstrated dose-related reductions in 2-deoxy-D-glucose (2DG)- and insulin-induced solid food intake with increasing dose (10, 25, and 50 mg/kg s.c.) of the NO-synthase (NOS) inhibitor, NG-nitro-L-arginine (L-NOARG), reaching statistical significance at 10 mg/kg L-NOARG when compared to vehicle controls.	Deoxyglucose	83-86	nitric oxide synthase 1, neuronal	Mus musculus	183-194
9678642-2	1998	One pair of experiments demonstrated dose-related reductions in 2-deoxy-D-glucose (2DG)- and insulin-induced solid food intake with increasing dose (10, 25, and 50 mg/kg s.c.) of the NO-synthase (NOS) inhibitor, NG-nitro-L-arginine (L-NOARG), reaching statistical significance at 10 mg/kg L-NOARG when compared to vehicle controls.	Nitroarginine	212-231	nitric oxide synthase 1, neuronal	Mus musculus	183-194
9678642-2	1998	One pair of experiments demonstrated dose-related reductions in 2-deoxy-D-glucose (2DG)- and insulin-induced solid food intake with increasing dose (10, 25, and 50 mg/kg s.c.) of the NO-synthase (NOS) inhibitor, NG-nitro-L-arginine (L-NOARG), reaching statistical significance at 10 mg/kg L-NOARG when compared to vehicle controls.	Nitroarginine	233-240	nitric oxide synthase 1, neuronal	Mus musculus	183-194
9678642-2	1998	One pair of experiments demonstrated dose-related reductions in 2-deoxy-D-glucose (2DG)- and insulin-induced solid food intake with increasing dose (10, 25, and 50 mg/kg s.c.) of the NO-synthase (NOS) inhibitor, NG-nitro-L-arginine (L-NOARG), reaching statistical significance at 10 mg/kg L-NOARG when compared to vehicle controls.	Nitroarginine	289-296	nitric oxide synthase 1, neuronal	Mus musculus	183-194
9714302-5	1998	Following cotreatment with N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, there was a significant increase in the intensity and the length of the infection.	NG-Nitroarginine Methyl Ester	27-61	nitric oxide synthase 1, neuronal	Mus musculus	88-99
9714302-5	1998	Following cotreatment with N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, there was a significant increase in the intensity and the length of the infection.	NG-Nitroarginine Methyl Ester	63-69	nitric oxide synthase 1, neuronal	Mus musculus	88-99
9607188-2	1998	In the kidneys of AT1a-/- mice, the activity of neuronal type nitric oxide synthase (N-NOS) was histochemically detected by nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase (NADPHd) reaction combined with N-NOS immunohistochemistry.	Phosphates	158-167	nitric oxide synthase 1, neuronal	Mus musculus	48-83
9607188-2	1998	In the kidneys of AT1a-/- mice, the activity of neuronal type nitric oxide synthase (N-NOS) was histochemically detected by nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase (NADPHd) reaction combined with N-NOS immunohistochemistry.	Phosphates	158-167	nitric oxide synthase 1, neuronal	Mus musculus	85-90
9607188-2	1998	In the kidneys of AT1a-/- mice, the activity of neuronal type nitric oxide synthase (N-NOS) was histochemically detected by nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase (NADPHd) reaction combined with N-NOS immunohistochemistry.	NADP	169-174	nitric oxide synthase 1, neuronal	Mus musculus	48-83
9607188-2	1998	In the kidneys of AT1a-/- mice, the activity of neuronal type nitric oxide synthase (N-NOS) was histochemically detected by nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase (NADPHd) reaction combined with N-NOS immunohistochemistry.	NADP	169-174	nitric oxide synthase 1, neuronal	Mus musculus	85-90
29090810-2	1998	The present study was undertaken to investigate whether the relatively selective, neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against METH-induced neurotoxicity.	7-nitroindazole	130-145	nitric oxide synthase 1, neuronal	Mus musculus	82-112
29090810-2	1998	The present study was undertaken to investigate whether the relatively selective, neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against METH-induced neurotoxicity.	7-nitroindazole	147-151	nitric oxide synthase 1, neuronal	Mus musculus	82-112
29090810-2	1998	The present study was undertaken to investigate whether the relatively selective, neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against METH-induced neurotoxicity.	Methamphetamine	171-175	nitric oxide synthase 1, neuronal	Mus musculus	82-112
9536086-2	1998	When dystrophin is absent, as in Duchenne muscular dystrophy patients and in mdx mice, nNOS is mislocalized to the interior of the muscle fiber where it continues to produce nitric oxide.	Nitric Oxide	174-186	nitric oxide synthase 1, neuronal	Mus musculus	87-91
9668670-2	1998	The present study was undertaken to investigate whether the relatively selective, neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against METH-induced neurotoxicity.	7-nitroindazole	130-145	nitric oxide synthase 1, neuronal	Mus musculus	82-112
9668670-2	1998	The present study was undertaken to investigate whether the relatively selective, neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against METH-induced neurotoxicity.	7-nitroindazole	147-151	nitric oxide synthase 1, neuronal	Mus musculus	82-112
9668670-2	1998	The present study was undertaken to investigate whether the relatively selective, neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against METH-induced neurotoxicity.	Methamphetamine	171-175	nitric oxide synthase 1, neuronal	Mus musculus	82-112
9597692-0	1998	Kinetic properties of nitric oxide synthase in cerebral cortex and cerebellum of morphine tolerant mice.	Morphine	81-89	nitric oxide synthase 1, neuronal	Mus musculus	22-43
9597692-1	1998	The effects of chronic morphine administration on the kinetics of nitric oxide synthase (NOS) activity were determined in the mouse cerebral cortex and cerebellum.	Morphine	23-31	nitric oxide synthase 1, neuronal	Mus musculus	66-87
9546715-6	1998	This production was reversibly inhibited by culture of embryos in medium containing a nonspecific NO synthase (NOS) inhibitor (NG-nitro-L-arginine).	Nitroarginine	127-146	nitric oxide synthase 1, neuronal	Mus musculus	98-109
9861634-0	1998	Effect of kainic acid and pentetrazole administration on the activity of nitric oxide synthase in the mouse brain.	Kainic Acid	10-21	nitric oxide synthase 1, neuronal	Mus musculus	73-94
9861634-0	1998	Effect of kainic acid and pentetrazole administration on the activity of nitric oxide synthase in the mouse brain.	Pentylenetetrazole	26-38	nitric oxide synthase 1, neuronal	Mus musculus	73-94
9861634-1	1998	The present study examined ex vivo effect of kainic acid and pentetrazole administration on the activity of nitric oxide synthase (NOS) in the mouse brain.	Kainic Acid	45-56	nitric oxide synthase 1, neuronal	Mus musculus	108-129
9861634-1	1998	The present study examined ex vivo effect of kainic acid and pentetrazole administration on the activity of nitric oxide synthase (NOS) in the mouse brain.	Pentylenetetrazole	61-73	nitric oxide synthase 1, neuronal	Mus musculus	108-129
9513897-1	1998	The present study investigates whether neuronal type nitric oxide synthase (N-NOS) in the macula densa participates in the regulation of renal renin expression during altered dietary salt intake in angiotensinogen gene-knockout (Atg-/-) mice.	Salts	183-187	nitric oxide synthase 1, neuronal	Mus musculus	76-81
9482791-9	1998	Furthermore, nNOS neurons from MnSOD -/- mice are markedly sensitive to NMDA toxicity.	N-Methylaspartate	72-76	nitric oxide synthase 1, neuronal	Mus musculus	13-17
9513897-5	1998	In animals fed a normal-salt diet, the renal expressions of N-NOS and renin were markedly increased in Atg-/- mice compared with Atg+/+ mice.	Salts	24-28	nitric oxide synthase 1, neuronal	Mus musculus	60-65
9513897-10	1998	These results suggest that the N-NOS expression in the macula densa is inversely regulated by salt intake and that the enzyme activity is functionally linked to renal renin production.	Salts	94-98	nitric oxide synthase 1, neuronal	Mus musculus	31-36
9513897-11	1998	Salt-modulated renal N-NOS and renin expressions are independent on angiotensin formation in Atg-/- mice.	Salts	0-4	nitric oxide synthase 1, neuronal	Mus musculus	21-26
9495865-0	1998	Resistance of neuronal nitric oxide synthase-deficient mice to methamphetamine-induced dopaminergic neurotoxicity.	Methamphetamine	63-78	nitric oxide synthase 1, neuronal	Mus musculus	14-44
9495865-2	1998	We have recently reported that blockade of the neuronal nitric oxide synthase (nNOS) isoform by 7-nitroindazole provides protection against METH-induced neurotoxicity in Swiss Webster mice.	7-nitroindazole	96-111	nitric oxide synthase 1, neuronal	Mus musculus	47-77
9495865-2	1998	We have recently reported that blockade of the neuronal nitric oxide synthase (nNOS) isoform by 7-nitroindazole provides protection against METH-induced neurotoxicity in Swiss Webster mice.	7-nitroindazole	96-111	nitric oxide synthase 1, neuronal	Mus musculus	79-83
9495865-2	1998	We have recently reported that blockade of the neuronal nitric oxide synthase (nNOS) isoform by 7-nitroindazole provides protection against METH-induced neurotoxicity in Swiss Webster mice.	Methamphetamine	140-144	nitric oxide synthase 1, neuronal	Mus musculus	47-77
9495865-2	1998	We have recently reported that blockade of the neuronal nitric oxide synthase (nNOS) isoform by 7-nitroindazole provides protection against METH-induced neurotoxicity in Swiss Webster mice.	Methamphetamine	140-144	nitric oxide synthase 1, neuronal	Mus musculus	79-83
9495865-3	1998	The present study was undertaken to investigate the effect of a neurotoxic dose of METH on mutant mice lacking the nNOS gene [nNOS(-/-)] and wild-type controls.	Methamphetamine	83-87	nitric oxide synthase 1, neuronal	Mus musculus	115-119
9495865-7	1998	This regimen of METH given to nNOS(-/-) mice affected neither the tissue content of dopamine and its metabolites nor the number of DAT binding sites.	Methamphetamine	16-20	nitric oxide synthase 1, neuronal	Mus musculus	30-34
9486242-8	1998	Our findings suggest that nNOS-guanosine 3",5"-cyclic monophosphate (cGMP)-dependent pathways dilate pial arterioles by compensatory mechanisms after eNOS gene disruption.	Cyclic GMP	69-73	nitric oxide synthase 1, neuronal	Mus musculus	26-30
9665659-4	1998	Poly(ADP-ribose) formation was attenuated in mice deficient for neuronal NO synthase (nNOS).	Poly Adenosine Diphosphate Ribose	0-16	nitric oxide synthase 1, neuronal	Mus musculus	86-90
9458885-1	1998	In macrophages and many other cell types, L-arginine is used as a substrate by both nitric oxide synthase (NOS) and arginase to produce nitric oxide (NO) and urea, respectively.	Arginine	42-52	nitric oxide synthase 1, neuronal	Mus musculus	84-105
9458885-1	1998	In macrophages and many other cell types, L-arginine is used as a substrate by both nitric oxide synthase (NOS) and arginase to produce nitric oxide (NO) and urea, respectively.	Urea	158-162	nitric oxide synthase 1, neuronal	Mus musculus	84-105
9495865-8	1998	Although a moderate reduction in the levels of dopamine (35%) and DAT binding sites (32%) occurred in striatum of heterozygote nNOS(+/-) mice, a more profound depletion of the dopaminergic markers (up to 68%) was observed in the wild-type animals.	Dopamine	47-55	nitric oxide synthase 1, neuronal	Mus musculus	127-131
9495865-9	1998	METH-induced hyperthermia was observed in all animal strains examined except the nNOS(-/-) mice.	Methamphetamine	0-4	nitric oxide synthase 1, neuronal	Mus musculus	81-85
9495865-11	1998	A low dose of METH (1.0 mg/kg) administered to naive animals (nNOS(-/-) and wild-type) resulted in a similar intensity of locomotor stimulation.	Methamphetamine	14-18	nitric oxide synthase 1, neuronal	Mus musculus	62-66
9495865-13	1998	Taken together, these results indicate that nNOS(-/-) mice are protected against METH-induced dopaminergic neurotoxicity and locomotor sensitization.	Methamphetamine	81-85	nitric oxide synthase 1, neuronal	Mus musculus	44-48
9619756-8	1998	Clearance effects of MIBG were mimicked by N-nitro-L-arginine methyl ester (L-NAME), a known inhibitor of nitric oxide synthase (NOS), and MIBG itself (100 microM) also inhibited NOS in vitro, suggesting that NOS inhibition by MIBG may have contributed to the observed reduction in renal clearance.	3-Iodobenzylguanidine	21-25	nitric oxide synthase 1, neuronal	Mus musculus	106-127
9472639-0	1998	Persistent induction of nitric oxide synthase in tumours from mice treated with the anti-tumour agent 5,6-dimethylxanthenone-4-acetic acid.	vadimezan	102-138	nitric oxide synthase 1, neuronal	Mus musculus	24-45
9472639-1	1998	An anti-tumour agent 5,6-dimethylxanthenone-4-acetic acid (5,6-MeXAA) induced nitric oxide synthase (NOS) in the tumour, spleen, thymus and small intestine, but not in the lung, liver, kidney, heart or skeletal muscle in B6D2F1 mice bearing subcutaneous colon 38 tumours.	vadimezan	21-57	nitric oxide synthase 1, neuronal	Mus musculus	78-99
9472639-1	1998	An anti-tumour agent 5,6-dimethylxanthenone-4-acetic acid (5,6-MeXAA) induced nitric oxide synthase (NOS) in the tumour, spleen, thymus and small intestine, but not in the lung, liver, kidney, heart or skeletal muscle in B6D2F1 mice bearing subcutaneous colon 38 tumours.	vadimezan	59-68	nitric oxide synthase 1, neuronal	Mus musculus	78-99
9619756-8	1998	Clearance effects of MIBG were mimicked by N-nitro-L-arginine methyl ester (L-NAME), a known inhibitor of nitric oxide synthase (NOS), and MIBG itself (100 microM) also inhibited NOS in vitro, suggesting that NOS inhibition by MIBG may have contributed to the observed reduction in renal clearance.	n-nitro-l-arginine methyl ester	43-74	nitric oxide synthase 1, neuronal	Mus musculus	106-127
9619756-8	1998	Clearance effects of MIBG were mimicked by N-nitro-L-arginine methyl ester (L-NAME), a known inhibitor of nitric oxide synthase (NOS), and MIBG itself (100 microM) also inhibited NOS in vitro, suggesting that NOS inhibition by MIBG may have contributed to the observed reduction in renal clearance.	NG-Nitroarginine Methyl Ester	76-82	nitric oxide synthase 1, neuronal	Mus musculus	106-127
9672112-10	1998	If NOS-I activity influences spatial learning as determined in the eight-arm radial maze, the areas with strongly elevated NADPH-d positive neurons may demarcate task-related cortical areas affected in mice with a reduced learning capacity.	NADP	123-128	nitric oxide synthase 1, neuronal	Mus musculus	3-8
9613715-5	1998	Mice treated with the neuronal nitric oxide synthase (NOS) inhibitor 7-nitroindazole show reduced toxicity to MPTP and knock-out mice lacking neuronal NOS show decreased MPTP susceptibility.	7-nitroindazole	69-84	nitric oxide synthase 1, neuronal	Mus musculus	22-52
9613715-5	1998	Mice treated with the neuronal nitric oxide synthase (NOS) inhibitor 7-nitroindazole show reduced toxicity to MPTP and knock-out mice lacking neuronal NOS show decreased MPTP susceptibility.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	110-114	nitric oxide synthase 1, neuronal	Mus musculus	22-52
9613715-5	1998	Mice treated with the neuronal nitric oxide synthase (NOS) inhibitor 7-nitroindazole show reduced toxicity to MPTP and knock-out mice lacking neuronal NOS show decreased MPTP susceptibility.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	170-174	nitric oxide synthase 1, neuronal	Mus musculus	22-52
9393670-9	1997	Addition of 50-750 microM EGCG, in a concentration-dependent manner, inhibited the enzyme activity of iNOS, to 85-14%, and neuronal nitric oxide synthase (nNOS), to 93-56%, as measured by citrulline formation.	epigallocatechin gallate	26-30	nitric oxide synthase 1, neuronal	Mus musculus	123-153
9488156-1	1998	The NO synthases (NOS) generate NO from L-arginine.	Arginine	40-50	nitric oxide synthase 1, neuronal	Mus musculus	4-16
9413858-0	1997	Sensitization to the locomotor stimulant activity of cocaine is associated with increases in nitric oxide synthase activity in brain regions and spinal cord of mice.	Cocaine	53-60	nitric oxide synthase 1, neuronal	Mus musculus	93-114
9413858-1	1997	Effects of multiple administrations of cocaine and subsequent cocaine withdrawal on the activity of nitric oxide synthase (NOS) in brain regions and spinal cord of male Swiss-Webster mice were determined.	Cocaine	39-46	nitric oxide synthase 1, neuronal	Mus musculus	100-121
9413858-1	1997	Effects of multiple administrations of cocaine and subsequent cocaine withdrawal on the activity of nitric oxide synthase (NOS) in brain regions and spinal cord of male Swiss-Webster mice were determined.	Cocaine	62-69	nitric oxide synthase 1, neuronal	Mus musculus	100-121
9452194-5	1997	After 3 h ischemia followed by 3 h reperfusion, the morphological damage and the decrease in [3H]PDBu binding in the ipsilateral striatum and the MCA region of cortex was smaller in mice lacking the expression of neuronal nitric oxide synthase (type I NOS) gene mutant mice compared to wild-type (SV-129 and C57black/6) mice.	Tritium	94-96	nitric oxide synthase 1, neuronal	Mus musculus	213-243
9347323-7	1997	Pretreatment with the nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine methylester (L-NAME), but not with D-NAME, significantly reduced the incidence of convulsions and lethality, as well as the increase in cyclic GMP.	Nitroarginine	61-80	nitric oxide synthase 1, neuronal	Mus musculus	22-43
9347323-7	1997	Pretreatment with the nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine methylester (L-NAME), but not with D-NAME, significantly reduced the incidence of convulsions and lethality, as well as the increase in cyclic GMP.	NG-Nitroarginine Methyl Ester	94-100	nitric oxide synthase 1, neuronal	Mus musculus	22-43
9347323-7	1997	Pretreatment with the nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine methylester (L-NAME), but not with D-NAME, significantly reduced the incidence of convulsions and lethality, as well as the increase in cyclic GMP.	Cyclic GMP	217-227	nitric oxide synthase 1, neuronal	Mus musculus	22-43
9383683-2	1997	These proinflammatory cytokines induce both cyclooxygenase (COX) and nitric oxide synthase (NOS) with the release of prostaglandin (PG) and NO, respectively.	Prostaglandins	117-130	nitric oxide synthase 1, neuronal	Mus musculus	69-90
9383683-2	1997	These proinflammatory cytokines induce both cyclooxygenase (COX) and nitric oxide synthase (NOS) with the release of prostaglandin (PG) and NO, respectively.	Prostaglandins	132-134	nitric oxide synthase 1, neuronal	Mus musculus	69-90
9393670-9	1997	Addition of 50-750 microM EGCG, in a concentration-dependent manner, inhibited the enzyme activity of iNOS, to 85-14%, and neuronal nitric oxide synthase (nNOS), to 93-56%, as measured by citrulline formation.	epigallocatechin gallate	26-30	nitric oxide synthase 1, neuronal	Mus musculus	155-159
9357865-4	1997	Airway responsiveness to methacholine (MCh), assessed by the log of the effective dose of MCh for a doubling of pulmonary resistance from baseline (ED(200)R(L)), was significantly lower in the -/- nNOS mice than in the wild-type mice (logED(200)R(L), 2.24 +/- 0.07 vs. 2.51 +/- 0.06 microg/kg, respectively; P = 0.003).	Methacholine Chloride	25-37	nitric oxide synthase 1, neuronal	Mus musculus	197-201
9357865-4	1997	Airway responsiveness to methacholine (MCh), assessed by the log of the effective dose of MCh for a doubling of pulmonary resistance from baseline (ED(200)R(L)), was significantly lower in the -/- nNOS mice than in the wild-type mice (logED(200)R(L), 2.24 +/- 0.07 vs. 2.51 +/- 0.06 microg/kg, respectively; P = 0.003).	Methacholine Chloride	39-42	nitric oxide synthase 1, neuronal	Mus musculus	197-201
9337148-1	1997	Nitric oxide (NO) from constitutive NO synthase (NOS) has been postulated to be a homeostatic regulator of leukocyte-endothelial cell interactions.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	36-47
9326308-1	1997	The ability of 7-nitroindazole (7-NI) to protect against MPTP-induced neurotoxicity has been attributed to its inhibition of neuronal nitric oxide synthase.	7-nitroindazole	15-30	nitric oxide synthase 1, neuronal	Mus musculus	125-155
9326308-1	1997	The ability of 7-nitroindazole (7-NI) to protect against MPTP-induced neurotoxicity has been attributed to its inhibition of neuronal nitric oxide synthase.	7-nitroindazole	32-36	nitric oxide synthase 1, neuronal	Mus musculus	125-155
9326308-1	1997	The ability of 7-nitroindazole (7-NI) to protect against MPTP-induced neurotoxicity has been attributed to its inhibition of neuronal nitric oxide synthase.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	57-61	nitric oxide synthase 1, neuronal	Mus musculus	125-155
9326308-6	1997	These data indicate that the mechanism by which 7-NI counteracts MPTP neurotoxicity in mice is not due solely to inhibition of neuronal nitric oxide synthase, but involves a reduction in MPP+ formation.	7-nitroindazole	48-52	nitric oxide synthase 1, neuronal	Mus musculus	127-157
9336332-5	1997	2-Ethylaminoguanidine displayed a high isoform selectivity for the iNOS compared with the nNOS and eNOS isoforms.	2-ethylaminoguanidine	0-21	nitric oxide synthase 1, neuronal	Mus musculus	90-94
9336332-9	1997	1-Amino-S-methylisothiourea by contrast with the aminoguanidines was identified as a mechanism-based inactivator selective for the nNOS isoform.	1-amino-s-methylisothiourea	0-27	nitric oxide synthase 1, neuronal	Mus musculus	131-135
9336332-9	1997	1-Amino-S-methylisothiourea by contrast with the aminoguanidines was identified as a mechanism-based inactivator selective for the nNOS isoform.	pimagedine	49-64	nitric oxide synthase 1, neuronal	Mus musculus	131-135
9374274-0	1997	Aggressive behavior in male mice lacking the gene for neuronal nitric oxide synthase requires testosterone.	Testosterone	94-106	nitric oxide synthase 1, neuronal	Mus musculus	54-84
9374274-5	1997	The present study sought to test the dependence of increased aggressive behavior in nNOS - / - males on testosterone.	Testosterone	104-116	nitric oxide synthase 1, neuronal	Mus musculus	84-88
9374274-9	1997	These data provide evidence that increased aggressive behavior of nNOS - /- mice, like aggression in WT mice, is testosterone-dependent.	Testosterone	113-125	nitric oxide synthase 1, neuronal	Mus musculus	66-70
9278526-1	1997	We investigated the role of neuronal (type I) nitric oxide synthase (nNOS) in NMDA-mediated excitotoxicity in wild-type (SV129 and C57BL/6J) and type I NOS knock-out (nNOS-/-) mice and examined its relationship to apoptosis.	N-Methylaspartate	78-82	nitric oxide synthase 1, neuronal	Mus musculus	69-73
9278526-6	1997	Pharmacological inhibition of nNOS by 7-nitroindazole (50 mg/kg, i.p.)	7-nitroindazole	38-53	nitric oxide synthase 1, neuronal	Mus musculus	30-34
9278526-15	1997	The mechanism of protection in nNOS-/- mice may relate to decreased oxygen free radical production and related NO reaction products and, in part, involves mechanisms of neuronal death associated with the delayed appearance of apoptosis.	oxygen free radical	68-87	nitric oxide synthase 1, neuronal	Mus musculus	31-35
9378246-0	1997	Effect of multiple injections of U-50, 488H, a kappa-opioid receptor agonist, on the activity of nitric oxide synthase in brain regions and spinal cord of mice.	u-50	33-37	nitric oxide synthase 1, neuronal	Mus musculus	97-118
9378246-0	1997	Effect of multiple injections of U-50, 488H, a kappa-opioid receptor agonist, on the activity of nitric oxide synthase in brain regions and spinal cord of mice.	488h	39-43	nitric oxide synthase 1, neuronal	Mus musculus	97-118
9378246-2	1997	The time course of the effects of multiple injections of U-50,488H, a kappa-opioid receptor agonist, and its subsequent termination on its analgesic action and nitric oxide synthase (NOS) activity was determined in the brain regions and spinal cord of the mouse.	u-50	57-61	nitric oxide synthase 1, neuronal	Mus musculus	160-181
9331267-1	1997	PURPOSE: Nitric oxide synthase (NOS) plays an essential role in neuronal function and is critical in the brain for normal and pathologic responses to glutamate.	Glutamic Acid	150-159	nitric oxide synthase 1, neuronal	Mus musculus	9-30
9331267-5	1997	RESULTS: Retinal ganglion cells in the nNOS-deficient mouse were relatively resistant to NMDA and to arterial occlusion.	N-Methylaspartate	89-93	nitric oxide synthase 1, neuronal	Mus musculus	39-43
9323712-4	1997	MATERIALS AND METHODS: Aggressive behavior, as well as brain citrulline levels, were monitored in adult male mice after treatment with a specific nNOS inhibitor, 7-nitroindazole (7-NI) (50 mg/kg i.p.	7-nitroindazole	162-177	nitric oxide synthase 1, neuronal	Mus musculus	146-150
9323712-4	1997	MATERIALS AND METHODS: Aggressive behavior, as well as brain citrulline levels, were monitored in adult male mice after treatment with a specific nNOS inhibitor, 7-nitroindazole (7-NI) (50 mg/kg i.p.	7-nitroindazole	179-183	nitric oxide synthase 1, neuronal	Mus musculus	146-150
9323712-11	1997	CONCLUSIONS: 7-NI augmented aggression in WT mice to levels displayed by nNOS- mice, strongly implying that nNOS is a major mediator of aggression.	7-nitroindazole	13-17	nitric oxide synthase 1, neuronal	Mus musculus	73-77
9323712-11	1997	CONCLUSIONS: 7-NI augmented aggression in WT mice to levels displayed by nNOS- mice, strongly implying that nNOS is a major mediator of aggression.	7-nitroindazole	13-17	nitric oxide synthase 1, neuronal	Mus musculus	108-112
9236188-3	1997	In previous studies, we showed that inhibiting NO production with the nonselective nitric oxide synthase (NOS) inhibitor NG-monomethyl-arginine reduced glomerulonephritis, arthritis, and vasculitis in MRL-lpr/lpr mice.	ng-monomethyl-arginine	121-143	nitric oxide synthase 1, neuronal	Mus musculus	83-104
9251903-0	1997	Time course of the changes in central nitric oxide synthase activity following chronic treatment with morphine in the mouse: reversal by naltrexone.	Morphine	102-110	nitric oxide synthase 1, neuronal	Mus musculus	38-59
9251903-0	1997	Time course of the changes in central nitric oxide synthase activity following chronic treatment with morphine in the mouse: reversal by naltrexone.	Naltrexone	137-147	nitric oxide synthase 1, neuronal	Mus musculus	38-59
9251903-2	1997	The time course of the effect of chronic administration of morphine on the activity of nitric oxide synthase (NOS) in the brain regions and spinal cord of the mouse was determined.	Morphine	59-67	nitric oxide synthase 1, neuronal	Mus musculus	87-108
9262311-0	1997	Modulation of cocaine- and methamphetamine-induced behavioral sensitization by inhibition of brain nitric oxide synthase.	Cocaine	14-21	nitric oxide synthase 1, neuronal	Mus musculus	99-120
9262311-0	1997	Modulation of cocaine- and methamphetamine-induced behavioral sensitization by inhibition of brain nitric oxide synthase.	Methamphetamine	27-42	nitric oxide synthase 1, neuronal	Mus musculus	99-120
9262311-2	1997	The present study was undertaken to investigate the effect of the relatively selective inhibitor of the neuronal nitric oxide synthase (NOS) isoform, 7-nitroindazole (7-NI), on the development of sensitization to the locomotor stimulating effect of cocaine and methamphetamine (METH).	7-nitroindazole	150-165	nitric oxide synthase 1, neuronal	Mus musculus	113-134
9262311-2	1997	The present study was undertaken to investigate the effect of the relatively selective inhibitor of the neuronal nitric oxide synthase (NOS) isoform, 7-nitroindazole (7-NI), on the development of sensitization to the locomotor stimulating effect of cocaine and methamphetamine (METH).	7-nitroindazole	167-171	nitric oxide synthase 1, neuronal	Mus musculus	113-134
9262311-2	1997	The present study was undertaken to investigate the effect of the relatively selective inhibitor of the neuronal nitric oxide synthase (NOS) isoform, 7-nitroindazole (7-NI), on the development of sensitization to the locomotor stimulating effect of cocaine and methamphetamine (METH).	Cocaine	249-256	nitric oxide synthase 1, neuronal	Mus musculus	113-134
9262311-2	1997	The present study was undertaken to investigate the effect of the relatively selective inhibitor of the neuronal nitric oxide synthase (NOS) isoform, 7-nitroindazole (7-NI), on the development of sensitization to the locomotor stimulating effect of cocaine and methamphetamine (METH).	Methamphetamine	261-276	nitric oxide synthase 1, neuronal	Mus musculus	113-134
9262311-2	1997	The present study was undertaken to investigate the effect of the relatively selective inhibitor of the neuronal nitric oxide synthase (NOS) isoform, 7-nitroindazole (7-NI), on the development of sensitization to the locomotor stimulating effect of cocaine and methamphetamine (METH).	Methamphetamine	278-282	nitric oxide synthase 1, neuronal	Mus musculus	113-134
9105232-12	1997	In nNOS knockout mice, isoflurane increased rCBF by 67 +/- 8%, 88 +/- 12%, and 112 +/- 18% at 1.2, 1.8, and 2.4 vol%, respectively.	Isoflurane	23-33	nitric oxide synthase 1, neuronal	Mus musculus	3-7
9183289-0	1997	[3H]L-NG-nitroarginine binding after transient focal ischemia and NMDA-induced excitotoxicity in type I and type III nitric oxide synthase null mice.	Tritium	1-3	nitric oxide synthase 1, neuronal	Mus musculus	117-138
9183289-0	1997	[3H]L-NG-nitroarginine binding after transient focal ischemia and NMDA-induced excitotoxicity in type I and type III nitric oxide synthase null mice.	Nitroarginine	6-22	nitric oxide synthase 1, neuronal	Mus musculus	117-138
9183289-1	1997	We investigated the density and distribution of nitric oxide synthase (NOS) binding by quantitative autoradiography using [3H]L-NG-nitroarginine ([3H]L-NNA) after transient focal ischemia or intrastriatal injection of N-methyl-D-aspartate (NMDA) in wild-type (SV-129 and C57black/6) and type I (neuronal) and type III (endothelial) NOS-deficient mice.	Tritium	123-125	nitric oxide synthase 1, neuronal	Mus musculus	48-69
9183289-1	1997	We investigated the density and distribution of nitric oxide synthase (NOS) binding by quantitative autoradiography using [3H]L-NG-nitroarginine ([3H]L-NNA) after transient focal ischemia or intrastriatal injection of N-methyl-D-aspartate (NMDA) in wild-type (SV-129 and C57black/6) and type I (neuronal) and type III (endothelial) NOS-deficient mice.	Nitroarginine	126-144	nitric oxide synthase 1, neuronal	Mus musculus	48-69
9183289-1	1997	We investigated the density and distribution of nitric oxide synthase (NOS) binding by quantitative autoradiography using [3H]L-NG-nitroarginine ([3H]L-NNA) after transient focal ischemia or intrastriatal injection of N-methyl-D-aspartate (NMDA) in wild-type (SV-129 and C57black/6) and type I (neuronal) and type III (endothelial) NOS-deficient mice.	[3h]l-nna	146-155	nitric oxide synthase 1, neuronal	Mus musculus	48-69
9096824-8	1997	RESULTS: NO synthesis precursor, L-arginine (20, 40, 200, 800 mg/kg), resulted in a dose-dependent decrease in the ACT in mice, while the NO synthase (NOS) inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME, 1.25, 2.50, 5.00 mg/kg, i.p.)	Arginine	33-43	nitric oxide synthase 1, neuronal	Mus musculus	138-149
9096824-8	1997	RESULTS: NO synthesis precursor, L-arginine (20, 40, 200, 800 mg/kg), resulted in a dose-dependent decrease in the ACT in mice, while the NO synthase (NOS) inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME, 1.25, 2.50, 5.00 mg/kg, i.p.)	NG-Nitroarginine Methyl Ester	167-199	nitric oxide synthase 1, neuronal	Mus musculus	138-149
9223342-0	1997	Functionally differentiating two neuronal nitric oxide synthase isoforms through antisense mapping: evidence for opposing NO actions on morphine analgesia and tolerance.	Morphine	136-144	nitric oxide synthase 1, neuronal	Mus musculus	33-63
9223342-4	1997	Down-regulation of nNOS-1 prevents the development of morphine tolerance.	Morphine	54-62	nitric oxide synthase 1, neuronal	Mus musculus	19-23
9223342-6	1997	Conversely, an antisense probe selectively targeting nNOS-2 blocks morphine analgesia, shifting the morphine dose-response curve over 2-fold to the right.	Morphine	67-75	nitric oxide synthase 1, neuronal	Mus musculus	53-57
9223342-6	1997	Conversely, an antisense probe selectively targeting nNOS-2 blocks morphine analgesia, shifting the morphine dose-response curve over 2-fold to the right.	Morphine	100-108	nitric oxide synthase 1, neuronal	Mus musculus	53-57
9223342-10	1997	Thus, antisense mapping distinguishes at the functional level two isoforms of nNOS with opposing actions on morphine actions.	Morphine	108-116	nitric oxide synthase 1, neuronal	Mus musculus	78-82
10456061-6	1997	Therefore, prolonged absence of nNOS allows atrophy of the signaling pathway downstream of cGMP.	Cyclic GMP	91-95	nitric oxide synthase 1, neuronal	Mus musculus	32-36
9105232-0	1997	Isoflurane-induced cerebral hyperemia in neuronal nitric oxide synthase gene deficient mice.	Isoflurane	0-10	nitric oxide synthase 1, neuronal	Mus musculus	41-71
9105232-15	1997	CONCLUSIONS: In nNOS knockout mice, the cerebral hyperemic response to isoflurane is preserved by compensatory mechanism(s) that is NO-independent at 2.4 vol%, although it may involve eNOS at 1.2 and 1.8 vol%.	Isoflurane	71-81	nitric oxide synthase 1, neuronal	Mus musculus	16-20
9105232-16	1997	It is suggested that in wild-type mice, eNOS and nNOS contribute to isoflurane-induced increase in rCBF.	Isoflurane	68-78	nitric oxide synthase 1, neuronal	Mus musculus	49-53
9058766-0	1997	Nitric oxide via an inducible isoform of nitric oxide synthase is a possible factor to eliminate inflammatory cells from the central nervous system of mice with experimental allergic encephalomyelitis.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	41-62
9096405-4	1997	To assess nNOS catalytic activity in intact animals we localized citrulline, which is formed stoichiometrically with NO, by immunohistochemistry.	Citrulline	65-75	nitric oxide synthase 1, neuronal	Mus musculus	10-14
9150796-6	1997	These data suggest that type II NMJ are provided with additional regulatory mechanisms, such as free radical signaling by the NOS I-derived NO which may exert modulatory effects on the choline acetyltransferase/ACh/AChE pathway.	Acetylcholine	211-214	nitric oxide synthase 1, neuronal	Mus musculus	126-131
9150796-7	1997	Furthermore, type II may represent those NMJ where recently glutamate-gated NMDA-type Ca2+ channels have been described, which in analogy to those in the nervous system may serve also in skeletal muscle fibers as NOS I activators.	Glutamic Acid	60-69	nitric oxide synthase 1, neuronal	Mus musculus	213-218
9065766-0	1997	Induction of nitric oxide synthesis in J774 cells lowers intracellular glutathione: effect of modulated glutathione redox status on nitric oxide synthase induction.	Glutathione	104-115	nitric oxide synthase 1, neuronal	Mus musculus	132-153
9125158-0	1997	Competitive inhibition of nitric oxide synthase by p-aminobenzamidine, a serine proteinase inhibitor.	4-aminobenzamidine	51-69	nitric oxide synthase 1, neuronal	Mus musculus	26-47
9125158-2	1997	Considering the structural and functional similarity between p-aminobenzamidine and the L-arginyl side chain in trypsin-like serine proteinases, we investigated the interaction of p-aminobenzamidine with mouse brain nitric oxide synthase (NOS), which uses L-arginine as the substrate for generating NO and L-citrulline.	4-aminobenzamidine	180-198	nitric oxide synthase 1, neuronal	Mus musculus	216-237
9001139-6	1997	We postulate that the smaller peri-infarct zone is a reflection of less severe metabolic disturbance after ischemia in nNOS- mice, possibly related to diminished production of nitric oxide (NO) or a related product.	Nitric Oxide	176-188	nitric oxide synthase 1, neuronal	Mus musculus	119-123
9138738-4	1997	N(G)-nitro-L-arginine (L-NNA), an inhibitor of NO synthase (NOS), (5 mg/kg, i.p.)	Nitroarginine	0-21	nitric oxide synthase 1, neuronal	Mus musculus	47-58
9129181-0	1997	5-Hydroxytryptamine-induced Ca2+ -independent cGMP formation is mediated by nitric oxide in a nitric oxide synthase-independent manner in NG108-15 cells.	Serotonin	0-19	nitric oxide synthase 1, neuronal	Mus musculus	94-115
9129181-0	1997	5-Hydroxytryptamine-induced Ca2+ -independent cGMP formation is mediated by nitric oxide in a nitric oxide synthase-independent manner in NG108-15 cells.	Cyclic GMP	46-50	nitric oxide synthase 1, neuronal	Mus musculus	94-115
9129181-0	1997	5-Hydroxytryptamine-induced Ca2+ -independent cGMP formation is mediated by nitric oxide in a nitric oxide synthase-independent manner in NG108-15 cells.	Nitric Oxide	76-88	nitric oxide synthase 1, neuronal	Mus musculus	94-115
9129181-7	1997	Ca2+ -independent cGMP formation was not inhibited by 1,2-bis(o-aminophenoxy)-ethane-N,N,N",N"-tetraacetic acid tetra(acetoxymethyl)ester (BAPTA-AM), N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), and various arginine-derivative nitric oxide synthase (NOS) inhibitors.	Cyclic GMP	18-22	nitric oxide synthase 1, neuronal	Mus musculus	240-261
9208212-0	1997	The developmental expression of neuronal nitric oxide synthase in cerebellar granule cells is sensitive to GABA and neurotrophins.	gamma-Aminobutyric Acid	107-111	nitric oxide synthase 1, neuronal	Mus musculus	32-62
9008461-4	1997	In addition, group 3 received supplemental L-arginine and group 4 received L-arginine and N omega-nitro-L-arginine (L-NA), an inhibitor of NO synthase (NOS).	Nitroarginine	90-114	nitric oxide synthase 1, neuronal	Mus musculus	139-150
9042165-12	1997	Furthermore, the selective inhibition of N-NOS activity by 7-nitrondazole significantly decreased the level of renal renin mRNA in Atg -/- mice.	7-nitrondazole	59-73	nitric oxide synthase 1, neuronal	Mus musculus	41-46
9208212-3	1997	Using primary cultures established from murine cerebella at different development stages, we analyzed the effects of the neurotransmitter GABA and the neurotrophins BDNF and NT-3 on nNOS expression in developing granule cells.	gamma-Aminobutyric Acid	138-142	nitric oxide synthase 1, neuronal	Mus musculus	182-186
9208212-4	1997	We show a biophasic effect of GABA on nNOS expression, which correlates with the ability of this transmitter to increase intracellular calcium levels.	gamma-Aminobutyric Acid	30-34	nitric oxide synthase 1, neuronal	Mus musculus	38-42
9208212-4	1997	We show a biophasic effect of GABA on nNOS expression, which correlates with the ability of this transmitter to increase intracellular calcium levels.	Calcium	135-142	nitric oxide synthase 1, neuronal	Mus musculus	38-42
9096253-0	1997	Adenosine and its receptor agonists potentiate nitric oxide synthase expression induced by lipopolysaccharide in RAW 264.7 murine macrophages.	Adenosine	0-9	nitric oxide synthase 1, neuronal	Mus musculus	47-68
9194695-1	1997	We have previously reported that 1-(2-trifluoromethylphenyl) imidazole (TRIM) is a potent inhibitor of mouse cerebellar neuronal NOS (nNOS) in vitro with very much reduced activity against bovine aortic endothelial NOS (eNOS).	1-(2-trifluoromethylphenyl)imidazole	33-70	nitric oxide synthase 1, neuronal	Mus musculus	120-132
9194695-1	1997	We have previously reported that 1-(2-trifluoromethylphenyl) imidazole (TRIM) is a potent inhibitor of mouse cerebellar neuronal NOS (nNOS) in vitro with very much reduced activity against bovine aortic endothelial NOS (eNOS).	1-(2-trifluoromethylphenyl)imidazole	33-70	nitric oxide synthase 1, neuronal	Mus musculus	134-138
9194695-1	1997	We have previously reported that 1-(2-trifluoromethylphenyl) imidazole (TRIM) is a potent inhibitor of mouse cerebellar neuronal NOS (nNOS) in vitro with very much reduced activity against bovine aortic endothelial NOS (eNOS).	1-(2-trifluoromethylphenyl)imidazole	72-76	nitric oxide synthase 1, neuronal	Mus musculus	120-132
9194695-1	1997	We have previously reported that 1-(2-trifluoromethylphenyl) imidazole (TRIM) is a potent inhibitor of mouse cerebellar neuronal NOS (nNOS) in vitro with very much reduced activity against bovine aortic endothelial NOS (eNOS).	1-(2-trifluoromethylphenyl)imidazole	72-76	nitric oxide synthase 1, neuronal	Mus musculus	134-138
9010449-2	1997	NO synthase (NOS) inhibitors, such as NG-nitro-L-arginine methyl ester (L-NAME) reduced all the manifestations of IL-2-induced capillary leakage, without compromising the antitumor effects of IL-2.	NG-Nitroarginine Methyl Ester	38-70	nitric oxide synthase 1, neuronal	Mus musculus	0-11
9010449-2	1997	NO synthase (NOS) inhibitors, such as NG-nitro-L-arginine methyl ester (L-NAME) reduced all the manifestations of IL-2-induced capillary leakage, without compromising the antitumor effects of IL-2.	NG-Nitroarginine Methyl Ester	72-78	nitric oxide synthase 1, neuronal	Mus musculus	0-11
9180370-0	1997	Aggravation of DMCM-induced seizure by nitric oxide synthase inhibitors in mice.	methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate	15-19	nitric oxide synthase 1, neuronal	Mus musculus	39-60
9180370-1	1997	The present study investigated the effects of nitric oxide synthase (NOS) inhibitors on the seizure threshold of DMCM in mice.	methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate	113-117	nitric oxide synthase 1, neuronal	Mus musculus	46-67
9331901-0	1997	MPP+ induced substantia nigra degeneration is attenuated in nNOS knockout mice.	mangion-purified polysaccharide (Candida albicans)	0-4	nitric oxide synthase 1, neuronal	Mus musculus	60-64
9331901-1	1997	Recent studies showed that neuronal nitric oxide synthase (nNOS) plays a role in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	81-125	nitric oxide synthase 1, neuronal	Mus musculus	27-57
9331901-1	1997	Recent studies showed that neuronal nitric oxide synthase (nNOS) plays a role in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	81-125	nitric oxide synthase 1, neuronal	Mus musculus	59-63
9331901-4	1997	The mice lacking nNOS showed a significant attenuation of MPP+(-) induced increases of 3-nitrotyrosine concentrations in the striatum.	3-nitrotyrosine	87-102	nitric oxide synthase 1, neuronal	Mus musculus	17-21
9096253-1	1997	The effect of adenosine and its agonists on nitric oxide synthase (NOS) activity and the production of nitrite induced by lipopolysaccharide (LPS) in RAW 264.7 cells were investigated.	Adenosine	14-23	nitric oxide synthase 1, neuronal	Mus musculus	44-65
8996510-0	1997	Tetrahydrobiopterin, a cofactor for nitric oxide synthase, produces endothelium-dependent dilation of mouse pial arterioles.	sapropterin	0-19	nitric oxide synthase 1, neuronal	Mus musculus	36-57
8996510-1	1997	BACKGROUND AND PURPOSE: Tetrahydrobiopterin (THBP) is an essential cofactor for nitric oxide synthase (NOS), which is responsible for the synthesis of the endothelium-derived relaxing factor (EDRF) responsible for mediating the vasorelaxation produced by acetylcholine (ACh).	sapropterin	24-43	nitric oxide synthase 1, neuronal	Mus musculus	80-101
8996510-1	1997	BACKGROUND AND PURPOSE: Tetrahydrobiopterin (THBP) is an essential cofactor for nitric oxide synthase (NOS), which is responsible for the synthesis of the endothelium-derived relaxing factor (EDRF) responsible for mediating the vasorelaxation produced by acetylcholine (ACh).	sapropterin	45-49	nitric oxide synthase 1, neuronal	Mus musculus	80-101
8996510-1	1997	BACKGROUND AND PURPOSE: Tetrahydrobiopterin (THBP) is an essential cofactor for nitric oxide synthase (NOS), which is responsible for the synthesis of the endothelium-derived relaxing factor (EDRF) responsible for mediating the vasorelaxation produced by acetylcholine (ACh).	Acetylcholine	255-268	nitric oxide synthase 1, neuronal	Mus musculus	80-101
8996510-1	1997	BACKGROUND AND PURPOSE: Tetrahydrobiopterin (THBP) is an essential cofactor for nitric oxide synthase (NOS), which is responsible for the synthesis of the endothelium-derived relaxing factor (EDRF) responsible for mediating the vasorelaxation produced by acetylcholine (ACh).	Acetylcholine	270-273	nitric oxide synthase 1, neuronal	Mus musculus	80-101
8990379-5	1996	NO synthesis was induced in DC by interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS), and was blocked by the inhibitor of nitric oxide synthase (NOS), NG-monomethyl-L-arginine (NMMA).	omega-N-Methylarginine	158-182	nitric oxide synthase 1, neuronal	Mus musculus	129-150
8990379-5	1996	NO synthesis was induced in DC by interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS), and was blocked by the inhibitor of nitric oxide synthase (NOS), NG-monomethyl-L-arginine (NMMA).	omega-N-Methylarginine	184-188	nitric oxide synthase 1, neuronal	Mus musculus	129-150
8951973-2	1996	Experiment 1 demonstrated a dose-related decrease in CP-induced solid food intake over a 60-min test period with increasing dose (10, 25, and 50 mg/ kg SC) of the NO-synthase (NOS) inhibitor, L-NG-nitro arginine (L-NOARG), reaching statistical significance at 10 mg/kg L-NOARG when compared to vehicle control.	Nitroarginine	192-211	nitric oxide synthase 1, neuronal	Mus musculus	163-174
8931477-0	1996	Role of nitric oxide in methamphetamine neurotoxicity: protection by 7-nitroindazole, an inhibitor of neuronal nitric oxide synthase.	7-nitroindazole	69-84	nitric oxide synthase 1, neuronal	Mus musculus	102-132
8931477-2	1996	in the neurotoxic effects of methamphetamine (METH) was evaluated using 7-nitroindazole (7-NI), a potent inhibitor of neuronal nitric oxide synthase.	Methamphetamine	29-44	nitric oxide synthase 1, neuronal	Mus musculus	118-148
8931477-2	1996	in the neurotoxic effects of methamphetamine (METH) was evaluated using 7-nitroindazole (7-NI), a potent inhibitor of neuronal nitric oxide synthase.	Methamphetamine	46-50	nitric oxide synthase 1, neuronal	Mus musculus	118-148
8931477-2	1996	in the neurotoxic effects of methamphetamine (METH) was evaluated using 7-nitroindazole (7-NI), a potent inhibitor of neuronal nitric oxide synthase.	7-nitroindazole	72-87	nitric oxide synthase 1, neuronal	Mus musculus	118-148
8931477-2	1996	in the neurotoxic effects of methamphetamine (METH) was evaluated using 7-nitroindazole (7-NI), a potent inhibitor of neuronal nitric oxide synthase.	7-nitroindazole	89-93	nitric oxide synthase 1, neuronal	Mus musculus	118-148
8896427-1	1996	Nitric oxide (NO) generated from L-arginine and molecular oxygen by nitric oxide synthase (NOS) has been shown to influence hepatocellular function and pathology in response to ischemia and certain hepatotoxins.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	68-89
8896427-1	1996	Nitric oxide (NO) generated from L-arginine and molecular oxygen by nitric oxide synthase (NOS) has been shown to influence hepatocellular function and pathology in response to ischemia and certain hepatotoxins.	Arginine	33-43	nitric oxide synthase 1, neuronal	Mus musculus	68-89
8896427-1	1996	Nitric oxide (NO) generated from L-arginine and molecular oxygen by nitric oxide synthase (NOS) has been shown to influence hepatocellular function and pathology in response to ischemia and certain hepatotoxins.	Oxygen	58-64	nitric oxide synthase 1, neuronal	Mus musculus	68-89
8871658-3	1996	NO production was inhibited by the nitric oxide synthase (NOS) inhibitor N(G)-monomethyl-L-arginine (NMMA).	omega-N-Methylarginine	73-99	nitric oxide synthase 1, neuronal	Mus musculus	35-56
8871658-3	1996	NO production was inhibited by the nitric oxide synthase (NOS) inhibitor N(G)-monomethyl-L-arginine (NMMA).	omega-N-Methylarginine	101-105	nitric oxide synthase 1, neuronal	Mus musculus	35-56
8916093-1	1996	The effect of the nitric oxide synthase (NOS) inhibitors N-nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole (7-NI) on seizures induced by N-methyl-D-aspartate (NMDA), pilocarpine (PIL) and pentylenetetrazol (PTZ), as well as on the electroconvulsive threshold was studied in mice.	N-Methylaspartate	148-168	nitric oxide synthase 1, neuronal	Mus musculus	18-39
8858965-0	1996	The neuronal nitric oxide synthase inhibitor, 7-nitroindazole, protects against methamphetamine-induced neurotoxicity in vivo.	7-nitroindazole	46-61	nitric oxide synthase 1, neuronal	Mus musculus	13-34
8904652-3	1996	In the present paper we have investigated, mainly with an in vivo approach, the influence and specificity of the NO synthase (NOS) blocker NG-nitro-L-arginine methyl ester (L-NAME) on L-arginine-induced secretion of insulin and glucagon.	NG-Nitroarginine Methyl Ester	139-171	nitric oxide synthase 1, neuronal	Mus musculus	113-124
8904652-3	1996	In the present paper we have investigated, mainly with an in vivo approach, the influence and specificity of the NO synthase (NOS) blocker NG-nitro-L-arginine methyl ester (L-NAME) on L-arginine-induced secretion of insulin and glucagon.	NG-Nitroarginine Methyl Ester	173-179	nitric oxide synthase 1, neuronal	Mus musculus	113-124
8904652-3	1996	In the present paper we have investigated, mainly with an in vivo approach, the influence and specificity of the NO synthase (NOS) blocker NG-nitro-L-arginine methyl ester (L-NAME) on L-arginine-induced secretion of insulin and glucagon.	Arginine	148-158	nitric oxide synthase 1, neuronal	Mus musculus	113-124
8904652-3	1996	In the present paper we have investigated, mainly with an in vivo approach, the influence and specificity of the NO synthase (NOS) blocker NG-nitro-L-arginine methyl ester (L-NAME) on L-arginine-induced secretion of insulin and glucagon.	Glucagon	228-236	nitric oxide synthase 1, neuronal	Mus musculus	113-124
8858965-0	1996	The neuronal nitric oxide synthase inhibitor, 7-nitroindazole, protects against methamphetamine-induced neurotoxicity in vivo.	Methamphetamine	80-95	nitric oxide synthase 1, neuronal	Mus musculus	13-34
8858965-1	1996	The present study was undertaken to investigate whether the relatively selective neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against methamphetamine (METH)-induced neurotoxicity.	7-nitroindazole	129-144	nitric oxide synthase 1, neuronal	Mus musculus	90-111
8858965-1	1996	The present study was undertaken to investigate whether the relatively selective neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against methamphetamine (METH)-induced neurotoxicity.	7-nitroindazole	146-150	nitric oxide synthase 1, neuronal	Mus musculus	90-111
8858965-1	1996	The present study was undertaken to investigate whether the relatively selective neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against methamphetamine (METH)-induced neurotoxicity.	Methamphetamine	170-185	nitric oxide synthase 1, neuronal	Mus musculus	90-111
8858965-1	1996	The present study was undertaken to investigate whether the relatively selective neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against methamphetamine (METH)-induced neurotoxicity.	Methamphetamine	187-191	nitric oxide synthase 1, neuronal	Mus musculus	90-111
8765472-3	1996	Inhibition was greatest if THC was added 1-4 hr before induction of nitric oxide synthase (NOS) by LPS and IFN-gamma, and declined with time after addition of the inducing agents.	Dronabinol	27-30	nitric oxide synthase 1, neuronal	Mus musculus	68-89
8806750-3	1996	The inhibition of citrulline formation by protoporphyrin IX occurs with IC50 values of 0.8, 4, and 5 microM for the nNOS, iNOS, and eNOS isoforms, respectively.	Citrulline	18-28	nitric oxide synthase 1, neuronal	Mus musculus	116-120
8806750-3	1996	The inhibition of citrulline formation by protoporphyrin IX occurs with IC50 values of 0.8, 4, and 5 microM for the nNOS, iNOS, and eNOS isoforms, respectively.	protoporphyrin IX	42-59	nitric oxide synthase 1, neuronal	Mus musculus	116-120
8806750-4	1996	Inhibition by N-methyl-protoporphyrin IX occurs at IC50 values of 6, 5, and 8 microM for the nNOS, iNOS, and eNOS isoforms, respectively.	N-methylprotoporphyrin IX	14-40	nitric oxide synthase 1, neuronal	Mus musculus	93-97
8806750-6	1996	Protoporphyrin IX reduces the maximal velocity of citrulline formation for both the iNOS and nNOS isoforms without altering the K(m) for the arginine substrate or the EC50 value for the tetrahydrobiopterin cofactor.	protoporphyrin IX	0-17	nitric oxide synthase 1, neuronal	Mus musculus	93-97
8806750-6	1996	Protoporphyrin IX reduces the maximal velocity of citrulline formation for both the iNOS and nNOS isoforms without altering the K(m) for the arginine substrate or the EC50 value for the tetrahydrobiopterin cofactor.	Citrulline	50-60	nitric oxide synthase 1, neuronal	Mus musculus	93-97
8806750-7	1996	Protoporphyrin IX inhibits the arginine-independent NADPH oxidase activity of nNOS with an IC50 value of 1 microM but has no effect on cytochrome c reductase activity at concentrations as high as 30 microM.	protoporphyrin IX	0-17	nitric oxide synthase 1, neuronal	Mus musculus	78-82
8806750-7	1996	Protoporphyrin IX inhibits the arginine-independent NADPH oxidase activity of nNOS with an IC50 value of 1 microM but has no effect on cytochrome c reductase activity at concentrations as high as 30 microM.	Arginine	31-39	nitric oxide synthase 1, neuronal	Mus musculus	78-82
8886430-5	1996	1-(2-Trifluoromethylphenyl) imidazole (TRIM) was a relatively potent inhibitor of nNOS and iNOS (IC50S of 28.2 microM and 27.0 microM respectively) but was a relatively weak inhibitor of eNOS (IC50, 1057.5 microM).	1-(2-trifluoromethylphenyl)imidazole	0-37	nitric oxide synthase 1, neuronal	Mus musculus	82-86
8886430-5	1996	1-(2-Trifluoromethylphenyl) imidazole (TRIM) was a relatively potent inhibitor of nNOS and iNOS (IC50S of 28.2 microM and 27.0 microM respectively) but was a relatively weak inhibitor of eNOS (IC50, 1057.5 microM).	1-(2-trifluoromethylphenyl)imidazole	39-43	nitric oxide synthase 1, neuronal	Mus musculus	82-86
8886430-6	1996	The parent compound, imidazole, was a weak inhibitor of all three NOS isoforms (IC50S: nNOS, 290.6 microM; eNOS, 101.3 microM; iNOS, 616.0 microM).	imidazole	21-30	nitric oxide synthase 1, neuronal	Mus musculus	87-91
8886430-7	1996	Substitution of imidazole with a phenyl group to yield I-phenylimidazole (PI) resulted in an isoform non-selective increase in inhibitory potency (IC50S: nNOS, 72.1 microM; eNOS, 86.9 microM; iNOS, 53.9 microM).	imidazole	16-25	nitric oxide synthase 1, neuronal	Mus musculus	154-158
8886430-7	1996	Substitution of imidazole with a phenyl group to yield I-phenylimidazole (PI) resulted in an isoform non-selective increase in inhibitory potency (IC50S: nNOS, 72.1 microM; eNOS, 86.9 microM; iNOS, 53.9 microM).	i-phenylimidazole	55-72	nitric oxide synthase 1, neuronal	Mus musculus	154-158
8886430-10	1996	The ability of TRIM to inhibit mouse cerebellar nNOS activity in vitro was influenced by the concentration of L-arginine (0.12-10.0 microM) in the incubation medium.	Arginine	110-120	nitric oxide synthase 1, neuronal	Mus musculus	48-52
8853353-0	1996	ACh dilates pial arterioles in endothelial and neuronal NOS knockout mice by NO-dependent mechanisms.	Acetylcholine	0-3	nitric oxide synthase 1, neuronal	Mus musculus	47-59
8853353-5	1996	NG-nitro-L-arginine (L-NNA, 1 mM) superfusion inhibited cortical NOS activity by > 70% and abrogated the response in wild-type mice while blocking the dilation by approximately 50% in eNOS mutant and nNOS mutant mice.	Nitroarginine	0-19	nitric oxide synthase 1, neuronal	Mus musculus	203-207
8853353-5	1996	NG-nitro-L-arginine (L-NNA, 1 mM) superfusion inhibited cortical NOS activity by > 70% and abrogated the response in wild-type mice while blocking the dilation by approximately 50% in eNOS mutant and nNOS mutant mice.	Nitroarginine	21-26	nitric oxide synthase 1, neuronal	Mus musculus	203-207
8853353-8	1996	Our findings indicate that 1) ACh dilates pial arterioles of wild-type mice by NOS-dependent mechanisms as reported in other species, 2) the response in nNOS mutant mice resembles the wild-type response except for enhanced dilation to ACh and reduced L-NNA sensitivity, and 3) surprisingly, the response in eNOS mutant mice is partially NOS dependent and attenuated by both TTX and L-NNA.	Acetylcholine	235-238	nitric oxide synthase 1, neuronal	Mus musculus	153-157
8853353-8	1996	Our findings indicate that 1) ACh dilates pial arterioles of wild-type mice by NOS-dependent mechanisms as reported in other species, 2) the response in nNOS mutant mice resembles the wild-type response except for enhanced dilation to ACh and reduced L-NNA sensitivity, and 3) surprisingly, the response in eNOS mutant mice is partially NOS dependent and attenuated by both TTX and L-NNA.	Nitroarginine	251-256	nitric oxide synthase 1, neuronal	Mus musculus	153-157
8853353-8	1996	Our findings indicate that 1) ACh dilates pial arterioles of wild-type mice by NOS-dependent mechanisms as reported in other species, 2) the response in nNOS mutant mice resembles the wild-type response except for enhanced dilation to ACh and reduced L-NNA sensitivity, and 3) surprisingly, the response in eNOS mutant mice is partially NOS dependent and attenuated by both TTX and L-NNA.	Tetrodotoxin	374-377	nitric oxide synthase 1, neuronal	Mus musculus	153-157
8853353-8	1996	Our findings indicate that 1) ACh dilates pial arterioles of wild-type mice by NOS-dependent mechanisms as reported in other species, 2) the response in nNOS mutant mice resembles the wild-type response except for enhanced dilation to ACh and reduced L-NNA sensitivity, and 3) surprisingly, the response in eNOS mutant mice is partially NOS dependent and attenuated by both TTX and L-NNA.	Nitroarginine	382-387	nitric oxide synthase 1, neuronal	Mus musculus	153-157
8853353-9	1996	Because nNOS is constitutively expressed in eNOS mutants, these findings coupled with the TTX results suggest that an nNOS-dependent mechanism may compensate for the chronic loss of eNOS activity after targeted gene disruption.	Tetrodotoxin	90-93	nitric oxide synthase 1, neuronal	Mus musculus	8-12
8853353-9	1996	Because nNOS is constitutively expressed in eNOS mutants, these findings coupled with the TTX results suggest that an nNOS-dependent mechanism may compensate for the chronic loss of eNOS activity after targeted gene disruption.	Tetrodotoxin	90-93	nitric oxide synthase 1, neuronal	Mus musculus	118-122
8782460-0	1996	Inhibition of neuronal nitric oxide synthase prevents MPTP-induced parkinsonism in baboons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	54-58	nitric oxide synthase 1, neuronal	Mus musculus	23-44
8782460-2	1996	7-Nitroindazole (7-NI) is a relatively selective inhibitor of the neuronal isoform of nitric oxide synthase (NOS) that blocks MPTP neurotoxicity in mice.	7-nitroindazole	0-15	nitric oxide synthase 1, neuronal	Mus musculus	86-107
8782460-2	1996	7-Nitroindazole (7-NI) is a relatively selective inhibitor of the neuronal isoform of nitric oxide synthase (NOS) that blocks MPTP neurotoxicity in mice.	7-nitroindazole	17-21	nitric oxide synthase 1, neuronal	Mus musculus	86-107
8782460-2	1996	7-Nitroindazole (7-NI) is a relatively selective inhibitor of the neuronal isoform of nitric oxide synthase (NOS) that blocks MPTP neurotoxicity in mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	126-130	nitric oxide synthase 1, neuronal	Mus musculus	86-107
8663207-1	1996	Nitric-oxide synthase (NOS) is responsible for the synthesis of nitric oxide which serves as a neural messenger in the central nervous system.	Nitric Oxide	64-76	nitric oxide synthase 1, neuronal	Mus musculus	0-21
8667023-0	1996	Striatal malonate lesions are attenuated in neuronal nitric oxide synthase knockout mice.	malonic acid	9-17	nitric oxide synthase 1, neuronal	Mus musculus	44-74
8683131-0	1996	IFN-alpha beta reconstitutes the deficiency in lipid A-activated AKR macrophages for nitric oxide synthase.	Lipid A	47-54	nitric oxide synthase 1, neuronal	Mus musculus	85-106
8683131-2	1996	We used AKR-PM as a model to further define the role of IFN-alpha beta in modulation of induction of macrophage nitric oxide synthase (NOS) in response to lipid A.	Lipid A	155-162	nitric oxide synthase 1, neuronal	Mus musculus	112-133
8667023-4	1996	Malonate striatal lesions were significantly attenuated in the nNOS mutant mice, and they were significantly increased in the eNOS mutant mice.	malonic acid	0-8	nitric oxide synthase 1, neuronal	Mus musculus	63-67
8667023-5	1996	Malonate-induced increases in levels of 2,3- and 2,5-dihydroxybenzoic acid/salicylate, markers of hydroxyl radical generation, were significantly attenuated in the nNOS knockout mice.	malonic acid	0-8	nitric oxide synthase 1, neuronal	Mus musculus	164-168
8667023-5	1996	Malonate-induced increases in levels of 2,3- and 2,5-dihydroxybenzoic acid/salicylate, markers of hydroxyl radical generation, were significantly attenuated in the nNOS knockout mice.	2,3- and 2,5-dihydroxybenzoic acid	40-74	nitric oxide synthase 1, neuronal	Mus musculus	164-168
8667023-5	1996	Malonate-induced increases in levels of 2,3- and 2,5-dihydroxybenzoic acid/salicylate, markers of hydroxyl radical generation, were significantly attenuated in the nNOS knockout mice.	Salicylates	75-85	nitric oxide synthase 1, neuronal	Mus musculus	164-168
8667023-5	1996	Malonate-induced increases in levels of 2,3- and 2,5-dihydroxybenzoic acid/salicylate, markers of hydroxyl radical generation, were significantly attenuated in the nNOS knockout mice.	Hydroxyl Radical	98-114	nitric oxide synthase 1, neuronal	Mus musculus	164-168
8667023-6	1996	Malonate-induced increases in 3-nitrotyrosine, a marker for peroxynitrite-mediated damage, were blocked in the nNOS mice, whereas a significant increase occurred in the eNOS mice.	malonic acid	0-8	nitric oxide synthase 1, neuronal	Mus musculus	111-115
8667023-6	1996	Malonate-induced increases in 3-nitrotyrosine, a marker for peroxynitrite-mediated damage, were blocked in the nNOS mice, whereas a significant increase occurred in the eNOS mice.	3-nitrotyrosine	30-45	nitric oxide synthase 1, neuronal	Mus musculus	111-115
8667023-6	1996	Malonate-induced increases in 3-nitrotyrosine, a marker for peroxynitrite-mediated damage, were blocked in the nNOS mice, whereas a significant increase occurred in the eNOS mice.	Peroxynitrous Acid	60-73	nitric oxide synthase 1, neuronal	Mus musculus	111-115
8667023-8	1996	produced by nNOS results in generation of peroxynitrite, which plays a role in malonate neurotoxicity.	Peroxynitrous Acid	42-55	nitric oxide synthase 1, neuronal	Mus musculus	12-16
8667023-8	1996	produced by nNOS results in generation of peroxynitrite, which plays a role in malonate neurotoxicity.	malonic acid	79-87	nitric oxide synthase 1, neuronal	Mus musculus	12-16
8797190-0	1996	7-Nitroindazole and methylene blue, inhibitors of neuronal nitric oxide synthase and NO-stimulated guanylate cyclase, block MK-801-elicited behaviors in mice.	7-nitroindazole	0-15	nitric oxide synthase 1, neuronal	Mus musculus	50-80
8797190-0	1996	7-Nitroindazole and methylene blue, inhibitors of neuronal nitric oxide synthase and NO-stimulated guanylate cyclase, block MK-801-elicited behaviors in mice.	Methylene Blue	20-34	nitric oxide synthase 1, neuronal	Mus musculus	50-80
8797190-0	1996	7-Nitroindazole and methylene blue, inhibitors of neuronal nitric oxide synthase and NO-stimulated guanylate cyclase, block MK-801-elicited behaviors in mice.	Dizocilpine Maleate	124-130	nitric oxide synthase 1, neuronal	Mus musculus	50-80
8797190-1	1996	We examined the abilities of 7-nitroindazole and methylene blue, inhibitors of the neuronal isoform of nitric oxide synthase (NOS) and nitric oxide-stimulated guanylate cyclase activity respectively, to attenuate explosive episodic jumping behavior(s) ("popping") elicited by MK-801 in mice.	7-nitroindazole	29-44	nitric oxide synthase 1, neuronal	Mus musculus	103-124
8784782-5	1996	RESULTS: Both intact animal penile erections and isolated erectile tissue function are maintained in nNOS mice, in agreement with demonstrated normal sexual behaviors, but is stereospecifically blocked by the NOS inhibitor, L-nitroarginine methyl ester (L-NAME).	NG-Nitroarginine Methyl Ester	254-260	nitric oxide synthase 1, neuronal	Mus musculus	101-105
8797190-1	1996	We examined the abilities of 7-nitroindazole and methylene blue, inhibitors of the neuronal isoform of nitric oxide synthase (NOS) and nitric oxide-stimulated guanylate cyclase activity respectively, to attenuate explosive episodic jumping behavior(s) ("popping") elicited by MK-801 in mice.	Methylene Blue	49-63	nitric oxide synthase 1, neuronal	Mus musculus	103-124
8796356-0	1996	Modification of kainate-induced behavioral and electrographic seizures following inhibition of nitric oxide synthase in mice.	Kainic Acid	16-23	nitric oxide synthase 1, neuronal	Mus musculus	95-116
8796356-1	1996	We assessed the effects of N(omega)-nitro-L-arginine-methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS), on behavioral and electrographic seizures elicited in mice by convulsant doses of kainate.	NG-Nitroarginine Methyl Ester	27-65	nitric oxide synthase 1, neuronal	Mus musculus	92-113
8796356-1	1996	We assessed the effects of N(omega)-nitro-L-arginine-methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS), on behavioral and electrographic seizures elicited in mice by convulsant doses of kainate.	NG-Nitroarginine Methyl Ester	67-73	nitric oxide synthase 1, neuronal	Mus musculus	92-113
8819145-0	1996	Effect of nitric oxide synthase inhibition on tolerance to the analgesic action of D-Pen2, D-Pen5 enkephalin and morphine in the mouse.	d-pen2	83-89	nitric oxide synthase 1, neuronal	Mus musculus	10-31
8819145-0	1996	Effect of nitric oxide synthase inhibition on tolerance to the analgesic action of D-Pen2, D-Pen5 enkephalin and morphine in the mouse.	d-pen5 enkephalin	91-108	nitric oxide synthase 1, neuronal	Mus musculus	10-31
8660797-5	1996	C3H-PM phi treated with C1q or Lipid A displayed increased TNF-R mRNA synthesis and in combination with Lipid A and anti-C1q antibody inhibited TNF-R and nitric oxide synthase (NOS) mRNA synthesis compared with Lipid A only, but had no effect on TNF mRNA synthesis.	Lipid A	104-111	nitric oxide synthase 1, neuronal	Mus musculus	154-175
8660797-5	1996	C3H-PM phi treated with C1q or Lipid A displayed increased TNF-R mRNA synthesis and in combination with Lipid A and anti-C1q antibody inhibited TNF-R and nitric oxide synthase (NOS) mRNA synthesis compared with Lipid A only, but had no effect on TNF mRNA synthesis.	Lipid A	104-111	nitric oxide synthase 1, neuronal	Mus musculus	154-175
8643444-2	1996	To study the role of NO radical in MPTP-induced neurotoxicity, we injected MPTP into mice in which nitric oxide synthase (NOS) was inhibited by 7-nitroindazole (7-NI) in a time- and dose-dependent fashion.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	75-79	nitric oxide synthase 1, neuronal	Mus musculus	99-120
8643444-2	1996	To study the role of NO radical in MPTP-induced neurotoxicity, we injected MPTP into mice in which nitric oxide synthase (NOS) was inhibited by 7-nitroindazole (7-NI) in a time- and dose-dependent fashion.	7-nitroindazole	144-159	nitric oxide synthase 1, neuronal	Mus musculus	99-120
8643444-2	1996	To study the role of NO radical in MPTP-induced neurotoxicity, we injected MPTP into mice in which nitric oxide synthase (NOS) was inhibited by 7-nitroindazole (7-NI) in a time- and dose-dependent fashion.	7-nitroindazole	161-165	nitric oxide synthase 1, neuronal	Mus musculus	99-120
9206098-1	1996	OBJECTIVE: To observe the changes of interleukin-1 (IL-1), nitric oxide (NO) and nitric oxide synthase (NOS) in mice with oleic acid-induced acute lung injury (ALI) and the protective effects of interleukin-1 receptor antagonist (IL-1ra).	Oleic Acid	122-132	nitric oxide synthase 1, neuronal	Mus musculus	81-102
8648734-4	1996	Treatment with Nomega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthetase (NOS) inhibitor, increased mortality to 100% (P < 0.05) in NSV-infected BALB/cJ mice, to 95% (P < 0.001) in BALB/cByJ mice, and to 100% in scid/CB17 mice.	NG-Nitroarginine Methyl Ester	15-51	nitric oxide synthase 1, neuronal	Mus musculus	64-87
8648734-4	1996	Treatment with Nomega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthetase (NOS) inhibitor, increased mortality to 100% (P < 0.05) in NSV-infected BALB/cJ mice, to 95% (P < 0.001) in BALB/cByJ mice, and to 100% in scid/CB17 mice.	NG-Nitroarginine Methyl Ester	53-59	nitric oxide synthase 1, neuronal	Mus musculus	64-87
8786424-3	1996	Neurotoxicity elicited by NMDA is markedly attenuated in nNOS- cortical cultures compared with wild-type cultures.	N-Methylaspartate	26-30	nitric oxide synthase 1, neuronal	Mus musculus	57-61
8786424-4	1996	The NOS inhibitor nitro-L-arginine is neuroprotective in wild-type but not nNOS-cultures, confirming the role of nNOS-derived NO in glutamate neurotoxicity.	Nitroarginine	18-34	nitric oxide synthase 1, neuronal	Mus musculus	113-117
8786424-4	1996	The NOS inhibitor nitro-L-arginine is neuroprotective in wild-type but not nNOS-cultures, confirming the role of nNOS-derived NO in glutamate neurotoxicity.	Glutamic Acid	132-141	nitric oxide synthase 1, neuronal	Mus musculus	113-117
8786424-5	1996	Confirming that the nNOS- cultures lack NMDA-stimulated nNOS activity, NMDA did not stimulate the formation of cGMP in nNOS- cultures, but markedly elevates cGMP in wild-type cultures.	N-Methylaspartate	40-44	nitric oxide synthase 1, neuronal	Mus musculus	56-60
8786424-5	1996	Confirming that the nNOS- cultures lack NMDA-stimulated nNOS activity, NMDA did not stimulate the formation of cGMP in nNOS- cultures, but markedly elevates cGMP in wild-type cultures.	N-Methylaspartate	40-44	nitric oxide synthase 1, neuronal	Mus musculus	56-60
8739302-1	1996	In the course of our studies on the local blood flow modulation in the NMRI-mouse placenta we have focussed on regulatory pathways involving recently appreciated gaseous messenger molecules nitric oxide (NO) and carbon monoxide (CO), which are generated by NO synthase (NOS) and heme oxygenase (HO)-2, respectively.	Nitric Oxide	190-202	nitric oxide synthase 1, neuronal	Mus musculus	257-268
8739302-1	1996	In the course of our studies on the local blood flow modulation in the NMRI-mouse placenta we have focussed on regulatory pathways involving recently appreciated gaseous messenger molecules nitric oxide (NO) and carbon monoxide (CO), which are generated by NO synthase (NOS) and heme oxygenase (HO)-2, respectively.	Carbon Monoxide	212-227	nitric oxide synthase 1, neuronal	Mus musculus	257-268
8739302-1	1996	In the course of our studies on the local blood flow modulation in the NMRI-mouse placenta we have focussed on regulatory pathways involving recently appreciated gaseous messenger molecules nitric oxide (NO) and carbon monoxide (CO), which are generated by NO synthase (NOS) and heme oxygenase (HO)-2, respectively.	Carbon Monoxide	229-231	nitric oxide synthase 1, neuronal	Mus musculus	257-268
8739302-9	1996	Since the intraplacental visceral epithelial yolk sac layer closely accompanies large fetal blood vessels entering the placental labyrinth from the chorionic plate it may be assumed that NO, generated by the NADPH-consuming NOS-I in the intraplacental yolk sac epithelium, acts to regulate the blood flow by relaxing smooth muscle cells in the wall of these fetal vessels.	NADP	208-213	nitric oxide synthase 1, neuronal	Mus musculus	224-229
8622563-14	1996	Nitric oxide synthase (NOS) inhibitors, superoxide dismutase (SOD), catalase, mannitol and cycloheximide, reversed the edema suppressions by TGF-beta1 +/- immunosuppressant at 30 min and 6 hr after Dex.	Dexamethasone	198-201	nitric oxide synthase 1, neuronal	Mus musculus	0-21
8660797-5	1996	C3H-PM phi treated with C1q or Lipid A displayed increased TNF-R mRNA synthesis and in combination with Lipid A and anti-C1q antibody inhibited TNF-R and nitric oxide synthase (NOS) mRNA synthesis compared with Lipid A only, but had no effect on TNF mRNA synthesis.	Lipid A	31-38	nitric oxide synthase 1, neuronal	Mus musculus	154-175
8692292-1	1996	The opiate withdrawal induced by administration of naloxone to morphine-dependent mice correlates with an increment of calcium- dependent nitric oxide synthase (NOS) activity in the cerebellum.	Opiate Alkaloids	4-10	nitric oxide synthase 1, neuronal	Mus musculus	138-159
8692292-1	1996	The opiate withdrawal induced by administration of naloxone to morphine-dependent mice correlates with an increment of calcium- dependent nitric oxide synthase (NOS) activity in the cerebellum.	Naloxone	51-59	nitric oxide synthase 1, neuronal	Mus musculus	138-159
8692292-1	1996	The opiate withdrawal induced by administration of naloxone to morphine-dependent mice correlates with an increment of calcium- dependent nitric oxide synthase (NOS) activity in the cerebellum.	Morphine	63-71	nitric oxide synthase 1, neuronal	Mus musculus	138-159
8851629-1	1996	Two potent inhibitors of nitric oxide synthase (NOS), namely, NG-nitro-L-arginine (NNA) and NG-monomethyl-L-arginine (NMMA) were administered intracerebroventricularly (i.c.v.)	Nitroarginine	62-81	nitric oxide synthase 1, neuronal	Mus musculus	25-46
9010608-5	1996	Destruction of the heme-thiolate catalytic site was observed when nNOS was exposed to PN suggesting that the irreversible oxidation of this bond may be the common mechanism of NOS inhibition.	heme-thiolate	19-32	nitric oxide synthase 1, neuronal	Mus musculus	66-70
8784782-5	1996	RESULTS: Both intact animal penile erections and isolated erectile tissue function are maintained in nNOS mice, in agreement with demonstrated normal sexual behaviors, but is stereospecifically blocked by the NOS inhibitor, L-nitroarginine methyl ester (L-NAME).	NG-Nitroarginine Methyl Ester	224-252	nitric oxide synthase 1, neuronal	Mus musculus	101-105
9173913-1	1996	We hypothesized that elimination of neuronal nitric oxide synthase (nNOS) by targeted disruption of the nNOS gene would result in amelioration of damage seen after hypoxia-ischemia in the developing brain since nitric oxide (NO) has been implicated in glutamate-mediated neurotoxicity after ischemia.	Nitric Oxide	45-57	nitric oxide synthase 1, neuronal	Mus musculus	68-72
9173913-1	1996	We hypothesized that elimination of neuronal nitric oxide synthase (nNOS) by targeted disruption of the nNOS gene would result in amelioration of damage seen after hypoxia-ischemia in the developing brain since nitric oxide (NO) has been implicated in glutamate-mediated neurotoxicity after ischemia.	Nitric Oxide	45-57	nitric oxide synthase 1, neuronal	Mus musculus	104-108
9173913-1	1996	We hypothesized that elimination of neuronal nitric oxide synthase (nNOS) by targeted disruption of the nNOS gene would result in amelioration of damage seen after hypoxia-ischemia in the developing brain since nitric oxide (NO) has been implicated in glutamate-mediated neurotoxicity after ischemia.	Glutamic Acid	252-261	nitric oxide synthase 1, neuronal	Mus musculus	36-66
9173913-1	1996	We hypothesized that elimination of neuronal nitric oxide synthase (nNOS) by targeted disruption of the nNOS gene would result in amelioration of damage seen after hypoxia-ischemia in the developing brain since nitric oxide (NO) has been implicated in glutamate-mediated neurotoxicity after ischemia.	Glutamic Acid	252-261	nitric oxide synthase 1, neuronal	Mus musculus	68-72
9173913-1	1996	We hypothesized that elimination of neuronal nitric oxide synthase (nNOS) by targeted disruption of the nNOS gene would result in amelioration of damage seen after hypoxia-ischemia in the developing brain since nitric oxide (NO) has been implicated in glutamate-mediated neurotoxicity after ischemia.	Glutamic Acid	252-261	nitric oxide synthase 1, neuronal	Mus musculus	104-108
9121609-0	1996	Attenuation of cocaine kindling by 7-nitroindazole, an inhibitor of brain nitric oxide synthase.	Cocaine	15-22	nitric oxide synthase 1, neuronal	Mus musculus	74-95
8795703-1	1996	Pretreatment with the nitric oxide synthase (NOS) inhibitor L-NG-nitro arginine methyl ester (L-NAME), injected intraperitoneally (i.p.)	l-ng-nitro arginine methyl ester	60-92	nitric oxide synthase 1, neuronal	Mus musculus	22-43
8795703-1	1996	Pretreatment with the nitric oxide synthase (NOS) inhibitor L-NG-nitro arginine methyl ester (L-NAME), injected intraperitoneally (i.p.)	NG-Nitroarginine Methyl Ester	94-100	nitric oxide synthase 1, neuronal	Mus musculus	22-43
8804071-0	1996	Nitric oxide synthase inhibition attenuates tolerance to morphine but not to [D-Ala2, Glu4] deltorphin II, a delta 2-opioid receptor agonist in mice.	Morphine	57-65	nitric oxide synthase 1, neuronal	Mus musculus	0-21
9121609-0	1996	Attenuation of cocaine kindling by 7-nitroindazole, an inhibitor of brain nitric oxide synthase.	7-nitroindazole	35-50	nitric oxide synthase 1, neuronal	Mus musculus	74-95
9121609-1	1996	Recent studies suggest the involvement of the N-methyl-D-aspartate (NMDA) type of glutamate receptors and nitric oxide synthase (NOS) in the process of increased sensitivity to the convulsive effect of cocaine ("cocaine kindling").	Cocaine	202-209	nitric oxide synthase 1, neuronal	Mus musculus	106-127
9121609-1	1996	Recent studies suggest the involvement of the N-methyl-D-aspartate (NMDA) type of glutamate receptors and nitric oxide synthase (NOS) in the process of increased sensitivity to the convulsive effect of cocaine ("cocaine kindling").	Cocaine	212-219	nitric oxide synthase 1, neuronal	Mus musculus	106-127
7485468-3	1995	Inhibition of nitric oxide synthase (NOS) blocks the cGMP response without affecting the peak amplitude of the intracellular Ca2+ signal, and it is concluded that Ca(2+)-dependent activation of NOS is required for cGMP production.	Cyclic GMP	53-57	nitric oxide synthase 1, neuronal	Mus musculus	14-35
7575577-7	1995	Both pre- or post-administration of NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine inhibited the NO generation.	omega-N-Methylarginine	65-89	nitric oxide synthase 1, neuronal	Mus musculus	36-47
8903681-1	1996	TH1-type proinflammatory cytokines induce the expression of phagocytic nitric oxide synthase (NOS) and prime the membrane-bound NADPH oxidase of neutrophils and monocytes of mice so as to attain an activated state, which upon a second stimulus releases up to 6-fold increased levels of reactive oxygen species (ROS) than do unprimed phagocytes.	Reactive Oxygen Species	286-309	nitric oxide synthase 1, neuronal	Mus musculus	71-92
8903681-1	1996	TH1-type proinflammatory cytokines induce the expression of phagocytic nitric oxide synthase (NOS) and prime the membrane-bound NADPH oxidase of neutrophils and monocytes of mice so as to attain an activated state, which upon a second stimulus releases up to 6-fold increased levels of reactive oxygen species (ROS) than do unprimed phagocytes.	Reactive Oxygen Species	311-314	nitric oxide synthase 1, neuronal	Mus musculus	71-92
7485468-3	1995	Inhibition of nitric oxide synthase (NOS) blocks the cGMP response without affecting the peak amplitude of the intracellular Ca2+ signal, and it is concluded that Ca(2+)-dependent activation of NOS is required for cGMP production.	Cyclic GMP	214-218	nitric oxide synthase 1, neuronal	Mus musculus	14-35
7545539-10	1995	Oral administration of N-monomethyl-L-arginine, an inhibitor of nitric oxide synthase (NOS), reduced urinary nitrate excretion and also the severity of myositis.	omega-N-Methylarginine	23-46	nitric oxide synthase 1, neuronal	Mus musculus	64-85
7545539-10	1995	Oral administration of N-monomethyl-L-arginine, an inhibitor of nitric oxide synthase (NOS), reduced urinary nitrate excretion and also the severity of myositis.	Nitrates	109-116	nitric oxide synthase 1, neuronal	Mus musculus	64-85
7545544-4	1995	The dystrophin complex interacts with an N-terminal domain of nNOS that contains a GLGF motif.	glgf	83-87	nitric oxide synthase 1, neuronal	Mus musculus	62-66
7545787-4	1995	Pharmacological blockade of NO production with arginine analogues such as L-nitroarginine (L-NA) or L-N-arginine methyl ester affects multiple isoforms of nitric oxide synthase (NOS), and so cannot distinguish their physiological roles.	Arginine	47-55	nitric oxide synthase 1, neuronal	Mus musculus	155-176
7545787-4	1995	Pharmacological blockade of NO production with arginine analogues such as L-nitroarginine (L-NA) or L-N-arginine methyl ester affects multiple isoforms of nitric oxide synthase (NOS), and so cannot distinguish their physiological roles.	H-Arg(NO2)-OH	74-89	nitric oxide synthase 1, neuronal	Mus musculus	155-176
7545787-4	1995	Pharmacological blockade of NO production with arginine analogues such as L-nitroarginine (L-NA) or L-N-arginine methyl ester affects multiple isoforms of nitric oxide synthase (NOS), and so cannot distinguish their physiological roles.	l-n-arginine methyl ester	100-125	nitric oxide synthase 1, neuronal	Mus musculus	155-176
7538492-7	1995	Both drugs acted directly on the nitric oxide synthase (NOS), since CsA and FK506 reduced by 35% and by 17%, respectively, NOS activity in the crude cytosolic fraction.	Cyclosporine	68-71	nitric oxide synthase 1, neuronal	Mus musculus	33-54
7542777-2	1995	In mice with deletion of the gene for neuronal NO synthase (NOS), CO2 inhalation augments cerebral blood flow to the same extent as in wild-type mice.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	66-69	nitric oxide synthase 1, neuronal	Mus musculus	47-58
7541615-11	1995	CONCLUSIONS: Although acute nonselective inhibition of nitric oxide synthase reduces the anesthetic requirements of wild-type mice, a chronic congenital deficiency of neuronal nitric oxide synthase or a week of L-NAME treatment of wild-type mice does not produce a state of greater sensitivity to the effects of isoflurane anesthesia.	Isoflurane	312-322	nitric oxide synthase 1, neuronal	Mus musculus	167-197
7541062-2	1995	In vitro, an inhibitor of NO synthase (NOS) reduced the candidacidal activity and nitrite-producing capacity of activated resident peritoneal macrophages from immunocompetent C.B-17 and immunodeficient SCID mice.	Nitrites	82-89	nitric oxide synthase 1, neuronal	Mus musculus	26-37
7540659-1	1995	It has been shown that nitric oxide (NO) regulates NO synthase (NOS) activity through negative feedback in cytosolic enzyme preparations in various cell types.	Nitric Oxide	23-35	nitric oxide synthase 1, neuronal	Mus musculus	51-62
7546627-1	1995	The majority of the data on nitric oxide (NO) in the central nervous system (CNS) relies on histochemical and immunohistochemical evidence concerning the distribution of the nitric oxide synthase (NOS), its inhibition by specific antagonists and its co-localization with the receptor enzyme guanylate cyclase (GC) in the same functional region.	Nitric Oxide	28-40	nitric oxide synthase 1, neuronal	Mus musculus	174-195
7539113-2	1995	It is generated from L-arginine by the enzyme NO synthase (NOS).	Arginine	21-31	nitric oxide synthase 1, neuronal	Mus musculus	46-57
7659439-6	1995	Intrathecal administration of L-arginine, a substrate of nitric oxide synthase (NOS), in conscious mice resulted in allodynia.	Arginine	30-40	nitric oxide synthase 1, neuronal	Mus musculus	57-78
7659444-16	1995	Finally, the NSAIDs, indomethacin and ibuprofen, the BK2 antagonist, Hoe 140 and the nitric oxide synthase (NOS) inhibitors, L-NAME and 7 nitroindazole, inhibited the LP (but not the EP) of FIL and (except for L-NAME) also reduced writhing: in contrast, they did not evoke ataxia and were inactive in the TF procedures.	Indomethacin	21-33	nitric oxide synthase 1, neuronal	Mus musculus	85-106
7659444-16	1995	Finally, the NSAIDs, indomethacin and ibuprofen, the BK2 antagonist, Hoe 140 and the nitric oxide synthase (NOS) inhibitors, L-NAME and 7 nitroindazole, inhibited the LP (but not the EP) of FIL and (except for L-NAME) also reduced writhing: in contrast, they did not evoke ataxia and were inactive in the TF procedures.	Ibuprofen	38-47	nitric oxide synthase 1, neuronal	Mus musculus	85-106
7659444-16	1995	Finally, the NSAIDs, indomethacin and ibuprofen, the BK2 antagonist, Hoe 140 and the nitric oxide synthase (NOS) inhibitors, L-NAME and 7 nitroindazole, inhibited the LP (but not the EP) of FIL and (except for L-NAME) also reduced writhing: in contrast, they did not evoke ataxia and were inactive in the TF procedures.	NG-Nitroarginine Methyl Ester	125-131	nitric oxide synthase 1, neuronal	Mus musculus	85-106
7659444-16	1995	Finally, the NSAIDs, indomethacin and ibuprofen, the BK2 antagonist, Hoe 140 and the nitric oxide synthase (NOS) inhibitors, L-NAME and 7 nitroindazole, inhibited the LP (but not the EP) of FIL and (except for L-NAME) also reduced writhing: in contrast, they did not evoke ataxia and were inactive in the TF procedures.	leucylproline	167-169	nitric oxide synthase 1, neuronal	Mus musculus	85-106
7537092-1	1995	Nitric oxide synthase (NOS) catalyzes the oxidation of L-arginine to citrulline and nitric oxide (.NO).	Arginine	55-65	nitric oxide synthase 1, neuronal	Mus musculus	0-21
7537092-1	1995	Nitric oxide synthase (NOS) catalyzes the oxidation of L-arginine to citrulline and nitric oxide (.NO).	Citrulline	69-79	nitric oxide synthase 1, neuronal	Mus musculus	0-21
7537092-1	1995	Nitric oxide synthase (NOS) catalyzes the oxidation of L-arginine to citrulline and nitric oxide (.NO).	Nitric Oxide	84-96	nitric oxide synthase 1, neuronal	Mus musculus	0-21
7538492-7	1995	Both drugs acted directly on the nitric oxide synthase (NOS), since CsA and FK506 reduced by 35% and by 17%, respectively, NOS activity in the crude cytosolic fraction.	Tacrolimus	76-81	nitric oxide synthase 1, neuronal	Mus musculus	33-54
8529104-1	1995	BACKGROUND: Nitric oxide (NO), a small effector molecule produced enzymatically from L-arginine by nitric oxide synthase (NOS), is a mediator not only of important homeostatic mechanisms (e.g., blood vessel tone and tissue perfusion), but also of key aspects of local and systemic inflammatory responses.	Nitric Oxide	12-24	nitric oxide synthase 1, neuronal	Mus musculus	99-120
8529104-1	1995	BACKGROUND: Nitric oxide (NO), a small effector molecule produced enzymatically from L-arginine by nitric oxide synthase (NOS), is a mediator not only of important homeostatic mechanisms (e.g., blood vessel tone and tissue perfusion), but also of key aspects of local and systemic inflammatory responses.	Arginine	85-95	nitric oxide synthase 1, neuronal	Mus musculus	99-120
7531495-1	1995	The ability of murine macrophage nitric oxide synthase (NOS) to utilize peroxides in place of O2 and NADPH was investigated using hydrogen peroxide (H2O2), tert-butylhydroperoxide, and cumene hydroperoxide with both L-arginine and NG-hydroxy-L-arginine (L-NHA) as substrates.	Peroxides	72-81	nitric oxide synthase 1, neuronal	Mus musculus	33-54
7538219-1	1995	Nitric oxide synthase (NOS) activity was determined by the rate of conversion of [3H]arginine to [3H]citrulline in brain regions (midbrain, hypothalamus, cerebellum, hippocampus, corpus striatum, cortex, pons-medulla and amygdala) and spinal cord of male Swiss Webster mice and male Sprague-Dawley rats.	[3h]arginine	81-93	nitric oxide synthase 1, neuronal	Mus musculus	0-21
7538219-1	1995	Nitric oxide synthase (NOS) activity was determined by the rate of conversion of [3H]arginine to [3H]citrulline in brain regions (midbrain, hypothalamus, cerebellum, hippocampus, corpus striatum, cortex, pons-medulla and amygdala) and spinal cord of male Swiss Webster mice and male Sprague-Dawley rats.	Tritium	82-84	nitric oxide synthase 1, neuronal	Mus musculus	0-21
7538219-1	1995	Nitric oxide synthase (NOS) activity was determined by the rate of conversion of [3H]arginine to [3H]citrulline in brain regions (midbrain, hypothalamus, cerebellum, hippocampus, corpus striatum, cortex, pons-medulla and amygdala) and spinal cord of male Swiss Webster mice and male Sprague-Dawley rats.	Citrulline	101-111	nitric oxide synthase 1, neuronal	Mus musculus	0-21
7531495-1	1995	The ability of murine macrophage nitric oxide synthase (NOS) to utilize peroxides in place of O2 and NADPH was investigated using hydrogen peroxide (H2O2), tert-butylhydroperoxide, and cumene hydroperoxide with both L-arginine and NG-hydroxy-L-arginine (L-NHA) as substrates.	Oxygen	94-96	nitric oxide synthase 1, neuronal	Mus musculus	33-54
7531495-1	1995	The ability of murine macrophage nitric oxide synthase (NOS) to utilize peroxides in place of O2 and NADPH was investigated using hydrogen peroxide (H2O2), tert-butylhydroperoxide, and cumene hydroperoxide with both L-arginine and NG-hydroxy-L-arginine (L-NHA) as substrates.	NADP	101-106	nitric oxide synthase 1, neuronal	Mus musculus	33-54
7531495-1	1995	The ability of murine macrophage nitric oxide synthase (NOS) to utilize peroxides in place of O2 and NADPH was investigated using hydrogen peroxide (H2O2), tert-butylhydroperoxide, and cumene hydroperoxide with both L-arginine and NG-hydroxy-L-arginine (L-NHA) as substrates.	Hydrogen Peroxide	130-147	nitric oxide synthase 1, neuronal	Mus musculus	33-54
7531495-1	1995	The ability of murine macrophage nitric oxide synthase (NOS) to utilize peroxides in place of O2 and NADPH was investigated using hydrogen peroxide (H2O2), tert-butylhydroperoxide, and cumene hydroperoxide with both L-arginine and NG-hydroxy-L-arginine (L-NHA) as substrates.	Hydrogen Peroxide	149-153	nitric oxide synthase 1, neuronal	Mus musculus	33-54
7531495-1	1995	The ability of murine macrophage nitric oxide synthase (NOS) to utilize peroxides in place of O2 and NADPH was investigated using hydrogen peroxide (H2O2), tert-butylhydroperoxide, and cumene hydroperoxide with both L-arginine and NG-hydroxy-L-arginine (L-NHA) as substrates.	tert-Butylhydroperoxide	156-179	nitric oxide synthase 1, neuronal	Mus musculus	33-54
7531495-1	1995	The ability of murine macrophage nitric oxide synthase (NOS) to utilize peroxides in place of O2 and NADPH was investigated using hydrogen peroxide (H2O2), tert-butylhydroperoxide, and cumene hydroperoxide with both L-arginine and NG-hydroxy-L-arginine (L-NHA) as substrates.	cumene hydroperoxide	185-205	nitric oxide synthase 1, neuronal	Mus musculus	33-54
7531495-1	1995	The ability of murine macrophage nitric oxide synthase (NOS) to utilize peroxides in place of O2 and NADPH was investigated using hydrogen peroxide (H2O2), tert-butylhydroperoxide, and cumene hydroperoxide with both L-arginine and NG-hydroxy-L-arginine (L-NHA) as substrates.	Arginine	216-226	nitric oxide synthase 1, neuronal	Mus musculus	33-54
7531495-1	1995	The ability of murine macrophage nitric oxide synthase (NOS) to utilize peroxides in place of O2 and NADPH was investigated using hydrogen peroxide (H2O2), tert-butylhydroperoxide, and cumene hydroperoxide with both L-arginine and NG-hydroxy-L-arginine (L-NHA) as substrates.	N(omega)-hydroxyarginine	231-252	nitric oxide synthase 1, neuronal	Mus musculus	33-54
7531495-1	1995	The ability of murine macrophage nitric oxide synthase (NOS) to utilize peroxides in place of O2 and NADPH was investigated using hydrogen peroxide (H2O2), tert-butylhydroperoxide, and cumene hydroperoxide with both L-arginine and NG-hydroxy-L-arginine (L-NHA) as substrates.	l-nha	254-259	nitric oxide synthase 1, neuronal	Mus musculus	33-54
7480796-0	1995	Prostaglandin E2 regulates inducible nitric oxide synthase in the murine macrophage cell line J774.	Dinoprostone	0-16	nitric oxide synthase 1, neuronal	Mus musculus	37-58
7531495-0	1995	Hydrogen peroxide-supported oxidation of NG-hydroxy-L-arginine by nitric oxide synthase.	Hydrogen Peroxide	0-17	nitric oxide synthase 1, neuronal	Mus musculus	66-87
7531495-0	1995	Hydrogen peroxide-supported oxidation of NG-hydroxy-L-arginine by nitric oxide synthase.	N(omega)-hydroxyarginine	41-62	nitric oxide synthase 1, neuronal	Mus musculus	66-87
7480796-1	1995	We have evaluated the role of prostaglandin E2 (PGE2) in the synthesis of nitric oxide (NO) by the activation of the inducible form of nitric oxide synthase (NOS) in the murine macrophage cell line, J774, stimulated with different doses of lipopolysaccharide (LPS).	Dinoprostone	30-46	nitric oxide synthase 1, neuronal	Mus musculus	135-156
7480796-1	1995	We have evaluated the role of prostaglandin E2 (PGE2) in the synthesis of nitric oxide (NO) by the activation of the inducible form of nitric oxide synthase (NOS) in the murine macrophage cell line, J774, stimulated with different doses of lipopolysaccharide (LPS).	Dinoprostone	48-52	nitric oxide synthase 1, neuronal	Mus musculus	135-156
7480796-1	1995	We have evaluated the role of prostaglandin E2 (PGE2) in the synthesis of nitric oxide (NO) by the activation of the inducible form of nitric oxide synthase (NOS) in the murine macrophage cell line, J774, stimulated with different doses of lipopolysaccharide (LPS).	Nitric Oxide	74-86	nitric oxide synthase 1, neuronal	Mus musculus	135-156
8630436-5	1995	By comparing NADPHd distribution with nitric oxide synthase (NOS) immunoreactivity (using a polyclonal antiserum raised against mouse cerebellar NOS) it was found that NADPHd labeling and NOS immunoreaction patterns generally matched.	nadphd	168-174	nitric oxide synthase 1, neuronal	Mus musculus	38-59
7539338-1	1995	Nitric oxide (NO) is produced in mammals by the enzyme NO synthase (NOS) in response to a number of agents, including the experimental antitumour agent flavone acetic acid (FAA) and the cytokine tumour necrosis factor-alpha (TNF).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	55-66
7539338-1	1995	Nitric oxide (NO) is produced in mammals by the enzyme NO synthase (NOS) in response to a number of agents, including the experimental antitumour agent flavone acetic acid (FAA) and the cytokine tumour necrosis factor-alpha (TNF).	flavone	152-159	nitric oxide synthase 1, neuronal	Mus musculus	55-66
7539338-1	1995	Nitric oxide (NO) is produced in mammals by the enzyme NO synthase (NOS) in response to a number of agents, including the experimental antitumour agent flavone acetic acid (FAA) and the cytokine tumour necrosis factor-alpha (TNF).	Acetic Acid	160-171	nitric oxide synthase 1, neuronal	Mus musculus	55-66
7539338-1	1995	Nitric oxide (NO) is produced in mammals by the enzyme NO synthase (NOS) in response to a number of agents, including the experimental antitumour agent flavone acetic acid (FAA) and the cytokine tumour necrosis factor-alpha (TNF).	flavone acetic acid	173-176	nitric oxide synthase 1, neuronal	Mus musculus	55-66
7542013-2	1995	Within the Leydig cell cytoplasm, immunocytochemical results suggested the occurrence of factors known to activate NOS-I such as glutamate and aspartate, as well as molecules involved in the regulation of the NOS-I activity such as calmodulin and Ca2+/calmodulin-dependent protein kinase II.	Glutamic Acid	129-138	nitric oxide synthase 1, neuronal	Mus musculus	115-120
7542013-2	1995	Within the Leydig cell cytoplasm, immunocytochemical results suggested the occurrence of factors known to activate NOS-I such as glutamate and aspartate, as well as molecules involved in the regulation of the NOS-I activity such as calmodulin and Ca2+/calmodulin-dependent protein kinase II.	Aspartic Acid	143-152	nitric oxide synthase 1, neuronal	Mus musculus	115-120
7542713-1	1995	Tetrahydrobiopterin (BH4) is the cofactor for the aromatic amino acid monoxygenase group of enzymes and for all known isoforms of nitric oxide synthase (NOS).	sapropterin	0-19	nitric oxide synthase 1, neuronal	Mus musculus	130-151
7542713-1	1995	Tetrahydrobiopterin (BH4) is the cofactor for the aromatic amino acid monoxygenase group of enzymes and for all known isoforms of nitric oxide synthase (NOS).	sapropterin	21-24	nitric oxide synthase 1, neuronal	Mus musculus	130-151
7869823-4	1995	In initial experiments employment of NG-monomethyl-L-arginine (L-NMMA) and dexamethasone, two specific inhibitors of nitric oxide synthase (NOS), confirmed the presence of inducible NOS activity in the cells.	omega-N-Methylarginine	37-61	nitric oxide synthase 1, neuronal	Mus musculus	117-138
7528781-3	1995	The maximal activity of NO synthase (NOS) was about 200-fold higher in cell lysates from the tEnd.1 endothelioma cell line than in lysates from nontransformed controls, whereas the affinity for arginine did not differ.	Arginine	194-202	nitric oxide synthase 1, neuronal	Mus musculus	24-35
7869823-4	1995	In initial experiments employment of NG-monomethyl-L-arginine (L-NMMA) and dexamethasone, two specific inhibitors of nitric oxide synthase (NOS), confirmed the presence of inducible NOS activity in the cells.	omega-N-Methylarginine	63-69	nitric oxide synthase 1, neuronal	Mus musculus	117-138
7869823-4	1995	In initial experiments employment of NG-monomethyl-L-arginine (L-NMMA) and dexamethasone, two specific inhibitors of nitric oxide synthase (NOS), confirmed the presence of inducible NOS activity in the cells.	Dexamethasone	75-88	nitric oxide synthase 1, neuronal	Mus musculus	117-138
7527442-5	1994	This lack of proliferation was determined not to be caused by impaired Ag processing, but rather was the result of IFN-gamma-stimulated nitric oxide (NO) release by the APC: 1) In vitro addition of the nitric oxide synthase (NOS) inhibitor NG-methyl-L-arginine (NMMA) restored the ability of the Gd-treated KC to stimulate clone proliferation.	Nitric Oxide	136-148	nitric oxide synthase 1, neuronal	Mus musculus	202-223
7525816-1	1994	Nitric oxide synthase (NOS) catalyzes the production of nitric oxide (NO), a short-lived radical gas with physiological or pathophysiological roles in nearly every organ system.	Nitric Oxide	56-68	nitric oxide synthase 1, neuronal	Mus musculus	0-21
7532830-1	1994	Under conditions in which NG-nitro-L-arginine (NOArg) treatment prevents morphine tolerance, NOArg induces a slow progressive inhibition of nitric oxide synthase (NOS), starting at approx.	Nitroarginine	93-98	nitric oxide synthase 1, neuronal	Mus musculus	140-161
7526856-1	1994	Nitric oxide synthase (NOS, EC 1.14.23) catalyzes the oxidation of the guanidino-nitrogen of L-arginine to form nitric oxide and L-citrulline.	guanidino-nitrogen	71-89	nitric oxide synthase 1, neuronal	Mus musculus	0-21
7526856-1	1994	Nitric oxide synthase (NOS, EC 1.14.23) catalyzes the oxidation of the guanidino-nitrogen of L-arginine to form nitric oxide and L-citrulline.	Arginine	93-103	nitric oxide synthase 1, neuronal	Mus musculus	0-21
7526856-1	1994	Nitric oxide synthase (NOS, EC 1.14.23) catalyzes the oxidation of the guanidino-nitrogen of L-arginine to form nitric oxide and L-citrulline.	Nitric Oxide	112-124	nitric oxide synthase 1, neuronal	Mus musculus	0-21
7526856-1	1994	Nitric oxide synthase (NOS, EC 1.14.23) catalyzes the oxidation of the guanidino-nitrogen of L-arginine to form nitric oxide and L-citrulline.	Citrulline	129-141	nitric oxide synthase 1, neuronal	Mus musculus	0-21
7520469-5	1994	In vitro experiments indicated that NO synthase (NOS) inhibition by N-nitro-L-arginine methyl ester (L-NAME) enhanced IFN-gamma and TNF production by splenocytes in response to SEB.	n-nitro-l-arginine methyl ester	68-99	nitric oxide synthase 1, neuronal	Mus musculus	36-47
7520469-5	1994	In vitro experiments indicated that NO synthase (NOS) inhibition by N-nitro-L-arginine methyl ester (L-NAME) enhanced IFN-gamma and TNF production by splenocytes in response to SEB.	NG-Nitroarginine Methyl Ester	101-107	nitric oxide synthase 1, neuronal	Mus musculus	36-47
7510883-3	1994	Nitric oxide is derived from L-arginine by isoforms of nitric-oxide synthase (NOS; EC 1.14.13.39): constitutive (cNOS; calcium-dependent) and inducible (iNOS; calcium-independent).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	55-76
7524106-1	1994	We recently reported that inhibition of nitric oxide (NO) production by the NO synthase (NOS) inhibitor L-NG-nitro arginine (L-NOARG) antagonized the behavioral effects of a benzodiazepine (BZ) in a mouse paradigm for screening anxiolytic drug activity.	Nitric Oxide	40-52	nitric oxide synthase 1, neuronal	Mus musculus	76-87
7524106-1	1994	We recently reported that inhibition of nitric oxide (NO) production by the NO synthase (NOS) inhibitor L-NG-nitro arginine (L-NOARG) antagonized the behavioral effects of a benzodiazepine (BZ) in a mouse paradigm for screening anxiolytic drug activity.	Nitroarginine	104-123	nitric oxide synthase 1, neuronal	Mus musculus	76-87
7524106-1	1994	We recently reported that inhibition of nitric oxide (NO) production by the NO synthase (NOS) inhibitor L-NG-nitro arginine (L-NOARG) antagonized the behavioral effects of a benzodiazepine (BZ) in a mouse paradigm for screening anxiolytic drug activity.	Nitroarginine	125-132	nitric oxide synthase 1, neuronal	Mus musculus	76-87
7524106-1	1994	We recently reported that inhibition of nitric oxide (NO) production by the NO synthase (NOS) inhibitor L-NG-nitro arginine (L-NOARG) antagonized the behavioral effects of a benzodiazepine (BZ) in a mouse paradigm for screening anxiolytic drug activity.	Benzodiazepines	174-188	nitric oxide synthase 1, neuronal	Mus musculus	76-87
7524106-1	1994	We recently reported that inhibition of nitric oxide (NO) production by the NO synthase (NOS) inhibitor L-NG-nitro arginine (L-NOARG) antagonized the behavioral effects of a benzodiazepine (BZ) in a mouse paradigm for screening anxiolytic drug activity.	Benzodiazepines	190-192	nitric oxide synthase 1, neuronal	Mus musculus	76-87
7518615-3	1994	One candidate retrograde messenger is the membrane-permeant gas nitric oxide (NO), which in the brain is released after activation of the neuronal-specific NO synthase isoform (nNOS).	Nitric Oxide	64-76	nitric oxide synthase 1, neuronal	Mus musculus	177-181
8182526-2	1994	In the mouse abdominal constriction test, pretreatment with the nitric oxide synthase (NOS) inhibitor L-NG-nitroarginine (L-NOARG) caused dose-related antagonism of the antinociceptive effect of N2O but not of either morphine or trans(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl] benzeneacetamide methane sulfonate.	Nitroarginine	102-120	nitric oxide synthase 1, neuronal	Mus musculus	64-85
8182526-2	1994	In the mouse abdominal constriction test, pretreatment with the nitric oxide synthase (NOS) inhibitor L-NG-nitroarginine (L-NOARG) caused dose-related antagonism of the antinociceptive effect of N2O but not of either morphine or trans(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl] benzeneacetamide methane sulfonate.	Nitroarginine	122-129	nitric oxide synthase 1, neuronal	Mus musculus	64-85
8182526-2	1994	In the mouse abdominal constriction test, pretreatment with the nitric oxide synthase (NOS) inhibitor L-NG-nitroarginine (L-NOARG) caused dose-related antagonism of the antinociceptive effect of N2O but not of either morphine or trans(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl] benzeneacetamide methane sulfonate.	Nitrous Oxide	195-198	nitric oxide synthase 1, neuronal	Mus musculus	64-85
8182526-2	1994	In the mouse abdominal constriction test, pretreatment with the nitric oxide synthase (NOS) inhibitor L-NG-nitroarginine (L-NOARG) caused dose-related antagonism of the antinociceptive effect of N2O but not of either morphine or trans(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl] benzeneacetamide methane sulfonate.	Morphine	217-225	nitric oxide synthase 1, neuronal	Mus musculus	64-85
7510678-0	1994	Regulation of nitric-oxide synthase mRNA expression by interferon-gamma and picolinic acid.	picolinic acid	76-90	nitric oxide synthase 1, neuronal	Mus musculus	14-35
7510678-2	1994	We studied whether picolinic acid could affect nitric-oxide synthase (NOS) expression at the gene level in the macrophage cell line ANA-1.	picolinic acid	19-33	nitric oxide synthase 1, neuronal	Mus musculus	47-68
7519084-0	1994	Carboxyebselen a potent and selective inhibitor of endothelial nitric oxide synthase.	carboxyebselen a	0-16	nitric oxide synthase 1, neuronal	Mus musculus	63-84
7519084-1	1994	Ebselen (Ebs) a glutathione peroxidase like agent has been recently described as an inhibitor of nitric oxide synthase (NOS).	ebselen	0-7	nitric oxide synthase 1, neuronal	Mus musculus	97-118
7519084-1	1994	Ebselen (Ebs) a glutathione peroxidase like agent has been recently described as an inhibitor of nitric oxide synthase (NOS).	ebselen	0-3	nitric oxide synthase 1, neuronal	Mus musculus	97-118
7509263-1	1994	Nitric oxide (NO) is generated intracellularly from L-arginine by the action of the enzyme nitric oxide synthase (NOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	91-112
7509263-1	1994	Nitric oxide (NO) is generated intracellularly from L-arginine by the action of the enzyme nitric oxide synthase (NOS).	Arginine	52-62	nitric oxide synthase 1, neuronal	Mus musculus	91-112
7507106-2	1994	In macrophages and other cell types, bacterial lipopolysaccharide and certain cytokines stimulate nitric oxide (NO) production via expression of the inducible isoform of nitric oxide synthase (NOS).	Nitric Oxide	98-110	nitric oxide synthase 1, neuronal	Mus musculus	170-191
7682975-0	1993	Diethyldithiocarbamate inhibits induction of macrophage NO synthase.	Ditiocarb	0-22	nitric oxide synthase 1, neuronal	Mus musculus	56-67
7509434-1	1994	Recent immunocytochemical studies of cerebellar nitric oxide synthase (NOS) and cGMP have aided dramatically in defining possible cellular sources of cGMP generation in the signal transduction cascade evoked by excitatory amino acids in the cerebellum.	Cyclic GMP	150-154	nitric oxide synthase 1, neuronal	Mus musculus	48-69
7509434-1	1994	Recent immunocytochemical studies of cerebellar nitric oxide synthase (NOS) and cGMP have aided dramatically in defining possible cellular sources of cGMP generation in the signal transduction cascade evoked by excitatory amino acids in the cerebellum.	Excitatory Amino Acids	211-233	nitric oxide synthase 1, neuronal	Mus musculus	48-69
7690590-1	1993	NG-Methyl-L-arginine (L-NMA) is one of the most commonly used inhibitors of the nitric oxide synthases (NOS).	ng-methyl-l-arginine	0-20	nitric oxide synthase 1, neuronal	Mus musculus	80-102
7690590-1	1993	NG-Methyl-L-arginine (L-NMA) is one of the most commonly used inhibitors of the nitric oxide synthases (NOS).	l-nma	22-27	nitric oxide synthase 1, neuronal	Mus musculus	80-102
7693278-0	1993	Characterization of the novel nitric oxide synthase inhibitor 7-nitro indazole and related indazoles: antinociceptive and cardiovascular effects.	7-nitroindazole	62-78	nitric oxide synthase 1, neuronal	Mus musculus	30-51
7693278-0	1993	Characterization of the novel nitric oxide synthase inhibitor 7-nitro indazole and related indazoles: antinociceptive and cardiovascular effects.	Indazoles	91-100	nitric oxide synthase 1, neuronal	Mus musculus	30-51
7693278-11	1993	The time course of 7-NI induced antinociception in the mouse was correlated with inhibition of brain (cerebellum) nitric oxide synthase (NOS) activity.	7-nitroindazole	19-23	nitric oxide synthase 1, neuronal	Mus musculus	114-135
7506289-3	1993	IL-1 beta-induced NOx production and intracellular cyclic GMP formation were similarly blocked by an NO synthase inhibitor, NG-monomethyl-L-arginine (LNMMA), whose effect was reversed by L-arginine, but not by D-arginine.	nicotine 1-N-oxide	18-21	nitric oxide synthase 1, neuronal	Mus musculus	101-112
7506289-3	1993	IL-1 beta-induced NOx production and intracellular cyclic GMP formation were similarly blocked by an NO synthase inhibitor, NG-monomethyl-L-arginine (LNMMA), whose effect was reversed by L-arginine, but not by D-arginine.	Cyclic GMP	51-61	nitric oxide synthase 1, neuronal	Mus musculus	101-112
7506289-3	1993	IL-1 beta-induced NOx production and intracellular cyclic GMP formation were similarly blocked by an NO synthase inhibitor, NG-monomethyl-L-arginine (LNMMA), whose effect was reversed by L-arginine, but not by D-arginine.	omega-N-Methylarginine	124-148	nitric oxide synthase 1, neuronal	Mus musculus	101-112
7506289-3	1993	IL-1 beta-induced NOx production and intracellular cyclic GMP formation were similarly blocked by an NO synthase inhibitor, NG-monomethyl-L-arginine (LNMMA), whose effect was reversed by L-arginine, but not by D-arginine.	omega-N-Methylarginine	150-155	nitric oxide synthase 1, neuronal	Mus musculus	101-112
7506289-3	1993	IL-1 beta-induced NOx production and intracellular cyclic GMP formation were similarly blocked by an NO synthase inhibitor, NG-monomethyl-L-arginine (LNMMA), whose effect was reversed by L-arginine, but not by D-arginine.	Arginine	138-148	nitric oxide synthase 1, neuronal	Mus musculus	101-112
7506289-3	1993	IL-1 beta-induced NOx production and intracellular cyclic GMP formation were similarly blocked by an NO synthase inhibitor, NG-monomethyl-L-arginine (LNMMA), whose effect was reversed by L-arginine, but not by D-arginine.	D-Arginine	210-220	nitric oxide synthase 1, neuronal	Mus musculus	101-112
7688473-2	1993	Induction of NO synthase (NOS) and COX (COX-2) in the mouse macrophage cell line RAW264.7 by Escherichia coli lipopolysaccharide (1 microgram/ml, 18 h) caused an increase in the release of nitrite (NO2-) and prostaglandin E2 (PGE2), products of NOS and COX, respectively.	Nitrites	189-196	nitric oxide synthase 1, neuronal	Mus musculus	13-24
7688473-2	1993	Induction of NO synthase (NOS) and COX (COX-2) in the mouse macrophage cell line RAW264.7 by Escherichia coli lipopolysaccharide (1 microgram/ml, 18 h) caused an increase in the release of nitrite (NO2-) and prostaglandin E2 (PGE2), products of NOS and COX, respectively.	Nitrogen Dioxide	198-201	nitric oxide synthase 1, neuronal	Mus musculus	13-24
7688473-2	1993	Induction of NO synthase (NOS) and COX (COX-2) in the mouse macrophage cell line RAW264.7 by Escherichia coli lipopolysaccharide (1 microgram/ml, 18 h) caused an increase in the release of nitrite (NO2-) and prostaglandin E2 (PGE2), products of NOS and COX, respectively.	Dinoprostone	208-224	nitric oxide synthase 1, neuronal	Mus musculus	13-24
7688473-2	1993	Induction of NO synthase (NOS) and COX (COX-2) in the mouse macrophage cell line RAW264.7 by Escherichia coli lipopolysaccharide (1 microgram/ml, 18 h) caused an increase in the release of nitrite (NO2-) and prostaglandin E2 (PGE2), products of NOS and COX, respectively.	Dinoprostone	226-230	nitric oxide synthase 1, neuronal	Mus musculus	13-24
8510824-2	1993	Exposure of cultures to 300 microM NMDA for 5 min resulted in death of 50-80% of neurons over the subsequent 24 h. This injury was not attenuated by hemoglobin, the nitric oxide synthase (NOS) inhibitors NG monomethyl-L-arginine (MMA) or N omega-nitro-L-arginine (NA), or L-arginine depletion.	N-Methylaspartate	35-39	nitric oxide synthase 1, neuronal	Mus musculus	165-186
7510883-3	1994	Nitric oxide is derived from L-arginine by isoforms of nitric-oxide synthase (NOS; EC 1.14.13.39): constitutive (cNOS; calcium-dependent) and inducible (iNOS; calcium-independent).	Arginine	29-39	nitric oxide synthase 1, neuronal	Mus musculus	55-76
7510883-3	1994	Nitric oxide is derived from L-arginine by isoforms of nitric-oxide synthase (NOS; EC 1.14.13.39): constitutive (cNOS; calcium-dependent) and inducible (iNOS; calcium-independent).	Calcium	119-126	nitric oxide synthase 1, neuronal	Mus musculus	55-76
7510883-3	1994	Nitric oxide is derived from L-arginine by isoforms of nitric-oxide synthase (NOS; EC 1.14.13.39): constitutive (cNOS; calcium-dependent) and inducible (iNOS; calcium-independent).	Calcium	159-166	nitric oxide synthase 1, neuronal	Mus musculus	55-76
7536060-1	1994	In the present study, nicotinamide adenine dinucleotide hydrogen phosphate-diaphorase (NADPH-d) histochemistry has been used as a marker for nitric oxide synthase (NOS).	nicotinamide adenine	22-42	nitric oxide synthase 1, neuronal	Mus musculus	141-162
7694580-0	1993	Dihydropyridine antagonists and agonists of calcium channels inhibit the induction of nitric oxide synthase by endotoxin in cultured macrophages.	1,4-dihydropyridine	0-15	nitric oxide synthase 1, neuronal	Mus musculus	86-107
7694580-1	1993	Here we investigate the effects of the dihydropyridine-type antagonists of calcium channels nitrendipine, nimodipine, nisoldipine and the calcium channel agonist BAY K 8644 on the induction of nitric oxide synthase (NOS) by bacterial endotoxin (lipopolysaccharide; LPS) in J774.2 macrophages cultured in vitro.	1,4-dihydropyridine	39-54	nitric oxide synthase 1, neuronal	Mus musculus	193-214
7694580-1	1993	Here we investigate the effects of the dihydropyridine-type antagonists of calcium channels nitrendipine, nimodipine, nisoldipine and the calcium channel agonist BAY K 8644 on the induction of nitric oxide synthase (NOS) by bacterial endotoxin (lipopolysaccharide; LPS) in J774.2 macrophages cultured in vitro.	Nitrendipine	92-104	nitric oxide synthase 1, neuronal	Mus musculus	193-214
7694580-1	1993	Here we investigate the effects of the dihydropyridine-type antagonists of calcium channels nitrendipine, nimodipine, nisoldipine and the calcium channel agonist BAY K 8644 on the induction of nitric oxide synthase (NOS) by bacterial endotoxin (lipopolysaccharide; LPS) in J774.2 macrophages cultured in vitro.	Nimodipine	106-116	nitric oxide synthase 1, neuronal	Mus musculus	193-214
7694580-1	1993	Here we investigate the effects of the dihydropyridine-type antagonists of calcium channels nitrendipine, nimodipine, nisoldipine and the calcium channel agonist BAY K 8644 on the induction of nitric oxide synthase (NOS) by bacterial endotoxin (lipopolysaccharide; LPS) in J774.2 macrophages cultured in vitro.	Nisoldipine	118-129	nitric oxide synthase 1, neuronal	Mus musculus	193-214
7682975-1	1993	We investigated whether sodium diethyldithiocarbamate (DETC), an inhibitor of the nuclear transcription factor kappa B (NFkappa B), modulates induction of NO synthase (NOS) in murine bone marrow-derived macrophages.	Ditiocarb	24-53	nitric oxide synthase 1, neuronal	Mus musculus	155-166
7682975-1	1993	We investigated whether sodium diethyldithiocarbamate (DETC), an inhibitor of the nuclear transcription factor kappa B (NFkappa B), modulates induction of NO synthase (NOS) in murine bone marrow-derived macrophages.	Ditiocarb	55-59	nitric oxide synthase 1, neuronal	Mus musculus	155-166
7680591-0	1993	7-Nitro indazole, an inhibitor of nitric oxide synthase, exhibits anti-nociceptive activity in the mouse without increasing blood pressure.	7-nitroindazole	0-16	nitric oxide synthase 1, neuronal	Mus musculus	34-55
7686743-1	1993	Nitric oxide (NO), generated from L-arginine by an enzymatic reaction of a NO synthase (NOS; EC 1.14.23), is a recently identified biological mediator suggested to be involved in a wide variety of biological processes.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	75-86
7686743-1	1993	Nitric oxide (NO), generated from L-arginine by an enzymatic reaction of a NO synthase (NOS; EC 1.14.23), is a recently identified biological mediator suggested to be involved in a wide variety of biological processes.	Arginine	34-44	nitric oxide synthase 1, neuronal	Mus musculus	75-86
7682617-2	1993	In this report, NMA is shown to irreversibly inhibit both mNOS (k(inact) = 0.08 min-1) and the recombinant constitutive brain NOS (bNOS).	nma	16-19	nitric oxide synthase 1, neuronal	Mus musculus	131-135
7682617-5	1993	Authentic NOHNMA, synthesized from L-ornithine, irreversibly inhibited both mNOS (k(inact) = 0.10 min-1) and bNOS in an NADPH-dependent reaction.	Ornithine	35-46	nitric oxide synthase 1, neuronal	Mus musculus	109-113
7682617-5	1993	Authentic NOHNMA, synthesized from L-ornithine, irreversibly inhibited both mNOS (k(inact) = 0.10 min-1) and bNOS in an NADPH-dependent reaction.	NADP	120-125	nitric oxide synthase 1, neuronal	Mus musculus	109-113
7680591-1	1993	7-Nitro indazole (7-NI) inhibits mouse cerebellar nitric oxide synthase (NOS) in vitro with an IC50 of 0.47 microM.	7-nitroindazole	0-16	nitric oxide synthase 1, neuronal	Mus musculus	50-71
7680591-1	1993	7-Nitro indazole (7-NI) inhibits mouse cerebellar nitric oxide synthase (NOS) in vitro with an IC50 of 0.47 microM.	7-nitroindazole	18-22	nitric oxide synthase 1, neuronal	Mus musculus	50-71
24805951-5	2014	Phenylephrine-induced vasoconstriction was significantly increased in vascular rings from ATP2B1(+/-) mice, and the difference in this contraction disappeared in the presence of a nitric oxide synthase (NOS) inhibitor.	Phenylephrine	0-13	nitric oxide synthase 1, neuronal	Mus musculus	180-201
1284437-2	1992	An inhibitor of nitric oxide synthase (NOS), N omega-nitro-L-arginine methyl ester (L-NAME), administered either systemically or intrathecally, blocked the NMDA-induced hyperalgesia.	NG-Nitroarginine Methyl Ester	45-82	nitric oxide synthase 1, neuronal	Mus musculus	16-37
1284437-2	1992	An inhibitor of nitric oxide synthase (NOS), N omega-nitro-L-arginine methyl ester (L-NAME), administered either systemically or intrathecally, blocked the NMDA-induced hyperalgesia.	NG-Nitroarginine Methyl Ester	84-90	nitric oxide synthase 1, neuronal	Mus musculus	16-37
1284437-2	1992	An inhibitor of nitric oxide synthase (NOS), N omega-nitro-L-arginine methyl ester (L-NAME), administered either systemically or intrathecally, blocked the NMDA-induced hyperalgesia.	N-Methylaspartate	156-160	nitric oxide synthase 1, neuronal	Mus musculus	16-37
1379468-0	1992	Macrophage nitric oxide synthase: relationship between enzyme-bound tetrahydrobiopterin and synthase activity.	sapropterin	68-87	nitric oxide synthase 1, neuronal	Mus musculus	11-32
1379468-1	1992	Nitric oxide synthase (NOS) (EC 1.14.23) catalyzes the oxidation of L-arginine to citrulline and nitric oxide.	Arginine	68-78	nitric oxide synthase 1, neuronal	Mus musculus	0-21
1379468-1	1992	Nitric oxide synthase (NOS) (EC 1.14.23) catalyzes the oxidation of L-arginine to citrulline and nitric oxide.	Citrulline	82-92	nitric oxide synthase 1, neuronal	Mus musculus	0-21
1379468-1	1992	Nitric oxide synthase (NOS) (EC 1.14.23) catalyzes the oxidation of L-arginine to citrulline and nitric oxide.	Nitric Oxide	97-109	nitric oxide synthase 1, neuronal	Mus musculus	0-21
1721880-4	1991	L-Homoarginine and L-arginine-containing small peptides, such as L-arginyl-L-phenylalanine, replaced L-arginine as a substrate for the NOSc in EC and the Ca(2+)-independent NOSi in J774.2 cells, but not the Ca(2+)-dependent NOSi.	Homoarginine	0-14	nitric oxide synthase 1, neuronal	Mus musculus	173-177
1721880-4	1991	L-Homoarginine and L-arginine-containing small peptides, such as L-arginyl-L-phenylalanine, replaced L-arginine as a substrate for the NOSc in EC and the Ca(2+)-independent NOSi in J774.2 cells, but not the Ca(2+)-dependent NOSi.	Homoarginine	0-14	nitric oxide synthase 1, neuronal	Mus musculus	224-228
1721880-4	1991	L-Homoarginine and L-arginine-containing small peptides, such as L-arginyl-L-phenylalanine, replaced L-arginine as a substrate for the NOSc in EC and the Ca(2+)-independent NOSi in J774.2 cells, but not the Ca(2+)-dependent NOSi.	Arginine	19-29	nitric oxide synthase 1, neuronal	Mus musculus	173-177
1721880-4	1991	L-Homoarginine and L-arginine-containing small peptides, such as L-arginyl-L-phenylalanine, replaced L-arginine as a substrate for the NOSc in EC and the Ca(2+)-independent NOSi in J774.2 cells, but not the Ca(2+)-dependent NOSi.	Arginine	19-29	nitric oxide synthase 1, neuronal	Mus musculus	224-228
1721880-4	1991	L-Homoarginine and L-arginine-containing small peptides, such as L-arginyl-L-phenylalanine, replaced L-arginine as a substrate for the NOSc in EC and the Ca(2+)-independent NOSi in J774.2 cells, but not the Ca(2+)-dependent NOSi.	Peptides	47-55	nitric oxide synthase 1, neuronal	Mus musculus	173-177
1721880-4	1991	L-Homoarginine and L-arginine-containing small peptides, such as L-arginyl-L-phenylalanine, replaced L-arginine as a substrate for the NOSc in EC and the Ca(2+)-independent NOSi in J774.2 cells, but not the Ca(2+)-dependent NOSi.	Peptides	47-55	nitric oxide synthase 1, neuronal	Mus musculus	224-228
1721880-4	1991	L-Homoarginine and L-arginine-containing small peptides, such as L-arginyl-L-phenylalanine, replaced L-arginine as a substrate for the NOSc in EC and the Ca(2+)-independent NOSi in J774.2 cells, but not the Ca(2+)-dependent NOSi.	arginylphenylalanine	65-90	nitric oxide synthase 1, neuronal	Mus musculus	173-177
1721880-4	1991	L-Homoarginine and L-arginine-containing small peptides, such as L-arginyl-L-phenylalanine, replaced L-arginine as a substrate for the NOSc in EC and the Ca(2+)-independent NOSi in J774.2 cells, but not the Ca(2+)-dependent NOSi.	arginylphenylalanine	65-90	nitric oxide synthase 1, neuronal	Mus musculus	224-228
1721880-4	1991	L-Homoarginine and L-arginine-containing small peptides, such as L-arginyl-L-phenylalanine, replaced L-arginine as a substrate for the NOSc in EC and the Ca(2+)-independent NOSi in J774.2 cells, but not the Ca(2+)-dependent NOSi.	Arginine	101-111	nitric oxide synthase 1, neuronal	Mus musculus	173-177
1721880-4	1991	L-Homoarginine and L-arginine-containing small peptides, such as L-arginyl-L-phenylalanine, replaced L-arginine as a substrate for the NOSc in EC and the Ca(2+)-independent NOSi in J774.2 cells, but not the Ca(2+)-dependent NOSi.	Arginine	101-111	nitric oxide synthase 1, neuronal	Mus musculus	224-228
33235613-12	2021	Treatment with Dex efficiently decreased the PSD95-NR2B-nNOS interaction, which reduced the TBI-induced neuronal death.	Dexmedetomidine	15-18	nitric oxide synthase 1, neuronal	Mus musculus	56-60
11475008-2	2001	Pretreatment with 7-nitroindazole, a fairly selective inhibitor of neuronal nitric oxide synthase in vivo, partially prevented DSP-4 induced NA depletion in mouse hippocampus measured seven days after the neurotoxic insult.	7-nitroindazole	18-33	nitric oxide synthase 1, neuronal	Mus musculus	67-97
21645517-1	2011	The exogenous administration of tetrahydrobiopterin (BH4), an essential cofactor of nitric oxide synthase (NOS), has been shown to reduce left ventricular hypertrophy, fibrosis, and cardiac dysfunction in mice with pre-established heart disease induced by pressure-overload.	sapropterin	32-51	nitric oxide synthase 1, neuronal	Mus musculus	84-105
21645517-1	2011	The exogenous administration of tetrahydrobiopterin (BH4), an essential cofactor of nitric oxide synthase (NOS), has been shown to reduce left ventricular hypertrophy, fibrosis, and cardiac dysfunction in mice with pre-established heart disease induced by pressure-overload.	sapropterin	53-56	nitric oxide synthase 1, neuronal	Mus musculus	84-105
15350652-1	2004	The present study investigated the role of neuronal nitric oxide synthase (nNOS) in carrageenan-induced inflammatory pain by combining genomic and pharmacological strategies.	Carrageenan	84-95	nitric oxide synthase 1, neuronal	Mus musculus	43-73
15350652-1	2004	The present study investigated the role of neuronal nitric oxide synthase (nNOS) in carrageenan-induced inflammatory pain by combining genomic and pharmacological strategies.	Carrageenan	84-95	nitric oxide synthase 1, neuronal	Mus musculus	75-79
15350652-2	2004	Intrathecal injection of the nNOS inhibitor 7-nitroindazole dose-dependently inhibited carrageenan-induced thermal hyperalgesia in both early and late phases in wild-type mice.	7-nitroindazole	44-59	nitric oxide synthase 1, neuronal	Mus musculus	29-33
15350652-2	2004	Intrathecal injection of the nNOS inhibitor 7-nitroindazole dose-dependently inhibited carrageenan-induced thermal hyperalgesia in both early and late phases in wild-type mice.	Carrageenan	87-98	nitric oxide synthase 1, neuronal	Mus musculus	29-33
15350652-3	2004	However in nNOS knockout mice, carrageenan-induced thermal hyperalgesia remained intact in the early phase but was reduced in the late phase.	Carrageenan	31-42	nitric oxide synthase 1, neuronal	Mus musculus	11-15
15350652-10	2004	Our current results indicate that nNOS plays different roles in the two phases of carrageenan-induced inflammatory pain.	Carrageenan	82-93	nitric oxide synthase 1, neuronal	Mus musculus	34-38
11015578-0	2000	nNOS and eNOS modulate cGMP formation and vascular response in contracting fast-twitch skeletal muscle.	Cyclic GMP	23-27	nitric oxide synthase 1, neuronal	Mus musculus	0-4
11015578-1	2000	Nitric oxide (NO) from Ca(2+)-dependent neuronal nitric oxide synthase (nNOS) in skeletal muscle fibers may modulate vascular tone by a cGMP-dependent pathway similar to NO derived from NOS in endothelial cells (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	40-70
11015578-1	2000	Nitric oxide (NO) from Ca(2+)-dependent neuronal nitric oxide synthase (nNOS) in skeletal muscle fibers may modulate vascular tone by a cGMP-dependent pathway similar to NO derived from NOS in endothelial cells (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	72-76
11015578-1	2000	Nitric oxide (NO) from Ca(2+)-dependent neuronal nitric oxide synthase (nNOS) in skeletal muscle fibers may modulate vascular tone by a cGMP-dependent pathway similar to NO derived from NOS in endothelial cells (eNOS).	Cyclic GMP	136-140	nitric oxide synthase 1, neuronal	Mus musculus	40-70
11015578-1	2000	Nitric oxide (NO) from Ca(2+)-dependent neuronal nitric oxide synthase (nNOS) in skeletal muscle fibers may modulate vascular tone by a cGMP-dependent pathway similar to NO derived from NOS in endothelial cells (eNOS).	Cyclic GMP	136-140	nitric oxide synthase 1, neuronal	Mus musculus	72-76
11015578-8	2000	These findings suggest that increases in cGMP and NO-dependent vascular relaxation in contracting fast-twitch skeletal muscle may require both nNOS and eNOS.	Cyclic GMP	41-45	nitric oxide synthase 1, neuronal	Mus musculus	143-147
11475008-5	2001	Thus, the contribution of neuronal nitric oxide synthase inhibition to the protective effect of 7-nitroindazole needs further studies.	7-nitroindazole	96-111	nitric oxide synthase 1, neuronal	Mus musculus	26-56
34954231-9	2022	Mechanistic studies subsequently showed that treatment of ALO increased the expression of NOS1, whereas NOS2 was decreased.	aloperine	58-61	nitric oxide synthase 1, neuronal	Mus musculus	90-94
34933049-4	2022	In the low EtOH consuming rodent models tested to date, EtOH enhancement of GC tonic GABAAR currents is mediated by inhibition of neuronal nitric oxide synthase (nNOS) which drives increased vesicular GABA release onto GCs and a consequent enhancement of tonic GABAAR currents.	Ethanol	56-60	nitric oxide synthase 1, neuronal	Mus musculus	130-160
34933049-4	2022	In the low EtOH consuming rodent models tested to date, EtOH enhancement of GC tonic GABAAR currents is mediated by inhibition of neuronal nitric oxide synthase (nNOS) which drives increased vesicular GABA release onto GCs and a consequent enhancement of tonic GABAAR currents.	Ethanol	56-60	nitric oxide synthase 1, neuronal	Mus musculus	162-166
34933049-5	2022	Consequently, genetic variation in nNOS expression across rodent genotypes is a key determinant of whether EtOH enhances or suppresses tonic GABAAR currents, and thus EtOH consumption.	Ethanol	107-111	nitric oxide synthase 1, neuronal	Mus musculus	35-39
34933049-5	2022	Consequently, genetic variation in nNOS expression across rodent genotypes is a key determinant of whether EtOH enhances or suppresses tonic GABAAR currents, and thus EtOH consumption.	Ethanol	167-171	nitric oxide synthase 1, neuronal	Mus musculus	35-39
34933049-10	2022	Collectively, our data demonstrate that despite being genetically similar, B6N mice consume significantly less EtOH than B6J mice, a behavioral difference paralleled by increased cerebellar nNOS expression and opposite EtOH action on GC tonic GABAAR currents in each genotype.	Ethanol	111-115	nitric oxide synthase 1, neuronal	Mus musculus	190-194
34310708-1	2021	Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor/uncoupler inducing vascular pathology.	dimethylarginine	11-27	nitric oxide synthase 1, neuronal	Mus musculus	52-73
34661719-0	2022	Targeting PSD95/nNOS by ZL006 alleviates social isolation-induced heightened attack behavior in mice.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	24-29	nitric oxide synthase 1, neuronal	Mus musculus	16-20
34661719-4	2022	METHODS: Pharmacological tools, biochemical methods, and behavioral tests were used to explore the potential therapeutic effects of ZL006 targeting postsynaptic density 95 (PSD95)/neuronal nitric oxide synthase (nNOS) pathway on escalation of attack behavior induced by SI in mice.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	132-137	nitric oxide synthase 1, neuronal	Mus musculus	180-210
34661719-4	2022	METHODS: Pharmacological tools, biochemical methods, and behavioral tests were used to explore the potential therapeutic effects of ZL006 targeting postsynaptic density 95 (PSD95)/neuronal nitric oxide synthase (nNOS) pathway on escalation of attack behavior induced by SI in mice.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	132-137	nitric oxide synthase 1, neuronal	Mus musculus	212-216
34657443-8	2021	In conclusion, the present study demonstrates that in the early stage of leptin receptor-deficient diabetes, the upregulation of macula densa NOS1 inhibits TGF and increases glomerular filtration rate, which counteracts renal sodium retention and limits the rise in blood pressure.	Sodium	226-232	nitric oxide synthase 1, neuronal	Mus musculus	142-146
34831251-10	2021	The treatment with vitamin C preserved the left kidney weight, restored renal function, reduced NO levels, decreased iNOS expression, elevated constitutive NOS isoforms, and improved oxygen consumption.	Ascorbic Acid	19-28	nitric oxide synthase 1, neuronal	Mus musculus	143-159
34944061-0	2021	Differences of Transport Activity of Arginine and Regulation on Neuronal Nitric Oxide Synthase and Oxidative Stress in Amyotrophic Lateral Sclerosis Model Cell Lines.	Arginine	37-45	nitric oxide synthase 1, neuronal	Mus musculus	64-94
34944061-9	2021	Pretreatment with arginine elevated nNOS mRNA levels in MT.	Arginine	18-26	nitric oxide synthase 1, neuronal	Mus musculus	36-40
34657443-4	2021	In this study, we hypothesize that in early diabetes, the macula densa neuronal nitric oxide synthase (NOS1)-derived nitric oxide (NO) production is enhanced, which blunts tubuloglomerular feedback (TGF) response, promotes glomerular hyperfiltration, and maintains normal blood pressure; conversely, insufficient NO generation by the macula densa induces hypertension by lowering glomerular filtration rate and thus inhibiting natriuresis.	Nitric Oxide	117-129	nitric oxide synthase 1, neuronal	Mus musculus	71-101
34657443-7	2021	Genetic knockout of macula densa NOS1 restored the TGF response and attenuated glomerular hyperfiltration in db/db mice but also further reduced fractional renal sodium excretion and substantially increased blood pressure.	Sodium	162-168	nitric oxide synthase 1, neuronal	Mus musculus	33-37
34547676-8	2021	Furthermore, melatonin triggers an increase in the iNOS expression and a decrease in the nNOS expression in the ipsilateral hemisphere at the earlier times in the post-ischemic recovery.	Melatonin	13-22	nitric oxide synthase 1, neuronal	Mus musculus	89-93
34547676-9	2021	At the 55th day of the post-ischemic recovery, melatonin administration enhanced the eNOS and nNOS protein expressions.	Melatonin	47-56	nitric oxide synthase 1, neuronal	Mus musculus	94-98
34739536-6	2021	R568 treatment increased the numbers of nitric oxide synthase-positive neurons and nitric oxide release but decreased the choline acetyl transferase-positive neurons and acetylcholine release in the myenteric plexuses.	N-(2-chlorophenylpropyl)-1-(3-methoxyphenyl)ethylamine	0-4	nitric oxide synthase 1, neuronal	Mus musculus	40-61
34830481-5	2021	First, nerinetide (Phase 3) and AVLX-144 (Phase 1) were designed to interfere with the coupling of the ternary complex formed by PSD-95 with GluN2B subunits of the N-methyl-D-aspartate type of glutamate receptors (NMDARs) and neuronal nitric oxide synthase (nNOS).	Tat-NR2B9c	7-17	nitric oxide synthase 1, neuronal	Mus musculus	226-256
34830481-5	2021	First, nerinetide (Phase 3) and AVLX-144 (Phase 1) were designed to interfere with the coupling of the ternary complex formed by PSD-95 with GluN2B subunits of the N-methyl-D-aspartate type of glutamate receptors (NMDARs) and neuronal nitric oxide synthase (nNOS).	Tat-NR2B9c	7-17	nitric oxide synthase 1, neuronal	Mus musculus	258-262
34830481-5	2021	First, nerinetide (Phase 3) and AVLX-144 (Phase 1) were designed to interfere with the coupling of the ternary complex formed by PSD-95 with GluN2B subunits of the N-methyl-D-aspartate type of glutamate receptors (NMDARs) and neuronal nitric oxide synthase (nNOS).	avlx-144	32-40	nitric oxide synthase 1, neuronal	Mus musculus	226-256
34830481-5	2021	First, nerinetide (Phase 3) and AVLX-144 (Phase 1) were designed to interfere with the coupling of the ternary complex formed by PSD-95 with GluN2B subunits of the N-methyl-D-aspartate type of glutamate receptors (NMDARs) and neuronal nitric oxide synthase (nNOS).	avlx-144	32-40	nitric oxide synthase 1, neuronal	Mus musculus	258-262
34506836-3	2021	In addition to NO, neuronal NOS (nNOS) produces H2O2, which contributes to vasodilation.	Hydrogen Peroxide	48-52	nitric oxide synthase 1, neuronal	Mus musculus	19-31
34506836-3	2021	In addition to NO, neuronal NOS (nNOS) produces H2O2, which contributes to vasodilation.	Hydrogen Peroxide	48-52	nitric oxide synthase 1, neuronal	Mus musculus	33-37
34506836-5	2021	In the present study, we assessed the possible role of nNOS-derived H2O2 and caveolins on endothelial vasodilation function following beta-AR overstimulation.	Hydrogen Peroxide	68-72	nitric oxide synthase 1, neuronal	Mus musculus	55-59
34506836-9	2021	However, this relaxation was significantly reduced in aortas from ISO compared to VHE when (1) caveolae were disrupted, (2) nNOS was pharmacologically inhibited or genetically suppressed and (3) H2O2 was scavenged.	Isoproterenol	66-69	nitric oxide synthase 1, neuronal	Mus musculus	124-128
34506836-11	2021	Aortas from ISO-treated mice showed increased expression of caveolin-1, nNOS and catalase, while caveolin-3 expression did not change.	Isoproterenol	12-15	nitric oxide synthase 1, neuronal	Mus musculus	72-76
34506836-12	2021	SIGNIFICANCE: The results suggest a role of caveolin-1 and the nNOS/H2O2 vasodilatory pathway in endothelium-dependent relaxation following beta-AR overstimulation and reinforce the protective role of nNOS in cardiovascular diseases associated with high adrenergic tone.	Hydrogen Peroxide	68-72	nitric oxide synthase 1, neuronal	Mus musculus	63-67
34310708-1	2021	Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor/uncoupler inducing vascular pathology.	N,N-dimethylarginine	29-33	nitric oxide synthase 1, neuronal	Mus musculus	52-73
34768842-5	2021	Pretreatment with L-NAME, which inhibits nitrix oxide synthases (NOS), decreased ACh-mediated vasorelaxation, whereby differences in vasorelaxation between groups disappeared.	NG-Nitroarginine Methyl Ester	18-24	nitric oxide synthase 1, neuronal	Mus musculus	41-63
34545607-11	2022	Also, the expression of nNOS protein in PTZ treated group was reversed by sumatriptan (P<0.01).	Pentylenetetrazole	40-43	nitric oxide synthase 1, neuronal	Mus musculus	24-28
34375928-4	2021	We induced obesity, impaired glucose tolerance, and cardiac hypertrophy with fibrosis, fat accumulation, and diastolic dysfunction in wild-type mice with a high-fat diet (HFD) and the nitric oxide synthase (NOS) inhibitor l-NAME for 16 weeks.	NG-Nitroarginine Methyl Ester	222-228	nitric oxide synthase 1, neuronal	Mus musculus	184-205
34665521-9	2021	Moreover, blocking aldosterone action with in vivo spironolactone treatment resulted in lower Kir 4.1 abundance and greater plasma K+ in the CDNOS1KO mice compared to controls.	Aldosterone	19-30	nitric oxide synthase 1, neuronal	Mus musculus	141-147
34665521-9	2021	Moreover, blocking aldosterone action with in vivo spironolactone treatment resulted in lower Kir 4.1 abundance and greater plasma K+ in the CDNOS1KO mice compared to controls.	Spironolactone	51-65	nitric oxide synthase 1, neuronal	Mus musculus	141-147
34827560-1	2021	In several systems, hydroxyurea has been shown to trigger nitric oxide (NO) release or activation of NO synthase (NOS).	Hydroxyurea	20-31	nitric oxide synthase 1, neuronal	Mus musculus	101-112
34437905-5	2021	A single injection with kisspeptin (Kp-10) or SNAP/BAY, a nitric oxide donor, significantly increased lordosis, whereas the nNOS inhibitor l-NAME decreased it.	NG-Nitroarginine Methyl Ester	139-145	nitric oxide synthase 1, neuronal	Mus musculus	124-128
34720852-3	2021	Using calcium photometry, we show that NOS1 neurons in MnPO/MPO are predominantly NREM and REM active, especially at the boundary of wake to NREM transitions, and in the later parts of REM bouts, with lower activity during wakefulness.	Calcium	6-13	nitric oxide synthase 1, neuronal	Mus musculus	39-43
34720852-4	2021	In addition to releasing nitric oxide, NOS1 neurons in MnPO/MPO can release GABA, glutamate and peptides.	Nitric Oxide	25-37	nitric oxide synthase 1, neuronal	Mus musculus	39-43
34720852-4	2021	In addition to releasing nitric oxide, NOS1 neurons in MnPO/MPO can release GABA, glutamate and peptides.	gamma-Aminobutyric Acid	76-80	nitric oxide synthase 1, neuronal	Mus musculus	39-43
34720852-4	2021	In addition to releasing nitric oxide, NOS1 neurons in MnPO/MPO can release GABA, glutamate and peptides.	Glutamic Acid	82-91	nitric oxide synthase 1, neuronal	Mus musculus	39-43
34720852-4	2021	In addition to releasing nitric oxide, NOS1 neurons in MnPO/MPO can release GABA, glutamate and peptides.	Peptides	96-104	nitric oxide synthase 1, neuronal	Mus musculus	39-43
34646422-11	2021	Furthermore, BRL treatment increased the neuronal NOS (nNOS) expression in cardiac hypertrophy.	brl	13-16	nitric oxide synthase 1, neuronal	Mus musculus	41-53
34646422-11	2021	Furthermore, BRL treatment increased the neuronal NOS (nNOS) expression in cardiac hypertrophy.	brl	13-16	nitric oxide synthase 1, neuronal	Mus musculus	55-59
34631224-10	2021	Western blotting of peri-infarct tissue detected increased expressions of VEGF, Ang-1 and reduced nNOS level in NBP-treated mice.	3-n-butylphthalide	112-115	nitric oxide synthase 1, neuronal	Mus musculus	98-102
34658750-2	2021	Nitric oxide (NO) is a major inhibitory neurotransmitter in the gut and blockade of nitric oxide synthase (NOS; responsible for NO synthesis) increases colonic motility in male mice ex vivo.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	84-105
34545607-11	2022	Also, the expression of nNOS protein in PTZ treated group was reversed by sumatriptan (P<0.01).	Sumatriptan	74-85	nitric oxide synthase 1, neuronal	Mus musculus	24-28
34630123-9	2021	Yeokwisan (400 mg/kg) significantly tempered the loperamide-induced alterations in the c-kit and nNOS levels (p < 0.01) as well as the expression of contraction- and ghrelin-related genes, such as 5-HT4 receptor (5-HT4R), anoctamin-1 (ANO1), ryanodine receptor 3 (RYR3) and smooth muscle myosin light chain kinase (smMLCK), in the stomach, but not in the small intestine.	Loperamide	49-59	nitric oxide synthase 1, neuronal	Mus musculus	97-101
34502247-1	2021	Previously, we showed that a nitric oxide synthase (NOS) inhibitor, compound T1023, induces transient hypoxia and prevents acute radiation syndrome (ARS) in mice.	T1023	77-82	nitric oxide synthase 1, neuronal	Mus musculus	29-50
34283253-11	2021	Protein expressions of p-Tau, p-ERK, pGSK3, iNOS, nNOS, PARP, Cytochrome c, caspase 3, and GluN2A were increased in the parietal cortex of STZ mice and significantly counteracted in M200 mice.	Streptozocin	139-142	nitric oxide synthase 1, neuronal	Mus musculus	50-54
34295228-8	2021	Finally, subthreshold dosage of YG combined with 7-nitroindazole (nNOS inhibitor) induced the antidepressant-like effects both in female and in male mice, while the single use of YG or 7-NI did not display any effect.	tyrosylglycine	32-34	nitric oxide synthase 1, neuronal	Mus musculus	66-70
34439529-7	2021	Although this stimulatory effect of 1,3-diCQA was not significantly affected by treatment with estrogen receptor agonist or antagonist, it was inhibited by 7-NI, an nNOS inhibitor.	1,3-dicaffeoylquinic acid	36-45	nitric oxide synthase 1, neuronal	Mus musculus	165-169
34439529-7	2021	Although this stimulatory effect of 1,3-diCQA was not significantly affected by treatment with estrogen receptor agonist or antagonist, it was inhibited by 7-NI, an nNOS inhibitor.	7-nitroindazole	156-160	nitric oxide synthase 1, neuronal	Mus musculus	165-169
34439529-9	2021	Our results suggest that 1,3-diCQA regulates nNOS in an estrogen recepters-independent manner to increase NO production in OVX mice.	1,3-dicaffeoylquinic acid	25-34	nitric oxide synthase 1, neuronal	Mus musculus	45-49
34325488-3	2021	In this study, we evaluated the possibility that the regulation by STEx of brain-derived neurotrophic factor (BDNF) and neuronal nitric oxide synthase (nNOS, encoded by NOS1), which are important molecules for anxiety regulation, might involve mechanisms of epigenetic modification, such as DNA methylation.	stex	67-71	nitric oxide synthase 1, neuronal	Mus musculus	169-173
34440315-1	2021	Hydroxyurea (HU) causes nitric oxide (NO) bioactivation, acting as both a NO donor and a stimulator of NO synthase (NOS).	Nitric Oxide	24-36	nitric oxide synthase 1, neuronal	Mus musculus	103-114
34295228-2	2021	This study aimed to investigate the sex difference mediated by calcium/calmodulin-dependent protein kinase II (CaMKII)-neuronal nitric oxide synthase (nNOS) signaling involved in the antidepressant-like effect of YG in mice.	Nitric Oxide	128-140	nitric oxide synthase 1, neuronal	Mus musculus	151-155
34295228-2	2021	This study aimed to investigate the sex difference mediated by calcium/calmodulin-dependent protein kinase II (CaMKII)-neuronal nitric oxide synthase (nNOS) signaling involved in the antidepressant-like effect of YG in mice.	tyrosylglycine	213-215	nitric oxide synthase 1, neuronal	Mus musculus	151-155
34295228-8	2021	Finally, subthreshold dosage of YG combined with 7-nitroindazole (nNOS inhibitor) induced the antidepressant-like effects both in female and in male mice, while the single use of YG or 7-NI did not display any effect.	7-nitroindazole	49-64	nitric oxide synthase 1, neuronal	Mus musculus	66-70
34295228-11	2021	The study revealed that chronic treatment with a subthreshold dose of YG also produced antidepressant-like effects in female mice, and these effects depended on the regulation of the CaMKII-nNOS signaling pathway.	tyrosylglycine	70-72	nitric oxide synthase 1, neuronal	Mus musculus	190-194
34295228-7	2021	Moreover, CUS significantly decreased the expression of nNOS and CaMKII, and both YG and ES could enhance the expression in the hippocampus of female mice, which was opposite to that in male mice, while endothelial nitric oxide synthase expression was not affected by stress or drug treatment neither in male mice nor in female mice.	cus	10-13	nitric oxide synthase 1, neuronal	Mus musculus	56-60
33151167-14	2021	In addition, tryptanthrin also suppressed the expression levels of NOS1, COX-2 and NF-kappaB in mouse tumor tissues, and regulated those of IL-2, IL-10 and TNF-alpha in the serum of tumor cells-transplanted mice.	tryptanthrine	13-25	nitric oxide synthase 1, neuronal	Mus musculus	67-71
35622265-11	2022	Also, MPTP-induced enhanced activation of Glial fibrillary acidic protein (GFAP) and neuronal nitric oxide synthase (nNOS) in the nigrostriatal pathway, which are the markers of inflammatory stress, were found to be ameliorated on GME treatment.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	6-10	nitric oxide synthase 1, neuronal	Mus musculus	85-115
35622265-11	2022	Also, MPTP-induced enhanced activation of Glial fibrillary acidic protein (GFAP) and neuronal nitric oxide synthase (nNOS) in the nigrostriatal pathway, which are the markers of inflammatory stress, were found to be ameliorated on GME treatment.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	6-10	nitric oxide synthase 1, neuronal	Mus musculus	117-121
35622265-11	2022	Also, MPTP-induced enhanced activation of Glial fibrillary acidic protein (GFAP) and neuronal nitric oxide synthase (nNOS) in the nigrostriatal pathway, which are the markers of inflammatory stress, were found to be ameliorated on GME treatment.	gme	231-234	nitric oxide synthase 1, neuronal	Mus musculus	85-115
35622265-11	2022	Also, MPTP-induced enhanced activation of Glial fibrillary acidic protein (GFAP) and neuronal nitric oxide synthase (nNOS) in the nigrostriatal pathway, which are the markers of inflammatory stress, were found to be ameliorated on GME treatment.	gme	231-234	nitric oxide synthase 1, neuronal	Mus musculus	117-121
35524664-10	2022	CONCLUSION- In molecular docking assay, which investigated potential targets, THL presented sat-isfactory energy values for: nNOs, SGC, IL-6, 5-HT1A, NMDAr, and D1.	Orlistat	78-81	nitric oxide synthase 1, neuronal	Mus musculus	125-129
35242008-2	2022	Cerebral ischemia triggers a series of complex harmful events, including excitotoxicity, inflammation and cell death, as well as increased nitric oxide production through the activation of nitric oxide synthase (NOS).	Nitric Oxide	139-151	nitric oxide synthase 1, neuronal	Mus musculus	189-210
35006609-8	2022	In addition, treating primary BG isolated from WT mice with the selective nNOS inhibitor 7N decreased the membrane expression of GLAST and influx of Ca2+ /Na+ , while treating nNOS-/- BG with SNAP increased the membrane expression of GLAST and Ca2+ /Na+ influx.	O(6)-benzylguanine	30-32	nitric oxide synthase 1, neuronal	Mus musculus	74-78
35006609-10	2022	Together, these results reveal a novel role for nNOS/NO signaling in BG development, regulated by a PKG-mediated mechanism.	O(6)-benzylguanine	69-71	nitric oxide synthase 1, neuronal	Mus musculus	48-52
35328344-4	2022	In C2C12 cells, but not in HeLa, Grp94 co-immunoprecipitated with non-client proteins, such as nNOS, SERCA2 and PMCA, which co-fractionated by sucrose gradient centrifugation in a distinct, medium density, ER vesicular compartment.	Sucrose	143-150	nitric oxide synthase 1, neuronal	Mus musculus	95-99
35328344-5	2022	Active nNOS was also required for Grp94-induced cytoprotection, since its inhibition by L-NNA disrupted the co-immunoprecipitation and co-fractionation of Grp94 with nNOS and SERCA2, and increased apoptosis.	Nitroarginine	88-93	nitric oxide synthase 1, neuronal	Mus musculus	7-11
35328344-5	2022	Active nNOS was also required for Grp94-induced cytoprotection, since its inhibition by L-NNA disrupted the co-immunoprecipitation and co-fractionation of Grp94 with nNOS and SERCA2, and increased apoptosis.	Nitroarginine	88-93	nitric oxide synthase 1, neuronal	Mus musculus	166-170
35084215-7	2022	To further demonstrate that loss of Nrf2 leads to inflammation, oxidative stress and reduces nNOS mediated gastric function, we have used streptozotocin (STZ)-induced diabetic and Nrf2 null female mice.	Streptozocin	154-157	nitric oxide synthase 1, neuronal	Mus musculus	93-97
35084215-9	2022	Supplementation of CNM normalized diabetes-induced altered gastric antrum protein expression of (1) p-AKT/p-p38MAPK/p-GSK-3beta, (2) BH4 (cofactor of nNOS) biosynthesis enzyme GCH-1, (3) nNOSalpha (4) TLR4, NFkappaB, and (5) inflammatory cytokines (TNF alpha, IL-1beta, IL-6).	sapropterin	133-136	nitric oxide synthase 1, neuronal	Mus musculus	150-154
35174211-8	2021	Increased superoxide formation in the brain was mirrored by a downregulation of neuronal nitric oxide synthase (Nos3) and transcription factor Foxo3 genes, whereas Vcam1 mRNA, a marker for inflammation was upregulated in all noise exposure groups.	Superoxides	10-20	nitric oxide synthase 1, neuronal	Mus musculus	80-110
35105915-8	2022	Using a human melanoma xenograft mouse model, the in vivo studies revealed that IFN-gamma increased tumor growth compared to control, which was inhibited by the co-administration of nNOS inhibitor MAC-3-190.	mac-3-190	197-206	nitric oxide synthase 1, neuronal	Mus musculus	182-186
35434279-12	2022	Finally, vitamin D supplementation for 10 weeks to AVD-deficient mice restored nNOS immunoreactivity to that seen in in control mice.	Vitamin D	9-18	nitric oxide synthase 1, neuronal	Mus musculus	79-83
34297798-0	2022	Disrupting the Interaction of nNOS with CAPON Prevents the Reinstatement of Morphine Conditioned Place Preference.	Morphine	76-84	nitric oxide synthase 1, neuronal	Mus musculus	30-34
34297798-5	2022	We found that morphine conditioned place preference (CPP) extinction training increased the association of nitric oxide synthase (nNOS) with its carboxy-terminal PDZ ligand (CAPON) in the dorsal hippocampus (dHPC) significantly and blocking the morphine-induced nNOS-CAPON association using Tat-CAPON-12C during and after extinction training reversed morphine-induced hippocampal neuroplasticity defect and prevented the reinstatement and spontaneous recovery of morphine CPP.	Morphine	14-22	nitric oxide synthase 1, neuronal	Mus musculus	130-134
34297798-5	2022	We found that morphine conditioned place preference (CPP) extinction training increased the association of nitric oxide synthase (nNOS) with its carboxy-terminal PDZ ligand (CAPON) in the dorsal hippocampus (dHPC) significantly and blocking the morphine-induced nNOS-CAPON association using Tat-CAPON-12C during and after extinction training reversed morphine-induced hippocampal neuroplasticity defect and prevented the reinstatement and spontaneous recovery of morphine CPP.	Morphine	14-22	nitric oxide synthase 1, neuronal	Mus musculus	262-266
34297798-5	2022	We found that morphine conditioned place preference (CPP) extinction training increased the association of nitric oxide synthase (nNOS) with its carboxy-terminal PDZ ligand (CAPON) in the dorsal hippocampus (dHPC) significantly and blocking the morphine-induced nNOS-CAPON association using Tat-CAPON-12C during and after extinction training reversed morphine-induced hippocampal neuroplasticity defect and prevented the reinstatement and spontaneous recovery of morphine CPP.	Nitric Oxide	107-119	nitric oxide synthase 1, neuronal	Mus musculus	130-134
35347247-11	2022	We further revealed that the protective effect of NE and DA against glutamate-induced oxidative cytotoxicity was mediated through inhibition of PDI-catalyzed dimerization of the neuronal nitric oxide synthase.	Dopamine	57-59	nitric oxide synthase 1, neuronal	Mus musculus	178-208
34297798-5	2022	We found that morphine conditioned place preference (CPP) extinction training increased the association of nitric oxide synthase (nNOS) with its carboxy-terminal PDZ ligand (CAPON) in the dorsal hippocampus (dHPC) significantly and blocking the morphine-induced nNOS-CAPON association using Tat-CAPON-12C during and after extinction training reversed morphine-induced hippocampal neuroplasticity defect and prevented the reinstatement and spontaneous recovery of morphine CPP.	Nitric Oxide	107-119	nitric oxide synthase 1, neuronal	Mus musculus	262-266
34297798-5	2022	We found that morphine conditioned place preference (CPP) extinction training increased the association of nitric oxide synthase (nNOS) with its carboxy-terminal PDZ ligand (CAPON) in the dorsal hippocampus (dHPC) significantly and blocking the morphine-induced nNOS-CAPON association using Tat-CAPON-12C during and after extinction training reversed morphine-induced hippocampal neuroplasticity defect and prevented the reinstatement and spontaneous recovery of morphine CPP.	Morphine	245-253	nitric oxide synthase 1, neuronal	Mus musculus	130-134
35347247-11	2022	We further revealed that the protective effect of NE and DA against glutamate-induced oxidative cytotoxicity was mediated through inhibition of PDI-catalyzed dimerization of the neuronal nitric oxide synthase.	Glutamic Acid	68-77	nitric oxide synthase 1, neuronal	Mus musculus	178-208
34297798-5	2022	We found that morphine conditioned place preference (CPP) extinction training increased the association of nitric oxide synthase (nNOS) with its carboxy-terminal PDZ ligand (CAPON) in the dorsal hippocampus (dHPC) significantly and blocking the morphine-induced nNOS-CAPON association using Tat-CAPON-12C during and after extinction training reversed morphine-induced hippocampal neuroplasticity defect and prevented the reinstatement and spontaneous recovery of morphine CPP.	Morphine	351-359	nitric oxide synthase 1, neuronal	Mus musculus	130-134
33342284-2	2021	Hepatic mitochondrial damage mediated by neuronal nitric oxide synthase- (nNOS) induced liver protein tyrosine nitration plays a critical role in the pathophysiology of APAP hepatotoxicity.	Acetaminophen	169-173	nitric oxide synthase 1, neuronal	Mus musculus	41-71
34297798-6	2022	Moreover, in the hippocampal selective ERK2 knock-out or nNOS knockout mice, the effect of Tat-CAPON-12C on the reinstatement of morphine CPP and hippocampal neuroplasticity disappeared, suggesting ERK2 is necessary for the effects of Tat-CAPON-12C.	Morphine	129-137	nitric oxide synthase 1, neuronal	Mus musculus	57-61
34297798-7	2022	Together, our findings suggest that nNOS-CAPON interaction in the dHPC may affect the consolidation of morphine CPP extinction and dissociating nNOS-CAPON prevents the reinstatement and spontaneous recovery of morphine CPP, possibly through ERK2-mediated neuroplasticity and extinction memory consolidation, offering a new target to prevent the reinstatement of drug abuse.	1,2-dihexadecyl-sn-glycero-3-phosphocholine	66-70	nitric oxide synthase 1, neuronal	Mus musculus	36-40
34297798-7	2022	Together, our findings suggest that nNOS-CAPON interaction in the dHPC may affect the consolidation of morphine CPP extinction and dissociating nNOS-CAPON prevents the reinstatement and spontaneous recovery of morphine CPP, possibly through ERK2-mediated neuroplasticity and extinction memory consolidation, offering a new target to prevent the reinstatement of drug abuse.	Morphine	103-111	nitric oxide synthase 1, neuronal	Mus musculus	36-40
34297798-7	2022	Together, our findings suggest that nNOS-CAPON interaction in the dHPC may affect the consolidation of morphine CPP extinction and dissociating nNOS-CAPON prevents the reinstatement and spontaneous recovery of morphine CPP, possibly through ERK2-mediated neuroplasticity and extinction memory consolidation, offering a new target to prevent the reinstatement of drug abuse.	Morphine	210-218	nitric oxide synthase 1, neuronal	Mus musculus	144-148
33831408-3	2021	The present study was designed to quantify the number of nNOS-containing hilar interneurons using stereology in pilocapine- and kainic acid (KA)-exposed transgenic adult mice that expressed GFP under the nNOS promoter.	pilocapine	112-122	nitric oxide synthase 1, neuronal	Mus musculus	57-61
33405022-7	2021	In both NP and P groups, progesterone significantly attenuated LPS-induced increase of nNOS and NF-kB, however with no effect on serum IL-6.	Progesterone	25-37	nitric oxide synthase 1, neuronal	Mus musculus	87-91
33722737-5	2021	Therefore, the aim of this study was to evaluate the effect of TCS on the expression of PPARgamma, NF-kappaB, nNOS, iNOS, and eNOS in mouse neocortical neurons.	Triclosan	63-66	nitric oxide synthase 1, neuronal	Mus musculus	110-114
33722737-9	2021	Moreover, under the influence of TCS, the expression of iNOS was increased and at the same time the expression of nNOS was decreased, which was probably caused by high levels of ROS.	Triclosan	33-36	nitric oxide synthase 1, neuronal	Mus musculus	114-118
33722737-9	2021	Moreover, under the influence of TCS, the expression of iNOS was increased and at the same time the expression of nNOS was decreased, which was probably caused by high levels of ROS.	ros	178-181	nitric oxide synthase 1, neuronal	Mus musculus	114-118
34058234-0	2021	Protective effect of alpha-lipoic acid on bisphenol A-induced learning and memory impairment in developing mice: nNOS and keap1/Nrf2 pathway.	Thioctic Acid	21-38	nitric oxide synthase 1, neuronal	Mus musculus	113-117
34058234-8	2021	ALA altered the protein levels of nNOS and keap1/Nrf2 pathway affected by BPA.	Thioctic Acid	0-3	nitric oxide synthase 1, neuronal	Mus musculus	34-38
34058234-9	2021	Our results suggested that impairments of learning and memory caused by BPA was related to the damage of hippocampal synapses mediated by oxidative stress, and ALA protected learning and memory by reducing the oxidative stress induced by BPA through regulating the nNOS and keap1/Nrf2 pathway.	Thioctic Acid	160-163	nitric oxide synthase 1, neuronal	Mus musculus	265-269
34058234-9	2021	Our results suggested that impairments of learning and memory caused by BPA was related to the damage of hippocampal synapses mediated by oxidative stress, and ALA protected learning and memory by reducing the oxidative stress induced by BPA through regulating the nNOS and keap1/Nrf2 pathway.	bisphenol A	238-241	nitric oxide synthase 1, neuronal	Mus musculus	265-269
33342284-2	2021	Hepatic mitochondrial damage mediated by neuronal nitric oxide synthase- (nNOS) induced liver protein tyrosine nitration plays a critical role in the pathophysiology of APAP hepatotoxicity.	Tyrosine	102-110	nitric oxide synthase 1, neuronal	Mus musculus	41-71
33342284-2	2021	Hepatic mitochondrial damage mediated by neuronal nitric oxide synthase- (nNOS) induced liver protein tyrosine nitration plays a critical role in the pathophysiology of APAP hepatotoxicity.	Tyrosine	102-110	nitric oxide synthase 1, neuronal	Mus musculus	74-78
33915274-6	2021	These effects were inhibited by L-NAME, a non-selective inhibitor of nitric oxide synthase (NOS); were partially inhibited by 7- Nitroindazole, a selective inhibitor of neuronal NOS (nNOS); and were abolished by L-NIL, a selective inhibitor of inducible NOS (iNOS).	L-NIL	212-217	nitric oxide synthase 1, neuronal	Mus musculus	169-181
33915274-6	2021	These effects were inhibited by L-NAME, a non-selective inhibitor of nitric oxide synthase (NOS); were partially inhibited by 7- Nitroindazole, a selective inhibitor of neuronal NOS (nNOS); and were abolished by L-NIL, a selective inhibitor of inducible NOS (iNOS).	L-NIL	212-217	nitric oxide synthase 1, neuronal	Mus musculus	183-187
34297798-5	2022	We found that morphine conditioned place preference (CPP) extinction training increased the association of nitric oxide synthase (nNOS) with its carboxy-terminal PDZ ligand (CAPON) in the dorsal hippocampus (dHPC) significantly and blocking the morphine-induced nNOS-CAPON association using Tat-CAPON-12C during and after extinction training reversed morphine-induced hippocampal neuroplasticity defect and prevented the reinstatement and spontaneous recovery of morphine CPP.	Morphine	463-471	nitric oxide synthase 1, neuronal	Mus musculus	130-134
33962017-0	2021	Alcohol hangover induces nitric oxide metabolism changes by impairing NMDA receptor-PSD95-nNOS pathway.	Alcohols	0-7	nitric oxide synthase 1, neuronal	Mus musculus	90-94
33962017-0	2021	Alcohol hangover induces nitric oxide metabolism changes by impairing NMDA receptor-PSD95-nNOS pathway.	Nitric Oxide	25-37	nitric oxide synthase 1, neuronal	Mus musculus	90-94
33962017-7	2021	A similar patter of response was observed for nNOS activity being decreased both in basal conditions and after glutamate addition.	Glutamic Acid	111-120	nitric oxide synthase 1, neuronal	Mus musculus	46-50
33915274-6	2021	These effects were inhibited by L-NAME, a non-selective inhibitor of nitric oxide synthase (NOS); were partially inhibited by 7- Nitroindazole, a selective inhibitor of neuronal NOS (nNOS); and were abolished by L-NIL, a selective inhibitor of inducible NOS (iNOS).	NG-Nitroarginine Methyl Ester	32-38	nitric oxide synthase 1, neuronal	Mus musculus	69-90
33915274-6	2021	These effects were inhibited by L-NAME, a non-selective inhibitor of nitric oxide synthase (NOS); were partially inhibited by 7- Nitroindazole, a selective inhibitor of neuronal NOS (nNOS); and were abolished by L-NIL, a selective inhibitor of inducible NOS (iNOS).	NG-Nitroarginine Methyl Ester	32-38	nitric oxide synthase 1, neuronal	Mus musculus	169-181
33915274-6	2021	These effects were inhibited by L-NAME, a non-selective inhibitor of nitric oxide synthase (NOS); were partially inhibited by 7- Nitroindazole, a selective inhibitor of neuronal NOS (nNOS); and were abolished by L-NIL, a selective inhibitor of inducible NOS (iNOS).	NG-Nitroarginine Methyl Ester	32-38	nitric oxide synthase 1, neuronal	Mus musculus	183-187
33915274-6	2021	These effects were inhibited by L-NAME, a non-selective inhibitor of nitric oxide synthase (NOS); were partially inhibited by 7- Nitroindazole, a selective inhibitor of neuronal NOS (nNOS); and were abolished by L-NIL, a selective inhibitor of inducible NOS (iNOS).	7-nitroindazole	126-142	nitric oxide synthase 1, neuronal	Mus musculus	169-181
33915274-6	2021	These effects were inhibited by L-NAME, a non-selective inhibitor of nitric oxide synthase (NOS); were partially inhibited by 7- Nitroindazole, a selective inhibitor of neuronal NOS (nNOS); and were abolished by L-NIL, a selective inhibitor of inducible NOS (iNOS).	7-nitroindazole	126-142	nitric oxide synthase 1, neuronal	Mus musculus	183-187
33876374-0	2021	Declining Levels of Specialized Synaptic Surface Proteins in nNOS-Expressing Interneurons in Mice Treated Prenatally with Valproic Acid.	Valproic Acid	122-135	nitric oxide synthase 1, neuronal	Mus musculus	61-65
33876374-3	2021	We have recently shown that neuronal nitric oxide synthase (nNOS) expression was reduced in the basolateral amygdala (BLA) of mice following postnatal valproic acid (VPA) exposure.	Valproic Acid	151-164	nitric oxide synthase 1, neuronal	Mus musculus	28-58
33876374-3	2021	We have recently shown that neuronal nitric oxide synthase (nNOS) expression was reduced in the basolateral amygdala (BLA) of mice following postnatal valproic acid (VPA) exposure.	Valproic Acid	151-164	nitric oxide synthase 1, neuronal	Mus musculus	60-64
33876374-3	2021	We have recently shown that neuronal nitric oxide synthase (nNOS) expression was reduced in the basolateral amygdala (BLA) of mice following postnatal valproic acid (VPA) exposure.	Valproic Acid	166-169	nitric oxide synthase 1, neuronal	Mus musculus	28-58
33876374-3	2021	We have recently shown that neuronal nitric oxide synthase (nNOS) expression was reduced in the basolateral amygdala (BLA) of mice following postnatal valproic acid (VPA) exposure.	Valproic Acid	166-169	nitric oxide synthase 1, neuronal	Mus musculus	60-64
33876374-4	2021	In the current study, we utilized a label-free proteomics approach to identify and quantify surface protein expression in nNOS-positive interneurons between VPA-treated and control mice.	Valproic Acid	157-160	nitric oxide synthase 1, neuronal	Mus musculus	122-126
33342284-2	2021	Hepatic mitochondrial damage mediated by neuronal nitric oxide synthase- (nNOS) induced liver protein tyrosine nitration plays a critical role in the pathophysiology of APAP hepatotoxicity.	Acetaminophen	169-173	nitric oxide synthase 1, neuronal	Mus musculus	74-78
33342284-11	2021	Notably, 80 mg/kg glycyrrhizin inhibited hepatic nNOS activity and its mRNA and protein expression levels by 16.9, 14.9, and 28.3%, respectively.	Glycyrrhizic Acid	18-30	nitric oxide synthase 1, neuronal	Mus musculus	49-53
33342284-14	2021	The present study indicates that post-treatment with glycyrrhizin can dose-dependently attenuate hepatic mitochondrial damage and inhibit the up-regulation of hepatic nNOS induced by APAP.	Glycyrrhizic Acid	53-65	nitric oxide synthase 1, neuronal	Mus musculus	167-171
33342284-14	2021	The present study indicates that post-treatment with glycyrrhizin can dose-dependently attenuate hepatic mitochondrial damage and inhibit the up-regulation of hepatic nNOS induced by APAP.	Acetaminophen	183-187	nitric oxide synthase 1, neuronal	Mus musculus	167-171
32661768-8	2021	nNOS inhibitor (ARL 17477)-treated stroke mice exhibited a significant functional improvement in speed at post-stroke day 10, when compared to stroke mice receiving vehicle (saline) only.	Sodium Chloride	174-180	nitric oxide synthase 1, neuronal	Mus musculus	0-4
33876374-6	2021	Our proteomics data revealed differentially expressed surface proteins in nNOS interneurons, e.g. Narp, AMPA-type glutamate (AMPA) receptor subunit GluA4 and Protein kinase C gamma (PKCgamma), which were validated by Western blotting in mice treated with VPA.	Valproic Acid	255-258	nitric oxide synthase 1, neuronal	Mus musculus	74-78
33859186-7	2021	These findings indicated that S-nitrosylation at Cys351 of PFKM by NOS1 contributes to the metabolic reprogramming of ovarian cancer cells, highlighting a critical role of endogenous nitrogen oxide on metabolism regulations in tumor progression.	Nitrogen	183-191	nitric oxide synthase 1, neuronal	Mus musculus	67-71
33846426-6	2021	6-OHDA lesioned mice had significantly fewer Hu+ neurons/ganglion (P < 0.02) and a reduced proportion of nNOS+ neurons in colon (P < 0.001).	Oxidopamine	0-6	nitric oxide synthase 1, neuronal	Mus musculus	105-109
33580591-7	2021	Mdx mice overexpressing dystrophins that localize neuronal nitric oxide synthase, restored dihydrobiopterin + tetrahydrobiopterin in mdx mice to wildtype levels while utrophin overexpression did not.	7,8-dihydrobiopterin	91-107	nitric oxide synthase 1, neuronal	Mus musculus	50-80
33580591-7	2021	Mdx mice overexpressing dystrophins that localize neuronal nitric oxide synthase, restored dihydrobiopterin + tetrahydrobiopterin in mdx mice to wildtype levels while utrophin overexpression did not.	sapropterin	110-129	nitric oxide synthase 1, neuronal	Mus musculus	50-80
33748496-11	2021	Therefore, pre- and post-treatment with pGz improves LPS-induced cardiomyocyte dysfunction, decreases iNOS expression, and increases cytoprotective eNOS and nNOS, with decreased pro-inflammatory response.	Methyl 2-O-[(S)-(Benzyloxy)(Hydroxy)phosphoryl]-3-Deoxy-3-{[(4-Methylphenyl)carbonyl]amino}-1-Thio-Beta-D-Galactopyranoside	40-43	nitric oxide synthase 1, neuronal	Mus musculus	157-161
33500273-7	2021	We demonstrate that nNOS-implicated mechanisms in NAc shell (NAcSh), including increased cell number, increased protein expression levels and increased specific enzyme activity, contribute the susceptibility to social defeat and the following depression-like behaviors.	nacsh	61-66	nitric oxide synthase 1, neuronal	Mus musculus	20-24
33500273-14	2021	Moreover, we discover the downstream mechanism of NAcSh nNOS in mediating the susceptibility is NO and S-nitrosylation of CDK5.	nacsh	50-55	nitric oxide synthase 1, neuronal	Mus musculus	56-60
33500273-15	2021	Thus, NAcSh nNOS mediates susceptibility to social defeat stress through CDK5 is a potential mechanism for depression, which may interpret how the brain transduces social stress exposure into depression.	nacsh	6-11	nitric oxide synthase 1, neuronal	Mus musculus	12-16
33494625-0	2021	BH4 Increases nNOS Activity and Preserves Left Ventricular Function in Diabetes.	sapropterin	0-3	nitric oxide synthase 1, neuronal	Mus musculus	14-18
33494625-2	2021	Oxidation of the nitric oxide synthase (NOS) co-factor tetrahydrobiopterin (BH4) and dysfunctional NOS activity have been implicated in the pathogenesis of the diabetic vascular and cardiomyopathic phenotype.Objective: Using mice models and human myocardial samples, we evaluated whether and by which mechanism increasing myocardial BH4 availability prevented or reversed LV dysfunction induced by diabetes.	sapropterin	55-74	nitric oxide synthase 1, neuronal	Mus musculus	17-38
33494625-2	2021	Oxidation of the nitric oxide synthase (NOS) co-factor tetrahydrobiopterin (BH4) and dysfunctional NOS activity have been implicated in the pathogenesis of the diabetic vascular and cardiomyopathic phenotype.Objective: Using mice models and human myocardial samples, we evaluated whether and by which mechanism increasing myocardial BH4 availability prevented or reversed LV dysfunction induced by diabetes.	sapropterin	76-79	nitric oxide synthase 1, neuronal	Mus musculus	17-38
33494625-2	2021	Oxidation of the nitric oxide synthase (NOS) co-factor tetrahydrobiopterin (BH4) and dysfunctional NOS activity have been implicated in the pathogenesis of the diabetic vascular and cardiomyopathic phenotype.Objective: Using mice models and human myocardial samples, we evaluated whether and by which mechanism increasing myocardial BH4 availability prevented or reversed LV dysfunction induced by diabetes.	sapropterin	333-336	nitric oxide synthase 1, neuronal	Mus musculus	17-38
33494625-5	2021	The protective effect of BH4 was abolished by CRISPR/Cas9-mediated knockout of neuronal NOS (nNOS) in mGCH1-Tg.	sapropterin	25-28	nitric oxide synthase 1, neuronal	Mus musculus	79-91
33494625-5	2021	The protective effect of BH4 was abolished by CRISPR/Cas9-mediated knockout of neuronal NOS (nNOS) in mGCH1-Tg.	sapropterin	25-28	nitric oxide synthase 1, neuronal	Mus musculus	93-97
33494625-8	2021	Conclusions: We uncovered a novel mechanism whereby myocardial BH4 prevents and reverses LV diastolic and systolic dysfunction associated with diabetes via a nNOS-mediated increase in non-insulin dependent myocardial glucose uptake and utilization.	sapropterin	63-66	nitric oxide synthase 1, neuronal	Mus musculus	158-162
33653689-5	2021	The action of nNOS on the beat frequency is mediated by guanylate cyclase; both NO donors and cGMP can augment fluid flow in the trachea and rescue the deficient flow in nNOS mutants.	Cyclic GMP	94-98	nitric oxide synthase 1, neuronal	Mus musculus	14-18
33653689-5	2021	The action of nNOS on the beat frequency is mediated by guanylate cyclase; both NO donors and cGMP can augment fluid flow in the trachea and rescue the deficient flow in nNOS mutants.	Cyclic GMP	94-98	nitric oxide synthase 1, neuronal	Mus musculus	170-174
33434144-2	2021	Previously, we had reported that NOS1AP enhanced hepatic insulin sensitivity through its PZD-binding domain, which suggested that nNOS might mediate the effect of NOS1AP.	3,6-bis(5-chloro-2-piperidyl)-2,5-piperazinedione	89-92	nitric oxide synthase 1, neuronal	Mus musculus	130-134
33434144-7	2021	The overexpression of nNOS in the liver of high-fat diet-induced obese mice exacerbated glucose intolerance, enhanced intrahepatic lipid accumulation, decreased glycogen storage, and blunted insulin-induced phosphorylation of IRbeta and Akt in the liver.	Glucose	88-95	nitric oxide synthase 1, neuronal	Mus musculus	22-26
33434144-7	2021	The overexpression of nNOS in the liver of high-fat diet-induced obese mice exacerbated glucose intolerance, enhanced intrahepatic lipid accumulation, decreased glycogen storage, and blunted insulin-induced phosphorylation of IRbeta and Akt in the liver.	Glycogen	161-169	nitric oxide synthase 1, neuronal	Mus musculus	22-26
33434144-9	2021	In contrast, treatment with Nomega-propyl-L-arginine (L-NPA), a selective nNOS inhibitor, improved glucose tolerance and upregulated insulin-induced phosphorylation of IRbeta and Akt in the liver of ob/ob mice.	N(omega)-propylarginine	28-52	nitric oxide synthase 1, neuronal	Mus musculus	74-78
33434144-9	2021	In contrast, treatment with Nomega-propyl-L-arginine (L-NPA), a selective nNOS inhibitor, improved glucose tolerance and upregulated insulin-induced phosphorylation of IRbeta and Akt in the liver of ob/ob mice.	l-npa	54-59	nitric oxide synthase 1, neuronal	Mus musculus	74-78
33434144-9	2021	In contrast, treatment with Nomega-propyl-L-arginine (L-NPA), a selective nNOS inhibitor, improved glucose tolerance and upregulated insulin-induced phosphorylation of IRbeta and Akt in the liver of ob/ob mice.	Glucose	99-106	nitric oxide synthase 1, neuronal	Mus musculus	74-78
33562035-5	2021	2-methoxyestradiol (2-ME), metabolite of 17beta-estradiol (E2) and potential anticancer agent, was demonstrated to inhibit cell growth of hippocampal HT22 cells by means of nitric oxide synthase (NOS) production and oxidative stress at both pharmacologically and also physiologically relevant concentrations.	2-Methoxyestradiol	0-18	nitric oxide synthase 1, neuronal	Mus musculus	173-194
33562035-5	2021	2-methoxyestradiol (2-ME), metabolite of 17beta-estradiol (E2) and potential anticancer agent, was demonstrated to inhibit cell growth of hippocampal HT22 cells by means of nitric oxide synthase (NOS) production and oxidative stress at both pharmacologically and also physiologically relevant concentrations.	2-Methoxyestradiol	20-24	nitric oxide synthase 1, neuronal	Mus musculus	173-194
33562035-5	2021	2-methoxyestradiol (2-ME), metabolite of 17beta-estradiol (E2) and potential anticancer agent, was demonstrated to inhibit cell growth of hippocampal HT22 cells by means of nitric oxide synthase (NOS) production and oxidative stress at both pharmacologically and also physiologically relevant concentrations.	Estradiol	59-61	nitric oxide synthase 1, neuronal	Mus musculus	173-194
33095056-8	2021	Nitric oxide synthase (NOS) inhibition with Nomega-nitro-l-arginine methyl ester hydrochloride eliminated both sex as well as diet-induced differences in endothelial dysfunction.	L-NAME hydrochloride	44-94	nitric oxide synthase 1, neuronal	Mus musculus	0-21
33533128-10	2021	Ethanol increases the expression of NOX-2 and NGP and decreases the expression of RAG1, NOS1, CD59a, S1PR5, PTPN22, GPR37, and Serpinb1b.	Ethanol	0-7	nitric oxide synthase 1, neuronal	Mus musculus	88-92
33290345-6	2021	The antidepressant-like effect of carbamazepine (40 mg/kg, intraperitoneal) was prevented by pretreatment with L-arginine [substrate for NO synthase (NOS), 750 mg/kg, intraperitoneal], sildenafil (a PDE-5 inhibitor, 5 mg/kg, intraperitoneal) and diazoxide (K channels opener, 10 mg/kg).	Carbamazepine	34-47	nitric oxide synthase 1, neuronal	Mus musculus	137-148
33290345-6	2021	The antidepressant-like effect of carbamazepine (40 mg/kg, intraperitoneal) was prevented by pretreatment with L-arginine [substrate for NO synthase (NOS), 750 mg/kg, intraperitoneal], sildenafil (a PDE-5 inhibitor, 5 mg/kg, intraperitoneal) and diazoxide (K channels opener, 10 mg/kg).	Arginine	111-121	nitric oxide synthase 1, neuronal	Mus musculus	137-148
33290345-6	2021	The antidepressant-like effect of carbamazepine (40 mg/kg, intraperitoneal) was prevented by pretreatment with L-arginine [substrate for NO synthase (NOS), 750 mg/kg, intraperitoneal], sildenafil (a PDE-5 inhibitor, 5 mg/kg, intraperitoneal) and diazoxide (K channels opener, 10 mg/kg).	Sildenafil Citrate	185-195	nitric oxide synthase 1, neuronal	Mus musculus	137-148
33290345-6	2021	The antidepressant-like effect of carbamazepine (40 mg/kg, intraperitoneal) was prevented by pretreatment with L-arginine [substrate for NO synthase (NOS), 750 mg/kg, intraperitoneal], sildenafil (a PDE-5 inhibitor, 5 mg/kg, intraperitoneal) and diazoxide (K channels opener, 10 mg/kg).	Diazoxide	246-255	nitric oxide synthase 1, neuronal	Mus musculus	137-148
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	8-27	nitric oxide synthase 1, neuronal	Mus musculus	180-210
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	8-27	nitric oxide synthase 1, neuronal	Mus musculus	212-216
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	29-32	nitric oxide synthase 1, neuronal	Mus musculus	180-210
33534356-5	2021	Chronic glyceryl trinitrate (GTN, 10 mg/kg) administration led to increased sensitivity to mechanical stimuli, and increased expression of phosphorylated protein kinase A (p-PKA), neuronal nitric oxide synthase (nNOS), and transient receptor potential ankyrin 1 (TRPA1) proteins in trigeminal ganglia.	Nitroglycerin	29-32	nitric oxide synthase 1, neuronal	Mus musculus	212-216
33534356-10	2021	Subsequent challenge with a previously ineffective low-dose GTN (0.1-0.3 mg/kg) revealed latent behavioral sensitization and increased expression of p-PKA, nNOS, and TRPA1 proteins in trigeminal ganglia.	Nitroglycerin	60-63	nitric oxide synthase 1, neuronal	Mus musculus	156-160
32755816-7	2020	The anticonvulsant effect of morphine was inhibited completely by the concomitant administration of NO synthase (NOS) inhibitors including nonspecific NOS inhibitor (L-NAME, 10 mg/kg), inducible NOS inhibitor (aminoguanidine, 50 mg/kg), and neuronal NOS inhibitor (7-nitroindazole (7-NI), 15 mg/kg) for five consecutive days.	Morphine	29-37	nitric oxide synthase 1, neuronal	Mus musculus	100-111
33106031-10	2021	The effects of 12,13-diHOME were absent in NOS1-/- mice and cardiomyocytes.	(+/-)12,13-Dihome	15-27	nitric oxide synthase 1, neuronal	Mus musculus	43-47
33569432-10	2021	Exposure to glyphosate alone or glyphosate plus hard water increased the levels of oxidative stress markers and inflammatory biomarkers, namely, thromboxane A2 (TX-A2), leukotriene B4 (LTB4), prostaglandin E2 (PGE2), nitric oxide synthase (NOS), and nitric oxide (NO).	glyphosate	12-22	nitric oxide synthase 1, neuronal	Mus musculus	217-238
33569432-10	2021	Exposure to glyphosate alone or glyphosate plus hard water increased the levels of oxidative stress markers and inflammatory biomarkers, namely, thromboxane A2 (TX-A2), leukotriene B4 (LTB4), prostaglandin E2 (PGE2), nitric oxide synthase (NOS), and nitric oxide (NO).	glyphosate	32-42	nitric oxide synthase 1, neuronal	Mus musculus	217-238
33569432-10	2021	Exposure to glyphosate alone or glyphosate plus hard water increased the levels of oxidative stress markers and inflammatory biomarkers, namely, thromboxane A2 (TX-A2), leukotriene B4 (LTB4), prostaglandin E2 (PGE2), nitric oxide synthase (NOS), and nitric oxide (NO).	Water	53-58	nitric oxide synthase 1, neuronal	Mus musculus	217-238
32594052-2	2020	ZL006 is shown to reduce over-produced nitric oxide and oxidative stress in ischemic stroke by interrupting the interaction of neuronal nitric oxide synthase and postsynaptic density protein 95.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	0-5	nitric oxide synthase 1, neuronal	Mus musculus	127-157
33238628-7	2020	Cisplatin-treated mice showed mucosal damage, inflammation, IL-1beta and IL-10 increase; decreased number of total neurons, ChAT- and nNOS-immunoreactive (IR) neurons; loss of SOX-10-IR cells and reduced expression of GFAP- and S100beta-glial markers in the myenteric plexus.	Cisplatin	0-9	nitric oxide synthase 1, neuronal	Mus musculus	134-138
33238628-8	2020	[Gly2]GLP-2 co-treatment partially prevented mucosal damage and counteracted the increase in cytokines and the loss of nNOS-IR and SOX-10-IR cells but not that of ChAT-IR neurons.	Glycylglycine	1-5	nitric oxide synthase 1, neuronal	Mus musculus	119-123
33203296-5	2021	The nitric oxide synthase (NOS) inhibitor Nomega-nitro-L-arginine abolished rCBF response to diazoxide suggesting NO was involved in the mediation of vasorelaxation.	Nitroarginine	42-65	nitric oxide synthase 1, neuronal	Mus musculus	4-25
33203296-5	2021	The nitric oxide synthase (NOS) inhibitor Nomega-nitro-L-arginine abolished rCBF response to diazoxide suggesting NO was involved in the mediation of vasorelaxation.	Diazoxide	93-102	nitric oxide synthase 1, neuronal	Mus musculus	4-25
33135877-2	2020	Among them, l-arginine is the substrate for nitric oxide synthases (NOS) to produce nitric oxide (NO), a key signaling molecule and second messenger.	Arginine	12-22	nitric oxide synthase 1, neuronal	Mus musculus	44-66
32663504-8	2020	The stimulation of cardiomyogenesis by ZOX was blunted by the nitric oxide synthase (NOS) inhibitor l-NAME, as well as CBX and NPPB.	NG-Nitroarginine Methyl Ester	100-106	nitric oxide synthase 1, neuronal	Mus musculus	62-83
32755816-7	2020	The anticonvulsant effect of morphine was inhibited completely by the concomitant administration of NO synthase (NOS) inhibitors including nonspecific NOS inhibitor (L-NAME, 10 mg/kg), inducible NOS inhibitor (aminoguanidine, 50 mg/kg), and neuronal NOS inhibitor (7-nitroindazole (7-NI), 15 mg/kg) for five consecutive days.	Morphine	29-37	nitric oxide synthase 1, neuronal	Mus musculus	241-253
32779043-0	2020	Berberine attenuates Abeta-induced neuronal damage through regulating miR-188/NOS1 in Alzheimer"s disease.	Berberine	0-9	nitric oxide synthase 1, neuronal	Mus musculus	78-82
32755816-7	2020	The anticonvulsant effect of morphine was inhibited completely by the concomitant administration of NO synthase (NOS) inhibitors including nonspecific NOS inhibitor (L-NAME, 10 mg/kg), inducible NOS inhibitor (aminoguanidine, 50 mg/kg), and neuronal NOS inhibitor (7-nitroindazole (7-NI), 15 mg/kg) for five consecutive days.	pimagedine	210-224	nitric oxide synthase 1, neuronal	Mus musculus	100-111
32755816-7	2020	The anticonvulsant effect of morphine was inhibited completely by the concomitant administration of NO synthase (NOS) inhibitors including nonspecific NOS inhibitor (L-NAME, 10 mg/kg), inducible NOS inhibitor (aminoguanidine, 50 mg/kg), and neuronal NOS inhibitor (7-nitroindazole (7-NI), 15 mg/kg) for five consecutive days.	7-nitroindazole	265-280	nitric oxide synthase 1, neuronal	Mus musculus	100-111
32755816-7	2020	The anticonvulsant effect of morphine was inhibited completely by the concomitant administration of NO synthase (NOS) inhibitors including nonspecific NOS inhibitor (L-NAME, 10 mg/kg), inducible NOS inhibitor (aminoguanidine, 50 mg/kg), and neuronal NOS inhibitor (7-nitroindazole (7-NI), 15 mg/kg) for five consecutive days.	7-nitroindazole	282-286	nitric oxide synthase 1, neuronal	Mus musculus	100-111
33016877-4	2020	Locomotion drove robust arterial dilation, increases in gamma band power in the local field potential (LFP), and increases calcium signals in pyramidal and neuronal nitric oxide synthase (nNOS)-expressing neurons.	Calcium	123-130	nitric oxide synthase 1, neuronal	Mus musculus	188-192
33841534-0	2020	Involvement of nNOS, and alpha1, alpha2, beta1, and beta2 Subunits of Soluble Guanylyl Cyclase Genes Expression in Anticonvulsant Effect of Sumatriptan on Pentylenetetrazole-Induced Seizure in Mice.	Sumatriptan	140-151	nitric oxide synthase 1, neuronal	Mus musculus	15-19
32812777-7	2020	Treatment with SB restored impaired gastric 1) Nrf2 and phase II antioxidant enzymes through PI3K/ERK/AKT mediated pathway; 2) tetrahydrobiopterin (BH4, cofactor of nNOS) biosynthesis enzyme DHFR; and 3) nNOSalpha dimerization in Obese/T2 diabetic female mice.	Antimony	15-17	nitric oxide synthase 1, neuronal	Mus musculus	165-169
32812777-7	2020	Treatment with SB restored impaired gastric 1) Nrf2 and phase II antioxidant enzymes through PI3K/ERK/AKT mediated pathway; 2) tetrahydrobiopterin (BH4, cofactor of nNOS) biosynthesis enzyme DHFR; and 3) nNOSalpha dimerization in Obese/T2 diabetic female mice.	sapropterin	127-146	nitric oxide synthase 1, neuronal	Mus musculus	165-169
32812777-7	2020	Treatment with SB restored impaired gastric 1) Nrf2 and phase II antioxidant enzymes through PI3K/ERK/AKT mediated pathway; 2) tetrahydrobiopterin (BH4, cofactor of nNOS) biosynthesis enzyme DHFR; and 3) nNOSalpha dimerization in Obese/T2 diabetic female mice.	sapropterin	148-151	nitric oxide synthase 1, neuronal	Mus musculus	165-169
33841534-11	2020	Furthermore, sumatriptan downregulated the PTZ-induced mRNA expression of nNOS (P <= 0.01), alpha1 (P <= 0.001), alpha2 (P <= 0.05), and beta1 (P <= 0.05) genes in cerebral cortex of mice.	Sumatriptan	13-24	nitric oxide synthase 1, neuronal	Mus musculus	74-78
33841534-11	2020	Furthermore, sumatriptan downregulated the PTZ-induced mRNA expression of nNOS (P <= 0.01), alpha1 (P <= 0.001), alpha2 (P <= 0.05), and beta1 (P <= 0.05) genes in cerebral cortex of mice.	Pentylenetetrazole	43-46	nitric oxide synthase 1, neuronal	Mus musculus	74-78
32360667-2	2020	We have previously shown that globally inhibiting protein synthesis mobilizes intracellular L-arginine "pools" in retinal neurons, which concomitantly enhances neuronal nitric oxide synthase-mediated nitric oxide production.	Arginine	92-102	nitric oxide synthase 1, neuronal	Mus musculus	160-190
32603891-9	2020	This study suggests the role of n-NOS in anti-convulsant effects of NLT and pro-convulsant effects of SNC80 in stress-induced seizure.	naltrindole	68-71	nitric oxide synthase 1, neuronal	Mus musculus	32-37
32778793-0	2020	Tau induces PSD95-neuronal NOS uncoupling and neurovascular dysfunction independent of neurodegeneration.	uridine triacetate	0-3	nitric oxide synthase 1, neuronal	Mus musculus	18-30
32982674-2	2020	We have recently shown that neuronal nitric oxide synthase (nNOS) expression was reduced in the basolateral amygdala of mice after postnatal valproic acid exposure.	Valproic Acid	141-154	nitric oxide synthase 1, neuronal	Mus musculus	28-58
32982674-2	2020	We have recently shown that neuronal nitric oxide synthase (nNOS) expression was reduced in the basolateral amygdala of mice after postnatal valproic acid exposure.	Valproic Acid	141-154	nitric oxide synthase 1, neuronal	Mus musculus	60-64
32479857-0	2020	Effects of inosine monophosphate and exercise training on neuronal nitric oxide synthase in the mouse brain.	Inosine Monophosphate	11-32	nitric oxide synthase 1, neuronal	Mus musculus	58-88
32479857-4	2020	However, whether inosine and exercise training have combined effects on nNOS pathway-related proteins in the brain remains unknown.	Inosine	17-24	nitric oxide synthase 1, neuronal	Mus musculus	72-76
32479857-5	2020	We found, for the first time, that inosine monophosphate (IMP), which is a precursor of inosine, decreases nNOS levels in the ventral hippocampus (vHp) and the cerebellum (Ce), but not in the dorsal hippocampus (dHp).	Inosine Monophosphate	35-56	nitric oxide synthase 1, neuronal	Mus musculus	107-111
32479857-5	2020	We found, for the first time, that inosine monophosphate (IMP), which is a precursor of inosine, decreases nNOS levels in the ventral hippocampus (vHp) and the cerebellum (Ce), but not in the dorsal hippocampus (dHp).	Inosine Monophosphate	58-61	nitric oxide synthase 1, neuronal	Mus musculus	107-111
32479857-5	2020	We found, for the first time, that inosine monophosphate (IMP), which is a precursor of inosine, decreases nNOS levels in the ventral hippocampus (vHp) and the cerebellum (Ce), but not in the dorsal hippocampus (dHp).	Inosine	35-42	nitric oxide synthase 1, neuronal	Mus musculus	107-111
32479857-11	2020	In conclusion, in the vHp, which is associated with emotional behavior, IMP decreased nNOS levels and activated CREB, suggesting that IMP can elicit anxiolytic effects.	Inosine Monophosphate	72-75	nitric oxide synthase 1, neuronal	Mus musculus	86-90
32479857-11	2020	In conclusion, in the vHp, which is associated with emotional behavior, IMP decreased nNOS levels and activated CREB, suggesting that IMP can elicit anxiolytic effects.	Inosine Monophosphate	134-137	nitric oxide synthase 1, neuronal	Mus musculus	86-90
32644793-3	2020	Here, in lipopolysaccharide-induced mice, we identified that a single administration of MH recovered depressive behaviors and down-regulated the expressions of neuronal nitric oxide synthase (nNOS) in the hippocampus after 1 day.	mh	88-90	nitric oxide synthase 1, neuronal	Mus musculus	160-190
32644793-3	2020	Here, in lipopolysaccharide-induced mice, we identified that a single administration of MH recovered depressive behaviors and down-regulated the expressions of neuronal nitric oxide synthase (nNOS) in the hippocampus after 1 day.	mh	88-90	nitric oxide synthase 1, neuronal	Mus musculus	192-196
32644793-4	2020	Activation of nNOS by l-arginine led to depressive behaviors, and inhibition of nNOS contributed to antidepressive behaviors.	Arginine	22-32	nitric oxide synthase 1, neuronal	Mus musculus	14-18
32644793-5	2020	Notably, MH only reversed the expression of nNOS"s downstream NF-kappaB and not the CREB/BDNF pathway in the hippocampus, and MH"s antidepressant-like effects were prevented by Asatone (an agonist of NF-kappaB) and not H89 (an antagonist of CREB).	ASATONE	177-184	nitric oxide synthase 1, neuronal	Mus musculus	44-48
32234538-13	2020	Mice given ampicillin had reduced colon motility compared with mice given only water, and their colonic LMMP had reduced numbers of nitrergic neurons, reduced nNOS production, and reduced colonic neurogenesis.	Ampicillin	11-21	nitric oxide synthase 1, neuronal	Mus musculus	159-163
32270464-1	2020	Nitric oxide (NO), specifically derived from neuronal nitric oxide synthase (nNOS), is a well-established regulator of synaptic transmission in Purkinje neurons (PNs), governing fundamental processes such as motor learning and coordination.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	45-75
32270464-1	2020	Nitric oxide (NO), specifically derived from neuronal nitric oxide synthase (nNOS), is a well-established regulator of synaptic transmission in Purkinje neurons (PNs), governing fundamental processes such as motor learning and coordination.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	77-81
32270464-2	2020	Previous phenotypic analyses showed similar cerebellar structures between neuronal nitric oxide null (nNOS-/-) and wild-type (WT) adult male mice, despite prominent ataxic behavior within nNOS-/- mice.	Nitric Oxide	83-95	nitric oxide synthase 1, neuronal	Mus musculus	102-106
32270464-10	2020	Together, these results indicate a novel role for nNOS/NO signaling in PN development, particularly by regulating an mGluR1-initiated calcium signaling mechanism.	Calcium	134-141	nitric oxide synthase 1, neuronal	Mus musculus	50-54
32447240-16	2020	NO synthase (NOS) inhibitors significantly augmented the anticonvulsant effects of combined low doses of thalidomide and morphine, whereas the inducible NOS inhibitor aminoguanidine (100 mg/kg, i.p.)	Thalidomide	105-116	nitric oxide synthase 1, neuronal	Mus musculus	0-11
32447240-16	2020	NO synthase (NOS) inhibitors significantly augmented the anticonvulsant effects of combined low doses of thalidomide and morphine, whereas the inducible NOS inhibitor aminoguanidine (100 mg/kg, i.p.)	Morphine	121-129	nitric oxide synthase 1, neuronal	Mus musculus	0-11
32612530-11	2020	Specifically, THC caused downregulation of let7a-5p which targeted SOCS1 and downregulation of miR-34-5p which caused increased expression of FoxP3, NOS1, and CSF1R.	Dronabinol	14-17	nitric oxide synthase 1, neuronal	Mus musculus	149-153
31975425-3	2020	In other organ systems, cAMP can increase neuronal NO production by stimulating PKA to phosphorylate neuronal NO synthase (nNOS) Serine-1412 (S1412).	Cyclic AMP	24-28	nitric oxide synthase 1, neuronal	Mus musculus	123-127
31975425-3	2020	In other organ systems, cAMP can increase neuronal NO production by stimulating PKA to phosphorylate neuronal NO synthase (nNOS) Serine-1412 (S1412).	3,9-dihydroxyoctahydrodibenzo(a,g)biphenylene	87-100	nitric oxide synthase 1, neuronal	Mus musculus	123-127
31975425-3	2020	In other organ systems, cAMP can increase neuronal NO production by stimulating PKA to phosphorylate neuronal NO synthase (nNOS) Serine-1412 (S1412).	cholecystokinin C-terminal flanking peptide	129-140	nitric oxide synthase 1, neuronal	Mus musculus	123-127
31975425-3	2020	In other organ systems, cAMP can increase neuronal NO production by stimulating PKA to phosphorylate neuronal NO synthase (nNOS) Serine-1412 (S1412).	cholecystokinin C-terminal flanking peptide	142-147	nitric oxide synthase 1, neuronal	Mus musculus	123-127
31975425-4	2020	We hypothesized that cAMP also increases nNOS S1412 phosphorylation by PKA in enteric neurons to augment nitrergic relaxation of mouse ileum.	Cyclic AMP	21-25	nitric oxide synthase 1, neuronal	Mus musculus	41-45
31975425-4	2020	We hypothesized that cAMP also increases nNOS S1412 phosphorylation by PKA in enteric neurons to augment nitrergic relaxation of mouse ileum.	cholecystokinin C-terminal flanking peptide	46-51	nitric oxide synthase 1, neuronal	Mus musculus	41-45
31975425-5	2020	EXPERIMENTAL APPROACH: We measured contractile force and nNOS S1412 phosphorylation in ileal rings suspended in physiologic organ bath.	cholecystokinin C-terminal flanking peptide	62-67	nitric oxide synthase 1, neuronal	Mus musculus	57-61
31975425-7	2020	KEY RESULTS: Forskolin stimulated phosphorylation of nNOS S1412 in mouse ileum.	Colforsin	13-22	nitric oxide synthase 1, neuronal	Mus musculus	53-57
31975425-7	2020	KEY RESULTS: Forskolin stimulated phosphorylation of nNOS S1412 in mouse ileum.	cholecystokinin C-terminal flanking peptide	58-63	nitric oxide synthase 1, neuronal	Mus musculus	53-57
31975425-9	2020	PKA inhibition blocked forskolin-induced nNOS phosphorylation and attenuated relaxation of wildtype but not nNOSS1412A ileum.	Colforsin	23-32	nitric oxide synthase 1, neuronal	Mus musculus	41-45
31975425-12	2020	CONCLUSION AND IMPLICATIONS: PKA phosphorylation of nNOS S1412 augments forskolin-induced nitrergic ileal relaxation.	cholecystokinin C-terminal flanking peptide	57-62	nitric oxide synthase 1, neuronal	Mus musculus	52-56
31975425-12	2020	CONCLUSION AND IMPLICATIONS: PKA phosphorylation of nNOS S1412 augments forskolin-induced nitrergic ileal relaxation.	Colforsin	72-81	nitric oxide synthase 1, neuronal	Mus musculus	52-56
31989159-1	2020	Excessive activation of N-methyl-D-aspartate receptors (NMDARs) and the resulting neuronal nitric oxide synthase (nNOS) activation plays a crucial role in the pathogenesis of traumatic brain injury (TBI).	N-Methylaspartate	24-44	nitric oxide synthase 1, neuronal	Mus musculus	82-112
31989159-1	2020	Excessive activation of N-methyl-D-aspartate receptors (NMDARs) and the resulting neuronal nitric oxide synthase (nNOS) activation plays a crucial role in the pathogenesis of traumatic brain injury (TBI).	N-Methylaspartate	24-44	nitric oxide synthase 1, neuronal	Mus musculus	114-118
32524520-5	2020	Because of the unclear etiology of morphine-induced adverse effects in the hippocampus, investigating the involvement of TRPM2 and NO synthetase (NOS) activations in the treatment of morphine-induced OS, apoptosis, and neuroinflammation is a major challenge.	Morphine	183-191	nitric oxide synthase 1, neuronal	Mus musculus	131-144
32635208-0	2020	Supplementation of 17beta-Estradiol Normalizes Rapid Gastric Emptying by Restoring Impaired Nrf2 and nNOS Function in Obesity-Induced Diabetic Ovariectomized Mice.	Estradiol	19-35	nitric oxide synthase 1, neuronal	Mus musculus	101-105
32238453-6	2020	Enhanced plaque stability by LEO was associated with the nitric oxide synthase (NOS)-nitric oxide (NO) system.	leonurine	29-32	nitric oxide synthase 1, neuronal	Mus musculus	57-78
32144123-10	2020	nNOS phosphorylation on positive (Ser-1412) regulatory site was decreased (P<0.05) in the bladder of SCD mice compared to WT and was not affected by NO-np.	Serine	34-37	nitric oxide synthase 1, neuronal	Mus musculus	0-4
32101284-0	2020	Effect of neuronal nitric oxide synthase serine-1412 phosphorylation on hypothalamic-pituitary-ovarian function and leptin response.	Serine	41-47	nitric oxide synthase 1, neuronal	Mus musculus	10-40
32101284-2	2020	The mechanism of hypothalamic nNOS activation is not clear but could be via nNOS serine1412 (S1412) phosphorylation, which increases nNOS activity and physiologic NO effects in other organ systems.	serine1412	81-91	nitric oxide synthase 1, neuronal	Mus musculus	30-34
32101284-2	2020	The mechanism of hypothalamic nNOS activation is not clear but could be via nNOS serine1412 (S1412) phosphorylation, which increases nNOS activity and physiologic NO effects in other organ systems.	serine1412	81-91	nitric oxide synthase 1, neuronal	Mus musculus	76-80
32101284-2	2020	The mechanism of hypothalamic nNOS activation is not clear but could be via nNOS serine1412 (S1412) phosphorylation, which increases nNOS activity and physiologic NO effects in other organ systems.	serine1412	81-91	nitric oxide synthase 1, neuronal	Mus musculus	76-80
32238672-1	2020	Dimethylarginine dimethylaminohydrolase-1 (DDAH1) maintains nitric oxide (NO) bioavailability by degrading asymmetric dimethylarginine (ADMA), which is an endogenous inhibitor of nitric oxide synthase (NOS).	Nitric Oxide	60-72	nitric oxide synthase 1, neuronal	Mus musculus	179-200
32238672-1	2020	Dimethylarginine dimethylaminohydrolase-1 (DDAH1) maintains nitric oxide (NO) bioavailability by degrading asymmetric dimethylarginine (ADMA), which is an endogenous inhibitor of nitric oxide synthase (NOS).	dimethylarginine	118-134	nitric oxide synthase 1, neuronal	Mus musculus	179-200
32238672-1	2020	Dimethylarginine dimethylaminohydrolase-1 (DDAH1) maintains nitric oxide (NO) bioavailability by degrading asymmetric dimethylarginine (ADMA), which is an endogenous inhibitor of nitric oxide synthase (NOS).	N,N-dimethylarginine	136-140	nitric oxide synthase 1, neuronal	Mus musculus	179-200
32462085-8	2020	Co-administration of citicoline and selective nitric oxide synthase (NOS) inhibitors amplified the anticonvulsant effect of citicoline.	Cytidine Diphosphate Choline	124-134	nitric oxide synthase 1, neuronal	Mus musculus	46-67
32427844-4	2020	Our results suggest that the pain signal becomes an anxiety signal after activation of vmPFC nNOS-expressing neurons, which causes subsequent release of nitric oxide (NO).	Nitric Oxide	153-165	nitric oxide synthase 1, neuronal	Mus musculus	93-97
32343709-10	2020	Finally, deletion of neuronal nitric oxide synthase (nNOS) in A53T alpha-syn transgenic mice reduced the levels of pSer129 alpha-syn and alpha-syn in an age dependent manner.	pser129	115-122	nitric oxide synthase 1, neuronal	Mus musculus	21-51
32113678-4	2020	Using morphine conditioned place preference (CPP) model, we show that association of neuronal nitric oxide synthase (nNOS) with postsynaptic density-95 (PSD-95) plays a significant role in morphine priming-induced reinstatement.	Morphine	6-14	nitric oxide synthase 1, neuronal	Mus musculus	85-115
32113678-4	2020	Using morphine conditioned place preference (CPP) model, we show that association of neuronal nitric oxide synthase (nNOS) with postsynaptic density-95 (PSD-95) plays a significant role in morphine priming-induced reinstatement.	Morphine	6-14	nitric oxide synthase 1, neuronal	Mus musculus	117-121
32113678-4	2020	Using morphine conditioned place preference (CPP) model, we show that association of neuronal nitric oxide synthase (nNOS) with postsynaptic density-95 (PSD-95) plays a significant role in morphine priming-induced reinstatement.	Morphine	189-197	nitric oxide synthase 1, neuronal	Mus musculus	85-115
32113678-4	2020	Using morphine conditioned place preference (CPP) model, we show that association of neuronal nitric oxide synthase (nNOS) with postsynaptic density-95 (PSD-95) plays a significant role in morphine priming-induced reinstatement.	Morphine	189-197	nitric oxide synthase 1, neuronal	Mus musculus	117-121
32113678-5	2020	The nNOS-PSD-95 coupling and c-Fos expression in the medial prefrontal cortex (mPFC) was significantly increased after extinction of morphine CPP.	Morphine	133-141	nitric oxide synthase 1, neuronal	Mus musculus	4-8
32113678-6	2020	Dissociation of nNOS-PSD-95 in the mPFC by ZL006 inhibited the reinstatement of morphine CPP induced by a priming dose of morphine.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	43-48	nitric oxide synthase 1, neuronal	Mus musculus	16-20
32113678-6	2020	Dissociation of nNOS-PSD-95 in the mPFC by ZL006 inhibited the reinstatement of morphine CPP induced by a priming dose of morphine.	Morphine	80-88	nitric oxide synthase 1, neuronal	Mus musculus	16-20
32113678-6	2020	Dissociation of nNOS-PSD-95 in the mPFC by ZL006 inhibited the reinstatement of morphine CPP induced by a priming dose of morphine.	Morphine	122-130	nitric oxide synthase 1, neuronal	Mus musculus	16-20
32113678-8	2020	Uncoupling nNOS-PSD-95 reversed the morphine-induced CREB dysfunction.	Morphine	36-44	nitric oxide synthase 1, neuronal	Mus musculus	11-15
32113678-9	2020	Moreover, effects of ZL006 on the reinstatement of morphine CPP and CREB activation depended on nNOS-PSD-95 target.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	21-26	nitric oxide synthase 1, neuronal	Mus musculus	96-100
32113678-9	2020	Moreover, effects of ZL006 on the reinstatement of morphine CPP and CREB activation depended on nNOS-PSD-95 target.	Morphine	51-59	nitric oxide synthase 1, neuronal	Mus musculus	96-100
32113678-10	2020	Together, our findings suggest that nNOS-PSD-95 in the mPFC contributes to reinstatement of morphine CPP, possibly through CREB dysfunction, offering a potential target to prevent relapse of drug abuse.	Morphine	92-100	nitric oxide synthase 1, neuronal	Mus musculus	36-40
32338170-7	2022	Acute amylin increased the expression of nNOS, ChAT, and uncoupling protein-1 in the IBAT of WT and sham mice, while no changes were observed in the denervated mice and pERK from the above effect.Conclusions: Intact SNS of IBAT influences amylin-induced suppression of food intake and body weight, thus affecting nNOS and ChAT signalling in the LDT and locus coeruleus.	ibat	85-89	nitric oxide synthase 1, neuronal	Mus musculus	41-45
32343709-10	2020	Finally, deletion of neuronal nitric oxide synthase (nNOS) in A53T alpha-syn transgenic mice reduced the levels of pSer129 alpha-syn and alpha-syn in an age dependent manner.	pser129	115-122	nitric oxide synthase 1, neuronal	Mus musculus	53-57
31882337-13	2020	Immunohistochemistry showed nNOS expression in the edaravone group to be significantly lower than that in the control group 96 hours after reperfusion.	Edaravone	51-60	nitric oxide synthase 1, neuronal	Mus musculus	28-32
31711126-7	2020	Interestingly, AMPA increased cGMP independently of NMDA receptors and dependent on NO synthase (NOS) activation.	alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid	15-19	nitric oxide synthase 1, neuronal	Mus musculus	84-95
31746324-5	2020	In the case of nNOS-interneurons, robust hemodynamic changes occurred with minimal changes in neural activity, suggesting that the ability of blood oxygen level dependent functional magnetic resonance imaging (BOLD fMRI) to reliably reflect changes in neuronal activity may be dependent on type of neuron recruited.	Oxygen	148-154	nitric oxide synthase 1, neuronal	Mus musculus	15-19
32412412-5	2020	Our study demonstrates generally that novel neural circuits can be identified from targeted connectomic analyses and specifically that the NOS-1 AC mediates long-range inhibition during night vision and is a major element of the RB pathway.	Rubidium	229-231	nitric oxide synthase 1, neuronal	Mus musculus	139-144
31863649-6	2020	Neuronal nitric oxide synthase (nNOS) mediated chronic stress-induced downregulation of 5-HT1A receptor in the DG through peroxynitrite anion (ONOO ) pathway but not cyclic guanosine monophosphate (cGMP) pathway.	Peroxynitrous Acid	122-135	nitric oxide synthase 1, neuronal	Mus musculus	0-30
31863649-6	2020	Neuronal nitric oxide synthase (nNOS) mediated chronic stress-induced downregulation of 5-HT1A receptor in the DG through peroxynitrite anion (ONOO ) pathway but not cyclic guanosine monophosphate (cGMP) pathway.	Peroxynitrous Acid	122-135	nitric oxide synthase 1, neuronal	Mus musculus	32-36
31863649-6	2020	Neuronal nitric oxide synthase (nNOS) mediated chronic stress-induced downregulation of 5-HT1A receptor in the DG through peroxynitrite anion (ONOO ) pathway but not cyclic guanosine monophosphate (cGMP) pathway.	tetramethylammonium peroxynitrite	143-147	nitric oxide synthase 1, neuronal	Mus musculus	0-30
31863649-6	2020	Neuronal nitric oxide synthase (nNOS) mediated chronic stress-induced downregulation of 5-HT1A receptor in the DG through peroxynitrite anion (ONOO ) pathway but not cyclic guanosine monophosphate (cGMP) pathway.	tetramethylammonium peroxynitrite	143-147	nitric oxide synthase 1, neuronal	Mus musculus	32-36
31863649-6	2020	Neuronal nitric oxide synthase (nNOS) mediated chronic stress-induced downregulation of 5-HT1A receptor in the DG through peroxynitrite anion (ONOO ) pathway but not cyclic guanosine monophosphate (cGMP) pathway.	Cyclic GMP	198-202	nitric oxide synthase 1, neuronal	Mus musculus	32-36
31863649-9	2020	Accordingly, we developed a "dentate nNOS-5-HT1A receptor closed-loop" theory (stress-glucocorticoids-nNOS-Nitric oxide-ONOO -5-HT1A receptor -nNOS) of stress-related anxiety.	tetramethylammonium peroxynitrite	107-124	nitric oxide synthase 1, neuronal	Mus musculus	37-41
31863649-9	2020	Accordingly, we developed a "dentate nNOS-5-HT1A receptor closed-loop" theory (stress-glucocorticoids-nNOS-Nitric oxide-ONOO -5-HT1A receptor -nNOS) of stress-related anxiety.	tetramethylammonium peroxynitrite	107-124	nitric oxide synthase 1, neuronal	Mus musculus	102-106
31863649-9	2020	Accordingly, we developed a "dentate nNOS-5-HT1A receptor closed-loop" theory (stress-glucocorticoids-nNOS-Nitric oxide-ONOO -5-HT1A receptor -nNOS) of stress-related anxiety.	tetramethylammonium peroxynitrite	107-124	nitric oxide synthase 1, neuronal	Mus musculus	102-106
32032718-5	2020	EXPERIMENTAL APPROACH: Mice were fed control or high fat diet (HFD) for 7 weeks in combination with the NO synthase (NOS) inhibitor l-NAME to induce metabolic syndrome.	NG-Nitroarginine Methyl Ester	132-138	nitric oxide synthase 1, neuronal	Mus musculus	104-115
31882337-14	2020	CONCLUSIONS: These in vivo data indicate that edaravone may have a neuroprotective effect by reducing levels of OH- metabolites, increasing NO production and decreasing nNOS expression in brain cells.	Edaravone	46-55	nitric oxide synthase 1, neuronal	Mus musculus	169-173
31895878-2	2020	We have previously demonstrated that endothelium-derived hydrogen peroxide (H2O2) is an EDH factor produced by all types of nitric oxide synthases (NOSs), including endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS.	Hydrogen Peroxide	57-74	nitric oxide synthase 1, neuronal	Mus musculus	189-201
31895878-2	2020	We have previously demonstrated that endothelium-derived hydrogen peroxide (H2O2) is an EDH factor produced by all types of nitric oxide synthases (NOSs), including endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS.	Hydrogen Peroxide	57-74	nitric oxide synthase 1, neuronal	Mus musculus	203-207
31895878-2	2020	We have previously demonstrated that endothelium-derived hydrogen peroxide (H2O2) is an EDH factor produced by all types of nitric oxide synthases (NOSs), including endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS.	Hydrogen Peroxide	76-80	nitric oxide synthase 1, neuronal	Mus musculus	189-201
31895878-2	2020	We have previously demonstrated that endothelium-derived hydrogen peroxide (H2O2) is an EDH factor produced by all types of nitric oxide synthases (NOSs), including endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS.	Hydrogen Peroxide	76-80	nitric oxide synthase 1, neuronal	Mus musculus	203-207
31895878-8	2020	Catalase, a specific H2O2 scavenger, markedly inhibited EDH-mediated relaxations in all 3 genotypes, indicating compensatory roles of nNOS-derived H2O2 as an EDH factor in coronary microcirculation.	Hydrogen Peroxide	147-151	nitric oxide synthase 1, neuronal	Mus musculus	134-138
31241990-4	2019	Nitric oxide is produced predominantly by nitric oxide synthase 1 (NOS1) in the CD and acts as a diuretic during salt loading.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	42-65
32039822-8	2020	After E2 treatment, GT1-7 cells expressed more GnRH and GPER was markedly elevated and reached a peak at 8 h. The KISS1, GPR54 and nNOS in GT1-7 cells were significantly increased with G1 induction, but were significantly decreased with G15 induction compared with E2 induction alone.	Estradiol	6-8	nitric oxide synthase 1, neuronal	Mus musculus	131-135
32039822-8	2020	After E2 treatment, GT1-7 cells expressed more GnRH and GPER was markedly elevated and reached a peak at 8 h. The KISS1, GPR54 and nNOS in GT1-7 cells were significantly increased with G1 induction, but were significantly decreased with G15 induction compared with E2 induction alone.	Estradiol	265-267	nitric oxide synthase 1, neuronal	Mus musculus	131-135
30857731-9	2019	Intestines from all treatment groups had similar PECAM staining, but intestines treated with dithizone had significantly decreased nNOS and iNOS gene expression compared to controls (p < 0.007).	Dithizone	93-102	nitric oxide synthase 1, neuronal	Mus musculus	131-135
31763675-0	2019	DDAH-2 alleviates contrast medium iopromide-induced acute kidney injury through nitric oxide synthase.	iopromide	34-43	nitric oxide synthase 1, neuronal	Mus musculus	80-101
31805977-6	2019	A biotin-switch assay was performed to detect the S-nitrosylation of HDAC2 by NOS1.	Biotin	2-8	nitric oxide synthase 1, neuronal	Mus musculus	78-82
31600544-2	2019	Research has revealed an alternative NO-generating pathway, independent of NO synthase (NOS), in which the inorganic anions nitrate (NO3-) and nitrite (NO2-) are serially reduced to form NO.	Nitrates	124-131	nitric oxide synthase 1, neuronal	Mus musculus	75-86
31600544-2	2019	Research has revealed an alternative NO-generating pathway, independent of NO synthase (NOS), in which the inorganic anions nitrate (NO3-) and nitrite (NO2-) are serially reduced to form NO.	Nitrites	143-150	nitric oxide synthase 1, neuronal	Mus musculus	75-86
33511058-8	2021	Anticonvulsant effect of onopordia was blocked by applying a single dose of a non-selective nitric oxide synthase (NOS) inhibitor, Nomega-nitro-l-arginine methyl ester hydrochloride (l-NAME; 10 mg/kg, i.p.	onopordia	25-34	nitric oxide synthase 1, neuronal	Mus musculus	92-113
33511058-12	2021	The results of the present study demonstrated the anticonvulsant effect of onopordia as a new lead compound and also contribution of NO/nNOS pathway on PTZ-induced seizure in mice.	Pentylenetetrazole	152-155	nitric oxide synthase 1, neuronal	Mus musculus	136-140
31543455-6	2019	Within the PO, various neuronal subtypes (e.g., GABA/galanin and glutamate/NOS1) induce NREM sleep [20-22] and concomitant body cooling [21, 22].	Glutamic Acid	65-74	nitric oxide synthase 1, neuronal	Mus musculus	75-79
31241990-4	2019	Nitric oxide is produced predominantly by nitric oxide synthase 1 (NOS1) in the CD and acts as a diuretic during salt loading.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	67-71
31241990-4	2019	Nitric oxide is produced predominantly by nitric oxide synthase 1 (NOS1) in the CD and acts as a diuretic during salt loading.	Cadmium	80-82	nitric oxide synthase 1, neuronal	Mus musculus	42-65
31241990-4	2019	Nitric oxide is produced predominantly by nitric oxide synthase 1 (NOS1) in the CD and acts as a diuretic during salt loading.	Cadmium	80-82	nitric oxide synthase 1, neuronal	Mus musculus	67-71
31283871-8	2019	Next, co-immunostaining of DARPP-32 and neuronal nitric oxide synthase (nNOS: expressed in a subtype of gamma-Aminobutyric acid (GABA interneurons) in ventral tegmental area (VTA) showed a colocalization of nNOS and DARPP-32.	gamma-Aminobutyric Acid	104-127	nitric oxide synthase 1, neuronal	Mus musculus	40-70
31283871-8	2019	Next, co-immunostaining of DARPP-32 and neuronal nitric oxide synthase (nNOS: expressed in a subtype of gamma-Aminobutyric acid (GABA interneurons) in ventral tegmental area (VTA) showed a colocalization of nNOS and DARPP-32.	gamma-Aminobutyric Acid	104-127	nitric oxide synthase 1, neuronal	Mus musculus	72-76
31283871-8	2019	Next, co-immunostaining of DARPP-32 and neuronal nitric oxide synthase (nNOS: expressed in a subtype of gamma-Aminobutyric acid (GABA interneurons) in ventral tegmental area (VTA) showed a colocalization of nNOS and DARPP-32.	gamma-Aminobutyric Acid	104-127	nitric oxide synthase 1, neuronal	Mus musculus	207-211
31283871-8	2019	Next, co-immunostaining of DARPP-32 and neuronal nitric oxide synthase (nNOS: expressed in a subtype of gamma-Aminobutyric acid (GABA interneurons) in ventral tegmental area (VTA) showed a colocalization of nNOS and DARPP-32.	gamma-Aminobutyric Acid	129-133	nitric oxide synthase 1, neuronal	Mus musculus	40-70
31283871-8	2019	Next, co-immunostaining of DARPP-32 and neuronal nitric oxide synthase (nNOS: expressed in a subtype of gamma-Aminobutyric acid (GABA interneurons) in ventral tegmental area (VTA) showed a colocalization of nNOS and DARPP-32.	gamma-Aminobutyric Acid	129-133	nitric oxide synthase 1, neuronal	Mus musculus	72-76
30957236-5	2019	Additionally, pretreatment with noneffective doses of an opioid receptor antagonist (naltrexone) and NMDA receptor antagonists (ketamine and MK-801) inhibited methadone"s proconvulsive activity in the acute phase, while l-NAME (a nonspecific nitric oxide synthase (NOS) inhibitor) did not affect that activity.	Naltrexone	85-95	nitric oxide synthase 1, neuronal	Mus musculus	242-263
31507355-4	2019	Canonical cGMP signaling in brain follows the activation of neuronal nitric oxide synthase (nNOS) and the generation of nitric oxide, which activates soluble guanylyl cyclase and cGMP synthesis.	Cyclic GMP	10-14	nitric oxide synthase 1, neuronal	Mus musculus	60-90
31507355-4	2019	Canonical cGMP signaling in brain follows the activation of neuronal nitric oxide synthase (nNOS) and the generation of nitric oxide, which activates soluble guanylyl cyclase and cGMP synthesis.	Cyclic GMP	10-14	nitric oxide synthase 1, neuronal	Mus musculus	92-96
31507355-4	2019	Canonical cGMP signaling in brain follows the activation of neuronal nitric oxide synthase (nNOS) and the generation of nitric oxide, which activates soluble guanylyl cyclase and cGMP synthesis.	Nitric Oxide	69-81	nitric oxide synthase 1, neuronal	Mus musculus	92-96
31507355-4	2019	Canonical cGMP signaling in brain follows the activation of neuronal nitric oxide synthase (nNOS) and the generation of nitric oxide, which activates soluble guanylyl cyclase and cGMP synthesis.	Cyclic GMP	179-183	nitric oxide synthase 1, neuronal	Mus musculus	60-90
31507355-4	2019	Canonical cGMP signaling in brain follows the activation of neuronal nitric oxide synthase (nNOS) and the generation of nitric oxide, which activates soluble guanylyl cyclase and cGMP synthesis.	Cyclic GMP	179-183	nitric oxide synthase 1, neuronal	Mus musculus	92-96
31507377-10	2019	These data suggest that secretin acts on GnRH neurons via secretin receptors whose activation triggers the cAMP/PKA/nNOS signaling pathway resulting in nitric oxide release and in the presynaptic terminals this retrograde NO machinery regulates the GABAergic input to GnRH neurons.	Cyclic AMP	107-111	nitric oxide synthase 1, neuronal	Mus musculus	116-120
31507377-10	2019	These data suggest that secretin acts on GnRH neurons via secretin receptors whose activation triggers the cAMP/PKA/nNOS signaling pathway resulting in nitric oxide release and in the presynaptic terminals this retrograde NO machinery regulates the GABAergic input to GnRH neurons.	Nitric Oxide	152-164	nitric oxide synthase 1, neuronal	Mus musculus	116-120
31268770-4	2019	Nitrergic neurons [neuronal nitric oxide synthase (nNOS)-positive neurons] expressing GCaMP3 exhibited higher levels of activity during periods of tonic inhibition than during CMMCs.	cmmcs	176-181	nitric oxide synthase 1, neuronal	Mus musculus	51-55
30957236-5	2019	Additionally, pretreatment with noneffective doses of an opioid receptor antagonist (naltrexone) and NMDA receptor antagonists (ketamine and MK-801) inhibited methadone"s proconvulsive activity in the acute phase, while l-NAME (a nonspecific nitric oxide synthase (NOS) inhibitor) did not affect that activity.	Ketamine	128-136	nitric oxide synthase 1, neuronal	Mus musculus	242-263
30957236-5	2019	Additionally, pretreatment with noneffective doses of an opioid receptor antagonist (naltrexone) and NMDA receptor antagonists (ketamine and MK-801) inhibited methadone"s proconvulsive activity in the acute phase, while l-NAME (a nonspecific nitric oxide synthase (NOS) inhibitor) did not affect that activity.	Dizocilpine Maleate	141-147	nitric oxide synthase 1, neuronal	Mus musculus	242-263
31034606-11	2019	The expression of Nos1 is frequently changed following alcohol exposure, and variants in this gene segregating among the BXD population may modulate alcohol intake in response to stress.	Alcohols	55-62	nitric oxide synthase 1, neuronal	Mus musculus	18-22
31401195-9	2019	Consequently, mice afflicted with painful cerulein-induced CP could be significantly relieved upon treatment with the specific nNOS inhibitor NPLA.	Ceruletide	42-50	nitric oxide synthase 1, neuronal	Mus musculus	127-131
31034606-11	2019	The expression of Nos1 is frequently changed following alcohol exposure, and variants in this gene segregating among the BXD population may modulate alcohol intake in response to stress.	Alcohols	149-156	nitric oxide synthase 1, neuronal	Mus musculus	18-22
30940567-7	2019	The BST pretreatment significantly tempered the loperamide-induced inactivation of c-kit and nNOS (p < 0.05 or 0.01) as well as the contraction-related gene expression, such as the 5HT4 receptor (5HT4R), anoctamin-1 (ANO1), ryanodine receptor 3 (RYR3) and smooth muscle myosin light chain kinase (smMLCK).	Loperamide	48-58	nitric oxide synthase 1, neuronal	Mus musculus	93-97
31091127-2	2019	SGLT1 also mediates macula densa (MD) sensing of an increase in luminal glucose, which increases nitric oxide (NO) synthase 1 (MD-NOS1)-mediated NO formation and potentially glomerular filtratrion rate (GFR).	Glucose	72-79	nitric oxide synthase 1, neuronal	Mus musculus	130-134
31091127-2	2019	SGLT1 also mediates macula densa (MD) sensing of an increase in luminal glucose, which increases nitric oxide (NO) synthase 1 (MD-NOS1)-mediated NO formation and potentially glomerular filtratrion rate (GFR).	nitric	97-103	nitric oxide synthase 1, neuronal	Mus musculus	130-134
31091127-13	2019	Potential mechanisms include its role in glucose-driven upregulation of MD-NOS1 expression.	Glucose	41-48	nitric oxide synthase 1, neuronal	Mus musculus	75-79
31087329-9	2019	This spreading potentiation was blocked by spinal application of l-NAME, an inhibitor of NO synthase (NOS).	NG-Nitroarginine Methyl Ester	65-71	nitric oxide synthase 1, neuronal	Mus musculus	89-100
31261859-6	2019	The aforementioned beneficial effects of S1P on EPCs could be inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitor of LY294002 and nitric oxide synthase (NOS) inhibitor of N"-nitro-L-arginine-methyl ester hydrochloride (L-NAME).	N'-Nitro-L-arginine-methyl ester hydrochloride	183-229	nitric oxide synthase 1, neuronal	Mus musculus	142-163
31223486-12	2019	Vascular relaxation after PCI34051 treatment was more dependent on vascular endothelial cells and it was blocked by an NO synthase (NOS) inhibitor.	PCI 34051	26-34	nitric oxide synthase 1, neuronal	Mus musculus	119-130
30926374-3	2019	Intrathecal administration of the nNOS-PSD95 interactions inhibitor, IC87201 on post-operative days 0-3 significantly reduced the CCI-induced increase in total NO levels in the lumbar spinal cord dorsal horn.	CCI	130-133	nitric oxide synthase 1, neuronal	Mus musculus	34-38
31160584-2	2019	CAPON is an adaptor protein of neuronal nitric oxide synthase (nNOS), and activated by the N-methyl-D-aspartate receptor.	N-Methylaspartate	91-111	nitric oxide synthase 1, neuronal	Mus musculus	31-61
31160584-2	2019	CAPON is an adaptor protein of neuronal nitric oxide synthase (nNOS), and activated by the N-methyl-D-aspartate receptor.	N-Methylaspartate	91-111	nitric oxide synthase 1, neuronal	Mus musculus	63-67
30399595-5	2019	Moreover, l-Arginine (a NO precursor; 750 mg/kg) or L-NAME (a non-selective nitric oxide synthase (NOS) inhibitor, 10 mg/kg) administration by itself decreased the immobility time in the FST.	NG-Nitroarginine Methyl Ester	52-58	nitric oxide synthase 1, neuronal	Mus musculus	76-97
30716330-10	2019	Also, combined blockade of COX and neuronal NOS (nNOS) blunted acetylcholine-induced vasodilation, while combined COX and inducible NOS (iNOS) inhibition had no effect.	Acetylcholine	63-76	nitric oxide synthase 1, neuronal	Mus musculus	35-47
30716330-10	2019	Also, combined blockade of COX and neuronal NOS (nNOS) blunted acetylcholine-induced vasodilation, while combined COX and inducible NOS (iNOS) inhibition had no effect.	Acetylcholine	63-76	nitric oxide synthase 1, neuronal	Mus musculus	49-53
30867247-2	2019	We propose that sodium-glucose cotransporter 1 (SGLT1) senses increases in luminal glucose at the macula densa, enhancing generation of neuronal nitric oxide synthase 1 (NOS1)-dependent nitric oxide (NO) in the macula densa and blunting the tubuloglomerular feedback (TGF) response, thereby promoting the rise in GFR.	Glucose	23-30	nitric oxide synthase 1, neuronal	Mus musculus	170-174
30867247-2	2019	We propose that sodium-glucose cotransporter 1 (SGLT1) senses increases in luminal glucose at the macula densa, enhancing generation of neuronal nitric oxide synthase 1 (NOS1)-dependent nitric oxide (NO) in the macula densa and blunting the tubuloglomerular feedback (TGF) response, thereby promoting the rise in GFR.	Nitric Oxide	145-157	nitric oxide synthase 1, neuronal	Mus musculus	170-174
30867247-7	2019	In addition, we demonstrated that glucose increases NOS1 expression and NOS1 phosphorylation at Ser1417 in mouse renal cortex and cultured human kidney tissue.	Glucose	34-41	nitric oxide synthase 1, neuronal	Mus musculus	52-56
30867247-7	2019	In addition, we demonstrated that glucose increases NOS1 expression and NOS1 phosphorylation at Ser1417 in mouse renal cortex and cultured human kidney tissue.	Glucose	34-41	nitric oxide synthase 1, neuronal	Mus musculus	72-76
30867247-9	2019	CONCLUSIONS: We identified a novel mechanism of acute hyperglycemia-induced hyperfiltration wherein increases in luminal glucose at the macula densa upregulate the expression and activity of NOS1 via SGLT1, blunting the TGF response and promoting glomerular hyperfiltration.	Glucose	121-128	nitric oxide synthase 1, neuronal	Mus musculus	191-195
30654106-7	2019	The results demonstrated a decrease in nNOS expression only in control mice treated with progesterone.	Progesterone	89-101	nitric oxide synthase 1, neuronal	Mus musculus	39-43
30611765-7	2019	This pathway culminated with nitric oxide and hydrogen peroxide production by neuronal nitric oxide synthase, being hydrogen peroxide most relevant for the anti-contractile effect of perivascular adipose tissue.	Hydrogen Peroxide	46-63	nitric oxide synthase 1, neuronal	Mus musculus	78-108
30611765-7	2019	This pathway culminated with nitric oxide and hydrogen peroxide production by neuronal nitric oxide synthase, being hydrogen peroxide most relevant for the anti-contractile effect of perivascular adipose tissue.	Hydrogen Peroxide	116-133	nitric oxide synthase 1, neuronal	Mus musculus	78-108
30728077-3	2019	Levels of arginine are regulated by the enzymes arginase 1,2 and nitric oxide synthase (NOS).	Arginine	10-18	nitric oxide synthase 1, neuronal	Mus musculus	65-86
29486595-2	2019	We previously found that NAADP activates the neuronal type of nitric oxide (NO) synthase (nNOS), the product of which, NO, activates guanylyl cyclase to produce cyclic guanosine monophosphate (cGMP), which, in turn, induces cADPR formation.	NAADP	25-30	nitric oxide synthase 1, neuronal	Mus musculus	90-94
29486595-2	2019	We previously found that NAADP activates the neuronal type of nitric oxide (NO) synthase (nNOS), the product of which, NO, activates guanylyl cyclase to produce cyclic guanosine monophosphate (cGMP), which, in turn, induces cADPR formation.	Nitric Oxide	62-74	nitric oxide synthase 1, neuronal	Mus musculus	90-94
29486595-2	2019	We previously found that NAADP activates the neuronal type of nitric oxide (NO) synthase (nNOS), the product of which, NO, activates guanylyl cyclase to produce cyclic guanosine monophosphate (cGMP), which, in turn, induces cADPR formation.	Cyclic GMP	161-191	nitric oxide synthase 1, neuronal	Mus musculus	90-94
29486595-2	2019	We previously found that NAADP activates the neuronal type of nitric oxide (NO) synthase (nNOS), the product of which, NO, activates guanylyl cyclase to produce cyclic guanosine monophosphate (cGMP), which, in turn, induces cADPR formation.	Cyclic GMP	193-197	nitric oxide synthase 1, neuronal	Mus musculus	90-94
29486595-4	2019	RESULTS: We show that NAADP-induced cGMP production by nNOS activation is dependent on carbon monoxide (CO) formation by heme oxygenase-2 (HO-2).	NAADP	22-27	nitric oxide synthase 1, neuronal	Mus musculus	55-59
29486595-4	2019	RESULTS: We show that NAADP-induced cGMP production by nNOS activation is dependent on carbon monoxide (CO) formation by heme oxygenase-2 (HO-2).	Cyclic GMP	36-40	nitric oxide synthase 1, neuronal	Mus musculus	55-59
29486595-4	2019	RESULTS: We show that NAADP-induced cGMP production by nNOS activation is dependent on carbon monoxide (CO) formation by heme oxygenase-2 (HO-2).	Carbon Monoxide	87-102	nitric oxide synthase 1, neuronal	Mus musculus	55-59
29486595-4	2019	RESULTS: We show that NAADP-induced cGMP production by nNOS activation is dependent on carbon monoxide (CO) formation by heme oxygenase-2 (HO-2).	Carbon Monoxide	104-106	nitric oxide synthase 1, neuronal	Mus musculus	55-59
30299277-4	2019	Therefore, the aim of this study was to verify if the antidepressant-like effect induced by a TRPV1 antagonist in mice submitted to the forced swimming test (FST) would be facilitated by combined treatment with neuronal nitric oxide synthase (nNOS) inhibition and N-methyl-D-aspartate (NMDA) blockade.	N-Methylaspartate	264-284	nitric oxide synthase 1, neuronal	Mus musculus	243-247
30299277-4	2019	Therefore, the aim of this study was to verify if the antidepressant-like effect induced by a TRPV1 antagonist in mice submitted to the forced swimming test (FST) would be facilitated by combined treatment with neuronal nitric oxide synthase (nNOS) inhibition and N-methyl-D-aspartate (NMDA) blockade.	N-Methylaspartate	286-290	nitric oxide synthase 1, neuronal	Mus musculus	211-241
30299277-4	2019	Therefore, the aim of this study was to verify if the antidepressant-like effect induced by a TRPV1 antagonist in mice submitted to the forced swimming test (FST) would be facilitated by combined treatment with neuronal nitric oxide synthase (nNOS) inhibition and N-methyl-D-aspartate (NMDA) blockade.	N-Methylaspartate	286-290	nitric oxide synthase 1, neuronal	Mus musculus	243-247
30292770-10	2019	Glutamate acting through the NMDA receptor has been found to regulate the expression of enzyme neuronal nitric oxide synthase (nNOS), which is responsible for the release of nitric oxide (NO), suggesting a possible link between NO and GSK-3 also.	Glutamic Acid	0-9	nitric oxide synthase 1, neuronal	Mus musculus	95-125
30292770-10	2019	Glutamate acting through the NMDA receptor has been found to regulate the expression of enzyme neuronal nitric oxide synthase (nNOS), which is responsible for the release of nitric oxide (NO), suggesting a possible link between NO and GSK-3 also.	Glutamic Acid	0-9	nitric oxide synthase 1, neuronal	Mus musculus	127-131
30292770-10	2019	Glutamate acting through the NMDA receptor has been found to regulate the expression of enzyme neuronal nitric oxide synthase (nNOS), which is responsible for the release of nitric oxide (NO), suggesting a possible link between NO and GSK-3 also.	Nitric Oxide	104-116	nitric oxide synthase 1, neuronal	Mus musculus	127-131
30523577-0	2019	Striatal Protection in nNOS Knock-Out Mice After Quinolinic Acid-Induced Oxidative Damage.	Quinolinic Acid	49-64	nitric oxide synthase 1, neuronal	Mus musculus	23-27
30523577-2	2019	The participation of neuronal nitric oxide synthase (nNOS) in the neurodegeneration mechanism has been reported; the activation of N-methyl-D-aspartate (NMDA) receptors by agonist quinolinic acid (QUIN) triggers an increase in nNOS function and promotes oxidative stress.	Quinolinic Acid	180-195	nitric oxide synthase 1, neuronal	Mus musculus	21-51
30523577-2	2019	The participation of neuronal nitric oxide synthase (nNOS) in the neurodegeneration mechanism has been reported; the activation of N-methyl-D-aspartate (NMDA) receptors by agonist quinolinic acid (QUIN) triggers an increase in nNOS function and promotes oxidative stress.	Quinolinic Acid	180-195	nitric oxide synthase 1, neuronal	Mus musculus	53-57
30523577-2	2019	The participation of neuronal nitric oxide synthase (nNOS) in the neurodegeneration mechanism has been reported; the activation of N-methyl-D-aspartate (NMDA) receptors by agonist quinolinic acid (QUIN) triggers an increase in nNOS function and promotes oxidative stress.	Quinolinic Acid	180-195	nitric oxide synthase 1, neuronal	Mus musculus	227-231
30523577-2	2019	The participation of neuronal nitric oxide synthase (nNOS) in the neurodegeneration mechanism has been reported; the activation of N-methyl-D-aspartate (NMDA) receptors by agonist quinolinic acid (QUIN) triggers an increase in nNOS function and promotes oxidative stress.	Quinolinic Acid	197-201	nitric oxide synthase 1, neuronal	Mus musculus	21-51
30523577-2	2019	The participation of neuronal nitric oxide synthase (nNOS) in the neurodegeneration mechanism has been reported; the activation of N-methyl-D-aspartate (NMDA) receptors by agonist quinolinic acid (QUIN) triggers an increase in nNOS function and promotes oxidative stress.	Quinolinic Acid	197-201	nitric oxide synthase 1, neuronal	Mus musculus	53-57
30523577-2	2019	The participation of neuronal nitric oxide synthase (nNOS) in the neurodegeneration mechanism has been reported; the activation of N-methyl-D-aspartate (NMDA) receptors by agonist quinolinic acid (QUIN) triggers an increase in nNOS function and promotes oxidative stress.	Quinolinic Acid	197-201	nitric oxide synthase 1, neuronal	Mus musculus	227-231
30523577-3	2019	The aim of the present work was to elucidate the participation of nNOS in QUIN-induced oxidative stress in knock-out mice (nNOS-/-).	Quinolinic Acid	74-78	nitric oxide synthase 1, neuronal	Mus musculus	66-70
30523577-5	2019	We found that the absence of nNOS provides a protection against striatal oxidative damage induced by QUIN, resulting in decreased circling behavior, oxidative stress, and a partial protection reflected in GABA depletion.	Quinolinic Acid	101-105	nitric oxide synthase 1, neuronal	Mus musculus	29-33
30523577-5	2019	We found that the absence of nNOS provides a protection against striatal oxidative damage induced by QUIN, resulting in decreased circling behavior, oxidative stress, and a partial protection reflected in GABA depletion.	gamma-Aminobutyric Acid	205-209	nitric oxide synthase 1, neuronal	Mus musculus	29-33
30523577-6	2019	We have shown that nNOS-derived NO is involved in neurological damage induced by oxidative stress in a QUIN-excitotoxic model.	Quinolinic Acid	103-107	nitric oxide synthase 1, neuronal	Mus musculus	19-23
30692916-9	2018	In contrast, inhibiting NO synthase (NOS) revealed the facial stimulation-induced MLI-PC LTD in EtOH consumption mice.	Ethanol	96-100	nitric oxide synthase 1, neuronal	Mus musculus	24-35
30035318-3	2018	However, little is known about the role of the nitric oxide (NO) mediator, induced by the enzyme nitric oxide synthase (NOS), in strongyloidiasis.	Nitric Oxide	47-59	nitric oxide synthase 1, neuronal	Mus musculus	97-118
30236052-4	2019	Since nitric oxide synthase (NOS) has been implicated in the regulation of glucose uptake during ex vivo and in situ muscle contractions and during exercise, and NO is increased with stretch, we examined whether the increase in muscle glucose uptake during stretching involves NOS.	Glucose	75-82	nitric oxide synthase 1, neuronal	Mus musculus	6-27
30744883-6	2019	Immunoreactivity of nNOS and Hsp70 including NF-kappaB mRNA expression increased in the PVN of PQ treated mice.	Paraquat	95-97	nitric oxide synthase 1, neuronal	Mus musculus	20-24
30236872-7	2018	Finally, we showed that inhibition of Sirt1 expression by EX527 attenuated arginine-induced increase in the protein levels of phospho-AMPK and slow MyHC, the mRNA level of nitric oxide synthase (NOS) and the contents of NOS and NO, as well as decrease in fast MyHC protein level.	Arginine	75-83	nitric oxide synthase 1, neuronal	Mus musculus	172-193
29629511-0	2018	Repeated Administration of 3,4-Methylenedioxymethamphetamine (MDMA) Elevates the Levels of Neuronal Nitric Oxide Synthase in the Nigrostriatal System: Possible Relevance to Neurotoxicity.	N-Methyl-3,4-methylenedioxyamphetamine	27-60	nitric oxide synthase 1, neuronal	Mus musculus	91-121
29629511-0	2018	Repeated Administration of 3,4-Methylenedioxymethamphetamine (MDMA) Elevates the Levels of Neuronal Nitric Oxide Synthase in the Nigrostriatal System: Possible Relevance to Neurotoxicity.	N-Methyl-3,4-methylenedioxyamphetamine	62-66	nitric oxide synthase 1, neuronal	Mus musculus	91-121
29629511-3	2018	To further elucidate this issue, we evaluated the levels of the enzyme nitric oxide synthase (nNOS), which catalyzes the production of NO, in mice treated with regimens of MDMA that induce progressive and persistent neurotoxicity in the dopaminergic nigrostriatal system.	N-Methyl-3,4-methylenedioxyamphetamine	172-176	nitric oxide synthase 1, neuronal	Mus musculus	94-98
29629511-7	2018	MDMA elevated the numbers of nNOS-positive neurons in the CPu of mice that received 28 or 36 drug administrations.	N-Methyl-3,4-methylenedioxyamphetamine	0-4	nitric oxide synthase 1, neuronal	Mus musculus	29-33
29629511-9	2018	Moreover, MDMA elevated the numbers of nNOS-positive neurons in the SNc.	N-Methyl-3,4-methylenedioxyamphetamine	10-14	nitric oxide synthase 1, neuronal	Mus musculus	39-43
30145742-6	2018	Both modulatory effects were blunted by pretreatment of L-NAME [nonspecific nitric oxide synthase (NOS) inhibitor; 10 mg/kg, i.p.	NG-Nitroarginine Methyl Ester	56-62	nitric oxide synthase 1, neuronal	Mus musculus	76-97
30456249-3	2018	nNOS+ and MOCK cells were exposed to proteostasis stress by treatment with rapamycin or serum-free starvation.	Sirolimus	75-84	nitric oxide synthase 1, neuronal	Mus musculus	0-4
30193808-6	2018	Systemic pre-treatment (but not post-treatment) of ZL006, a small molecule that disrupts PSD-95-nNOS interaction, alleviated these pain hypersensitivities.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	51-56	nitric oxide synthase 1, neuronal	Mus musculus	96-100
30193808-8	2018	Mechanistically, ZL006 blocked the hemorrhage-induced increase of binding of PSD-95 with nNOS and membrane translocation of nNOS in thalamic neurons.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	17-22	nitric oxide synthase 1, neuronal	Mus musculus	89-93
30193808-8	2018	Mechanistically, ZL006 blocked the hemorrhage-induced increase of binding of PSD-95 with nNOS and membrane translocation of nNOS in thalamic neurons.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	17-22	nitric oxide synthase 1, neuronal	Mus musculus	124-128
30125872-2	2018	Nitric oxide (NO), which is generated by nitric oxide synthase (NOS), has been considered to modulate learning and memory.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	41-62
30254218-3	2018	A1 competes with nitric oxide synthase (NOS) for their common substrate L-arginine.	Arginine	72-82	nitric oxide synthase 1, neuronal	Mus musculus	17-38
30249002-7	2018	In kidney, insulin infusion: (1) increased total and phosphorylated (serine-1177) endothelial nitric oxide synthase (eNOS) band densities; (2) reduced band density of the uncoupled form of eNOS; and (3) increased renal homogenate nitric oxide synthase (NOS) activity.	Serine	69-75	nitric oxide synthase 1, neuronal	Mus musculus	94-115
29751018-1	2018	The interaction between distinctive nitric oxide synthase (NOS) isoforms and the dopamine system provides new avenues to the development of pharmacological tools for the pathophysiological conditions of the dopaminergic system.	Dopamine	81-89	nitric oxide synthase 1, neuronal	Mus musculus	36-57
29957842-4	2018	The objective of this study was to determine whether a null mutation of neuronal nitric oxide synthase (nNOS) can increase the vulnerability of some brain regions, but not others, to alcohol-induced neuronal losses.	Alcohols	183-190	nitric oxide synthase 1, neuronal	Mus musculus	72-102
29957842-4	2018	The objective of this study was to determine whether a null mutation of neuronal nitric oxide synthase (nNOS) can increase the vulnerability of some brain regions, but not others, to alcohol-induced neuronal losses.	Alcohols	183-190	nitric oxide synthase 1, neuronal	Mus musculus	104-108
29957842-10	2018	However, null mutation of nNOS more than doubled alcohol-induced cell death in the olfactory bulb granule cells, while the mutation had no effect on the facial nucleus neurons.	Alcohols	49-56	nitric oxide synthase 1, neuronal	Mus musculus	26-30
29957842-11	2018	As a result, in nNOS-/- mice, alcohol caused substantially more cell loss in the olfactory bulb than in the facial nucleus.	Alcohols	30-37	nitric oxide synthase 1, neuronal	Mus musculus	16-20
29957842-12	2018	CONCLUSIONS: Mutation of the nNOS gene substantially increases vulnerability to alcohol-induced cell loss in a brain region where the gene is expressed (olfactory bulb), but not in a separate brain region, where the gene is not expressed (facial nucleus).	Alcohols	80-87	nitric oxide synthase 1, neuronal	Mus musculus	29-33
30127396-1	2019	Neuronal and endothelial nitric oxide synthases (nNOS and eNOS respectively) play major roles in generating the nitric oxide bioactivity necessary for erectile function.	Nitric Oxide	25-37	nitric oxide synthase 1, neuronal	Mus musculus	49-53
31574503-2	2019	Conversely, elevated luminal shear stress (SS) promotes outward remodeling of arteries in vivo and prevents inward remodeling in culture in a nitric oxide synthase (NOS)-dependent manner.	Phenobarbital	21-28	nitric oxide synthase 1, neuronal	Mus musculus	142-163
30503614-0	2019	Neuronal nitric oxide synthase (nNOS) splice variant function: Insights into nitric oxide signaling from skeletal muscle.	Nitric Oxide	9-21	nitric oxide synthase 1, neuronal	Mus musculus	32-36
30503614-4	2019	The first focus of this review is how the differential targeting of nNOS splice variants creates spatially and functionally distinct nitric oxide (NO) signaling compartments at the sarcolemma, Golgi complex, and cytoplasm.	Nitric Oxide	133-145	nitric oxide synthase 1, neuronal	Mus musculus	68-72
30503614-6	2019	The second major focus is to review current understanding of cGMP-mediated nNOS signaling in skeletal muscle and its emergence as a therapeutic target in DMD and BMD.	Cyclic GMP	61-65	nitric oxide synthase 1, neuronal	Mus musculus	75-79
30320383-5	2018	Furthermore, the results of ELISA and western blot analysis demonstrated that EGCG administration restored acetylcholinesterase activity and modulated the expression levels of neuronal nitric oxide synthase (nNOS), beta-amyloid and amyloid precursor protein in anesthesia-induced mice.	epigallocatechin gallate	78-82	nitric oxide synthase 1, neuronal	Mus musculus	176-206
30320383-5	2018	Furthermore, the results of ELISA and western blot analysis demonstrated that EGCG administration restored acetylcholinesterase activity and modulated the expression levels of neuronal nitric oxide synthase (nNOS), beta-amyloid and amyloid precursor protein in anesthesia-induced mice.	epigallocatechin gallate	78-82	nitric oxide synthase 1, neuronal	Mus musculus	208-212
30320383-6	2018	The present study also employed L-arginine as an nNOS substrate and 7-nitroindazole as an nNOS inhibitor, which were demonstrated to inhibit or potentiate the effects of EGCG, respectively, on anesthesia-induced memory deficit in mice.	7-nitroindazole	68-83	nitric oxide synthase 1, neuronal	Mus musculus	90-94
30320383-6	2018	The present study also employed L-arginine as an nNOS substrate and 7-nitroindazole as an nNOS inhibitor, which were demonstrated to inhibit or potentiate the effects of EGCG, respectively, on anesthesia-induced memory deficit in mice.	epigallocatechin gallate	170-174	nitric oxide synthase 1, neuronal	Mus musculus	90-94
29298528-1	2018	CONTEXT: Exogenous nitrogen oxides must be made bioavailable to sustain normal physiology because nitric oxide synthase (NOS) deficient mice are viable.	Nitrogen Oxides	19-34	nitric oxide synthase 1, neuronal	Mus musculus	98-119
30196988-10	2018	HEMA inhibited the LPS-stimulated expression of NOS (nitric oxide synthase) to produce NO but counteracted the expression of Nox2, which forms superoxide anions that combine with NO to peroxynitrite.	hydroxyethyl methacrylate	0-4	nitric oxide synthase 1, neuronal	Mus musculus	53-74
30055993-2	2018	Arginase competes with nitric oxide synthase for substrate arginine to produce orthinine and urea.	Arginine	59-67	nitric oxide synthase 1, neuronal	Mus musculus	23-44
30150925-3	2018	Here, stereology was used to quantify the number of nNOS-expressing interneurons in valproic acid (VPA)-exposed C57BL/6J (B6) and BTBR T+Itpr3tf/J (BTBR) mice models of autism.	Valproic Acid	84-97	nitric oxide synthase 1, neuronal	Mus musculus	52-56
30150925-3	2018	Here, stereology was used to quantify the number of nNOS-expressing interneurons in valproic acid (VPA)-exposed C57BL/6J (B6) and BTBR T+Itpr3tf/J (BTBR) mice models of autism.	Valproic Acid	99-102	nitric oxide synthase 1, neuronal	Mus musculus	52-56
30079374-8	2018	These results indicate that estradiol acts directly on GnRH neurons via the ERbeta/Akt/nNOS pathway at proestrus afternoon generating NO that retrogradely accelerates GABA and glutamate release from the presynaptic terminals contacting GnRH neurons.	Estradiol	28-37	nitric oxide synthase 1, neuronal	Mus musculus	87-91
30079374-8	2018	These results indicate that estradiol acts directly on GnRH neurons via the ERbeta/Akt/nNOS pathway at proestrus afternoon generating NO that retrogradely accelerates GABA and glutamate release from the presynaptic terminals contacting GnRH neurons.	gamma-Aminobutyric Acid	167-171	nitric oxide synthase 1, neuronal	Mus musculus	87-91
30079374-8	2018	These results indicate that estradiol acts directly on GnRH neurons via the ERbeta/Akt/nNOS pathway at proestrus afternoon generating NO that retrogradely accelerates GABA and glutamate release from the presynaptic terminals contacting GnRH neurons.	Glutamic Acid	176-185	nitric oxide synthase 1, neuronal	Mus musculus	87-91
30055993-1	2018	Arginine is a semi-essential amino acid which serves as a substrate for nitric oxide (NO) production by nitric oxide synthase (NOS) and a precursor for various metabolites including ornithine, creatine, polyamines, and agmatine.	Arginine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	104-125
30055993-1	2018	Arginine is a semi-essential amino acid which serves as a substrate for nitric oxide (NO) production by nitric oxide synthase (NOS) and a precursor for various metabolites including ornithine, creatine, polyamines, and agmatine.	Nitric Oxide	72-84	nitric oxide synthase 1, neuronal	Mus musculus	104-125
30055993-2	2018	Arginase competes with nitric oxide synthase for substrate arginine to produce orthinine and urea.	orthinine	79-88	nitric oxide synthase 1, neuronal	Mus musculus	23-44
30055993-2	2018	Arginase competes with nitric oxide synthase for substrate arginine to produce orthinine and urea.	Urea	93-97	nitric oxide synthase 1, neuronal	Mus musculus	23-44
29909247-7	2018	The 6-OHDA-induced increases in nigrostriatal expression of inducible nitric oxide synthase (iNOS) and decreases in that of nNOS were also reversed by honokiol posttreatment.	Oxidopamine	4-10	nitric oxide synthase 1, neuronal	Mus musculus	124-128
29909247-7	2018	The 6-OHDA-induced increases in nigrostriatal expression of inducible nitric oxide synthase (iNOS) and decreases in that of nNOS were also reversed by honokiol posttreatment.	honokiol	151-159	nitric oxide synthase 1, neuronal	Mus musculus	124-128
29361881-7	2018	Also, regulating the NF-kappaB pathway, DMF treatment decreased the severity of inflammation through a modulation of neuronal nitric oxide synthase, interleukin 1, tumor necrosis factor, cyclooxygenase 2, and myeloperoxidase activity, reducing ionized calcium-binding adapter molecule 1 and glial fibrillary acidic protein expression.	Dimethyl Fumarate	40-43	nitric oxide synthase 1, neuronal	Mus musculus	117-147
30105819-10	2018	In WT and cav-1 KO, dilation to ACh was enhanced by MO through increased role for NOS and cyclooxygenase.	Acetylcholine	32-35	nitric oxide synthase 1, neuronal	Mus musculus	82-104
29525685-0	2018	Involvement of neuronal nitric oxide synthase in cross-sensitization between chronic unpredictable stress and ethanol in adolescent and adult mice.	Ethanol	110-117	nitric oxide synthase 1, neuronal	Mus musculus	15-45
29768197-2	2018	Argininosuccinate lyase (ASL) is the only enzyme able to produce arginine, the substrate for NO generation by nitric oxide synthase (NOS) isoforms.	Arginine	65-73	nitric oxide synthase 1, neuronal	Mus musculus	110-131
29266319-2	2018	L-arginine can be metabolized by NO synthase (NOS) to form L-citrulline and NO, a potent vasodilator.	Arginine	0-10	nitric oxide synthase 1, neuronal	Mus musculus	33-44
29266319-2	2018	L-arginine can be metabolized by NO synthase (NOS) to form L-citrulline and NO, a potent vasodilator.	Citrulline	59-71	nitric oxide synthase 1, neuronal	Mus musculus	33-44
29525685-6	2018	A neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7NI), was administered along with ethanol and CUS to test its effects on behavioral sensitization.	7-nitroindazole	51-66	nitric oxide synthase 1, neuronal	Mus musculus	2-32
29525685-6	2018	A neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7NI), was administered along with ethanol and CUS to test its effects on behavioral sensitization.	7-nitroindazole	51-66	nitric oxide synthase 1, neuronal	Mus musculus	34-38
29525685-6	2018	A neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7NI), was administered along with ethanol and CUS to test its effects on behavioral sensitization.	7-nitroindazole	68-71	nitric oxide synthase 1, neuronal	Mus musculus	2-32
29525685-6	2018	A neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7NI), was administered along with ethanol and CUS to test its effects on behavioral sensitization.	7-nitroindazole	68-71	nitric oxide synthase 1, neuronal	Mus musculus	34-38
29525685-8	2018	nNOS inhibition by 7NI reduced both ethanol sensitization and cross-sensitization.	7ni reduced	19-30	nitric oxide synthase 1, neuronal	Mus musculus	0-4
29525685-8	2018	nNOS inhibition by 7NI reduced both ethanol sensitization and cross-sensitization.	Ethanol	36-43	nitric oxide synthase 1, neuronal	Mus musculus	0-4
29121483-8	2018	High concentrations of NCG (1.0mM) and ARG (4.0mM) inhibited (P&lt;0.05) GnRH and nNOS mRNA abundance in GT1-7 cells.	Arginine	39-42	nitric oxide synthase 1, neuronal	Mus musculus	82-86
29476751-12	2018	injection of NG-nitro-l-arginine methyl ester [a nonselective nitric oxide synthetase (NOS) inhibitor] significantly blocked mechanical allodynia on day 3 after BCAO and i.t.	NG-Nitroarginine Methyl Ester	13-45	nitric oxide synthase 1, neuronal	Mus musculus	62-85
29447430-12	2018	CONCLUSIONS AND IMPLICATIONS: Aucubin suppresses oxidative stress during cardiac remodelling by increasing the expression of nNOS in a process that requires activation of the beta3 -adrenoceptor/AC/cAMP pathway.	Cyclic AMP	198-202	nitric oxide synthase 1, neuronal	Mus musculus	125-129
29378248-2	2018	Mice with a NOS1 knockout have markedly reduced muscle nitrate levels, suggesting NO production by NOS and its reaction with oxymyoglobin as a source of nitrate.	Nitrates	55-62	nitric oxide synthase 1, neuronal	Mus musculus	12-16
29378248-2	2018	Mice with a NOS1 knockout have markedly reduced muscle nitrate levels, suggesting NO production by NOS and its reaction with oxymyoglobin as a source of nitrate.	Nitrates	153-160	nitric oxide synthase 1, neuronal	Mus musculus	12-16
29410249-7	2018	The anti-convulsant effects of sumatriptan was potentiated by L-NAME, a non-selective NOS inhibitor, 7-NI, a selective nNOS inhibitor, but not AG, an iNOS inhibitor.	Sumatriptan	31-42	nitric oxide synthase 1, neuronal	Mus musculus	119-123
29167164-1	2018	Nuclear factor erythyroid factor 2 (Nrf2) transcribes genes in cultured endothelial cells that reduce reactive oxygen species (ROS) and generate nitric oxide (NO) or metabolize asymmetric dimethylarginine (ADMA), which inhibits NO synthase (NOS).	Reactive Oxygen Species	102-125	nitric oxide synthase 1, neuronal	Mus musculus	228-239
29410249-7	2018	The anti-convulsant effects of sumatriptan was potentiated by L-NAME, a non-selective NOS inhibitor, 7-NI, a selective nNOS inhibitor, but not AG, an iNOS inhibitor.	7-nitroindazole	101-105	nitric oxide synthase 1, neuronal	Mus musculus	119-123
29410249-11	2018	Our data revealed that anti-convulsive effects of sumatriptan is mediated by interaction between non-serotonergic 5-HT1B/D receptors and nNOS/NO pathway.	Sumatriptan	50-61	nitric oxide synthase 1, neuronal	Mus musculus	137-141
29223784-9	2018	Thalidomide alone or in combination with PI3K inhibitor, Akt inhibitor or nitric oxide synthase (NOS) inhibitors significantly reduced naloxone induced withdrawal signs in morphine dependent mice.	Thalidomide	0-11	nitric oxide synthase 1, neuronal	Mus musculus	74-95
29223784-9	2018	Thalidomide alone or in combination with PI3K inhibitor, Akt inhibitor or nitric oxide synthase (NOS) inhibitors significantly reduced naloxone induced withdrawal signs in morphine dependent mice.	Naloxone	135-143	nitric oxide synthase 1, neuronal	Mus musculus	74-95
29102713-3	2018	For this purpose, acute and chronic effect of lithium in seizure animal model and the interaction of NMDA receptor antagonist (MK-801) and neuronal nitric oxide synthase (nNOS) inhibitor (7-NI) with these neuroprotection has been studied.	7-nitroindazole	188-192	nitric oxide synthase 1, neuronal	Mus musculus	139-169
29102713-3	2018	For this purpose, acute and chronic effect of lithium in seizure animal model and the interaction of NMDA receptor antagonist (MK-801) and neuronal nitric oxide synthase (nNOS) inhibitor (7-NI) with these neuroprotection has been studied.	7-nitroindazole	188-192	nitric oxide synthase 1, neuronal	Mus musculus	171-175
29487540-4	2018	About 8% of all myenteric neurons were found to be GABA-immunoreactive (GABA+) including some Calretinin+ and some neuronal nitric oxide synthase (nNOS+) neurons.	gamma-Aminobutyric Acid	51-55	nitric oxide synthase 1, neuronal	Mus musculus	115-145
29487540-6	2018	Exogenous GABA increased the intracellular calcium concentration, [Ca2+]i of some myenteric neurons including many that did not express GABA or nNOS (the majority), some GABA+, Calretinin+ or Neurofilament-M (NFM)+ but rarely nNOS+ neurons.	gamma-Aminobutyric Acid	10-14	nitric oxide synthase 1, neuronal	Mus musculus	226-230
29167164-1	2018	Nuclear factor erythyroid factor 2 (Nrf2) transcribes genes in cultured endothelial cells that reduce reactive oxygen species (ROS) and generate nitric oxide (NO) or metabolize asymmetric dimethylarginine (ADMA), which inhibits NO synthase (NOS).	Reactive Oxygen Species	127-130	nitric oxide synthase 1, neuronal	Mus musculus	228-239
29167164-1	2018	Nuclear factor erythyroid factor 2 (Nrf2) transcribes genes in cultured endothelial cells that reduce reactive oxygen species (ROS) and generate nitric oxide (NO) or metabolize asymmetric dimethylarginine (ADMA), which inhibits NO synthase (NOS).	Nitric Oxide	145-157	nitric oxide synthase 1, neuronal	Mus musculus	228-239
29167164-1	2018	Nuclear factor erythyroid factor 2 (Nrf2) transcribes genes in cultured endothelial cells that reduce reactive oxygen species (ROS) and generate nitric oxide (NO) or metabolize asymmetric dimethylarginine (ADMA), which inhibits NO synthase (NOS).	dimethylarginine	188-204	nitric oxide synthase 1, neuronal	Mus musculus	228-239
29167164-1	2018	Nuclear factor erythyroid factor 2 (Nrf2) transcribes genes in cultured endothelial cells that reduce reactive oxygen species (ROS) and generate nitric oxide (NO) or metabolize asymmetric dimethylarginine (ADMA), which inhibits NO synthase (NOS).	N,N-dimethylarginine	206-210	nitric oxide synthase 1, neuronal	Mus musculus	228-239
29053192-0	2018	Dissociation of nNOS from PSD-95 promotes functional recovery after cerebral ischaemia in mice through reducing excessive tonic GABA release from reactive astrocytes.	gamma-Aminobutyric Acid	128-132	nitric oxide synthase 1, neuronal	Mus musculus	16-20
29053192-7	2018	Treatments with Tat-nNOS-N1-133 or ZL006 after ischaemia inhibited astrocyte activation and GABA production, prevented the reversal of GAT-3/4, and consequently decreased excessive tonic inhibition and ameliorated functional outcome.	gamma-Aminobutyric Acid	92-96	nitric oxide synthase 1, neuronal	Mus musculus	20-24
28815720-3	2018	Chloroquine stimulates neuronal nitric oxide synthase (nNOS) activity to over-producing NO in the skin.	Chloroquine	0-11	nitric oxide synthase 1, neuronal	Mus musculus	55-59
29193716-8	2018	The effect of ATAin vivo and ex vivo was abolished by the neuronal nitric oxide synthase (nNOS) inhibitor Vinyl-l-NIO.	N(5)-(1-imino-3-butenyl)ornithine	106-117	nitric oxide synthase 1, neuronal	Mus musculus	58-88
29193716-8	2018	The effect of ATAin vivo and ex vivo was abolished by the neuronal nitric oxide synthase (nNOS) inhibitor Vinyl-l-NIO.	N(5)-(1-imino-3-butenyl)ornithine	106-117	nitric oxide synthase 1, neuronal	Mus musculus	90-94
29126791-1	2018	The production of nitric oxide (NO) by nitric oxide synthases (NOS) depends on the bioavailability of L-arginine as NOS competes with arginase for this common substrate.	Nitric Oxide	18-30	nitric oxide synthase 1, neuronal	Mus musculus	39-61
29053192-9	2018	The nNOS-PSD-95 interaction is thus a potential target for functional restoration after stroke and ZL006, a small molecule inhibitor of this interaction, is a promising pharmacological lead compound.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	99-104	nitric oxide synthase 1, neuronal	Mus musculus	4-8
29126791-1	2018	The production of nitric oxide (NO) by nitric oxide synthases (NOS) depends on the bioavailability of L-arginine as NOS competes with arginase for this common substrate.	Arginine	102-112	nitric oxide synthase 1, neuronal	Mus musculus	39-61
29563358-1	2018	Localization of the nitric oxide (NO)-producing enzyme, nitric oxide synthase (NOS), and its functions are currently being investigated in several tissues and organs.	Nitric Oxide	20-32	nitric oxide synthase 1, neuronal	Mus musculus	56-77
29145710-3	2018	Given the critical role of androgens in erection physiology and NO synthase (NOS)/PDE5 expression, we hypothesized that testosterone replacement to eugonadal testosterone levels reduces priapism by reversing impaired endothelial (e)NOS activity and molecular abnormalities involving PDE5.	Testosterone	120-132	nitric oxide synthase 1, neuronal	Mus musculus	64-75
30504686-8	2018	nNOS inhibitor 7-nitroindazole (25 mg/kg, i.p.)	7-nitroindazole	15-30	nitric oxide synthase 1, neuronal	Mus musculus	0-4
29577226-0	2018	Neuronal nitric oxide synthase phosphorylation induced by docosahexaenoic acid protects dopaminergic neurons in an experimental model of Parkinson"s disease.	Docosahexaenoic Acids	58-78	nitric oxide synthase 1, neuronal	Mus musculus	0-30
29723849-8	2018	However, zingerone-induced pacemaker potential inhibition was blocked by 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ; a guanylate cyclase inhibitor), KT5823 (a protein kinase G (PKG) inhibitor), and L-NAME (a non-selective nitric oxide synthase (NOS) inhibitor).	zingerone	9-18	nitric oxide synthase 1, neuronal	Mus musculus	231-252
29723849-8	2018	However, zingerone-induced pacemaker potential inhibition was blocked by 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ; a guanylate cyclase inhibitor), KT5823 (a protein kinase G (PKG) inhibitor), and L-NAME (a non-selective nitric oxide synthase (NOS) inhibitor).	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	121-124	nitric oxide synthase 1, neuronal	Mus musculus	231-252
29577226-2	2018	The aim of this study was to investigate if the DHA acts on neurons of substantia nigra (SN) by phosphorylation of neuronal nitric oxide synthase (nNOS) in an experimental mouse model of PD.	Docosahexaenoic Acids	48-51	nitric oxide synthase 1, neuronal	Mus musculus	115-145
29577226-2	2018	The aim of this study was to investigate if the DHA acts on neurons of substantia nigra (SN) by phosphorylation of neuronal nitric oxide synthase (nNOS) in an experimental mouse model of PD.	Docosahexaenoic Acids	48-51	nitric oxide synthase 1, neuronal	Mus musculus	147-151
29577226-13	2018	DHA treatment significantly decreased nNOS and increased p-nNOS immunoreactivities in the DHA + MPTP group compared to the MPTP group.	Docosahexaenoic Acids	0-3	nitric oxide synthase 1, neuronal	Mus musculus	38-42
29577226-13	2018	DHA treatment significantly decreased nNOS and increased p-nNOS immunoreactivities in the DHA + MPTP group compared to the MPTP group.	Docosahexaenoic Acids	0-3	nitric oxide synthase 1, neuronal	Mus musculus	59-63
29577226-13	2018	DHA treatment significantly decreased nNOS and increased p-nNOS immunoreactivities in the DHA + MPTP group compared to the MPTP group.	Docosahexaenoic Acids	90-93	nitric oxide synthase 1, neuronal	Mus musculus	59-63
29577226-13	2018	DHA treatment significantly decreased nNOS and increased p-nNOS immunoreactivities in the DHA + MPTP group compared to the MPTP group.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	96-100	nitric oxide synthase 1, neuronal	Mus musculus	59-63
29577226-14	2018	CONCLUSIONS: These results indicate that DHA treatment protects dopaminergic neurons in SN via increasing nNOS serine 852 phosphorylation in the experimental mice model of PD.	Docosahexaenoic Acids	41-44	nitric oxide synthase 1, neuronal	Mus musculus	106-110
29577226-14	2018	CONCLUSIONS: These results indicate that DHA treatment protects dopaminergic neurons in SN via increasing nNOS serine 852 phosphorylation in the experimental mice model of PD.	Serine	111-117	nitric oxide synthase 1, neuronal	Mus musculus	106-110
29789101-12	2018	CONCLUSIONS: NO down-regulation possibly through iNOS and nNOS inhibition may involve in the antidepressant property of licofelone.	licofelone	120-130	nitric oxide synthase 1, neuronal	Mus musculus	58-62
29386447-3	2018	Dopamine receptor antagonists, N-methyl-D-aspartic acid (NMDA) receptor antagonists, Nitric Oxide Synthase (NOS) inhibitors and free radical scavengers significantly attenuate methamphetamine-induced SIB.	Methamphetamine	176-191	nitric oxide synthase 1, neuronal	Mus musculus	85-106
28875428-7	2018	TiNS-CBL also thwarted increased alpha-synuclein levels in the brain and in the cerebrospinal fluid (CSF) as well as neuronal nitric oxide synthase (nNOS) in the in PD brain as compared to untreated group.	tins-cbl	0-8	nitric oxide synthase 1, neuronal	Mus musculus	117-147
29032115-8	2017	Nitric Oxide Synthase (NOS) activity was measured by conversion of [3H]-l-arginine to [3H]-l-citrulline, systemic TNF-alpha levels by ELISA, and reactive oxygen species (ROS) by immunofluorescence.	[3h]-l-arginine	67-82	nitric oxide synthase 1, neuronal	Mus musculus	0-21
29183804-7	2018	We demonstrate here that acetylcholine (Ach)-induced relaxation is completely abolished by nNOS inhibition in eNOS silenced mice aorta which also decreased NO and H2O2 concentrations.	Acetylcholine	25-38	nitric oxide synthase 1, neuronal	Mus musculus	91-95
29183804-7	2018	We demonstrate here that acetylcholine (Ach)-induced relaxation is completely abolished by nNOS inhibition in eNOS silenced mice aorta which also decreased NO and H2O2 concentrations.	Acetylcholine	40-43	nitric oxide synthase 1, neuronal	Mus musculus	91-95
29183804-7	2018	We demonstrate here that acetylcholine (Ach)-induced relaxation is completely abolished by nNOS inhibition in eNOS silenced mice aorta which also decreased NO and H2O2 concentrations.	Hydrogen Peroxide	163-167	nitric oxide synthase 1, neuronal	Mus musculus	91-95
29032115-8	2017	Nitric Oxide Synthase (NOS) activity was measured by conversion of [3H]-l-arginine to [3H]-l-citrulline, systemic TNF-alpha levels by ELISA, and reactive oxygen species (ROS) by immunofluorescence.	[3h]-l-citrulline	86-103	nitric oxide synthase 1, neuronal	Mus musculus	0-21
29032115-8	2017	Nitric Oxide Synthase (NOS) activity was measured by conversion of [3H]-l-arginine to [3H]-l-citrulline, systemic TNF-alpha levels by ELISA, and reactive oxygen species (ROS) by immunofluorescence.	Reactive Oxygen Species	145-168	nitric oxide synthase 1, neuronal	Mus musculus	0-21
29032115-8	2017	Nitric Oxide Synthase (NOS) activity was measured by conversion of [3H]-l-arginine to [3H]-l-citrulline, systemic TNF-alpha levels by ELISA, and reactive oxygen species (ROS) by immunofluorescence.	Reactive Oxygen Species	170-173	nitric oxide synthase 1, neuronal	Mus musculus	0-21
28705804-7	2017	Colons from W/Wv, Nos1-/- , and Prkg1-/- mice displayed augmented neural release of purines that was likely due to altered nitrergic neuromodulation.	Purines	84-91	nitric oxide synthase 1, neuronal	Mus musculus	18-22
29158387-5	2017	Chronic nicotine treatment altered the translational profile of more than 1,000 genes in alpha5- Amigo1 neurons, including neuronal nitric oxide synthase (Nos1) and somatostatin (Sst).	Nicotine	8-16	nitric oxide synthase 1, neuronal	Mus musculus	123-153
29158387-5	2017	Chronic nicotine treatment altered the translational profile of more than 1,000 genes in alpha5- Amigo1 neurons, including neuronal nitric oxide synthase (Nos1) and somatostatin (Sst).	Nicotine	8-16	nitric oxide synthase 1, neuronal	Mus musculus	155-159
29158387-9	2017	This loss of nicotine reward was mimicked by shRNA-mediated knockdown of Nos1 in the IPN.	Nicotine	13-21	nitric oxide synthase 1, neuronal	Mus musculus	73-77
29234274-5	2017	By genetic deletion of nNOS gene, we further demonstrated that nNOS acts through peroxynitrite, an important member of reactive nitrogen species, to trigger hippocampal ER stress and oxidative damage in the PTZ-kindled mice.	Peroxynitrous Acid	81-94	nitric oxide synthase 1, neuronal	Mus musculus	23-27
29234274-5	2017	By genetic deletion of nNOS gene, we further demonstrated that nNOS acts through peroxynitrite, an important member of reactive nitrogen species, to trigger hippocampal ER stress and oxidative damage in the PTZ-kindled mice.	Peroxynitrous Acid	81-94	nitric oxide synthase 1, neuronal	Mus musculus	63-67
29234274-5	2017	By genetic deletion of nNOS gene, we further demonstrated that nNOS acts through peroxynitrite, an important member of reactive nitrogen species, to trigger hippocampal ER stress and oxidative damage in the PTZ-kindled mice.	Reactive Nitrogen Species	119-144	nitric oxide synthase 1, neuronal	Mus musculus	23-27
29234274-5	2017	By genetic deletion of nNOS gene, we further demonstrated that nNOS acts through peroxynitrite, an important member of reactive nitrogen species, to trigger hippocampal ER stress and oxidative damage in the PTZ-kindled mice.	Reactive Nitrogen Species	119-144	nitric oxide synthase 1, neuronal	Mus musculus	63-67
29234274-5	2017	By genetic deletion of nNOS gene, we further demonstrated that nNOS acts through peroxynitrite, an important member of reactive nitrogen species, to trigger hippocampal ER stress and oxidative damage in the PTZ-kindled mice.	Pentylenetetrazole	207-210	nitric oxide synthase 1, neuronal	Mus musculus	23-27
29234274-5	2017	By genetic deletion of nNOS gene, we further demonstrated that nNOS acts through peroxynitrite, an important member of reactive nitrogen species, to trigger hippocampal ER stress and oxidative damage in the PTZ-kindled mice.	Pentylenetetrazole	207-210	nitric oxide synthase 1, neuronal	Mus musculus	63-67
28778482-5	2017	These CRP-mediated detrimental effects on cell viability and insulin secretion were significantly reversed by adding NAC (a potent antioxidant), apocynin (a selective NADPH oxidase inhibitor), L-NAME (a non-selective nitric oxide synthase (NOS) inhibitor), aminoguanidine (a selective iNOS inhibitor), PDTC (a selective NFkappaB inhibitor) or Enbrel (an anti-TNFalpha fusion protein).	NG-Nitroarginine Methyl Ester	193-199	nitric oxide synthase 1, neuronal	Mus musculus	217-238
28585346-9	2017	Neuronal nitric oxide synthase (nNOS) and vasoactive intestinal polypeptide (VIP) were significantly up-regulated due to Tarc2 deficiency, contributing to enhanced nitric oxide (NO) signaling in the stomach of Tacr2-/- mice.	Nitric Oxide	9-21	nitric oxide synthase 1, neuronal	Mus musculus	32-36
28515388-1	2017	Nitric oxide (NO), generated from L-arginine by three different isoforms of nitric oxide synthase (NOS), is a pleiotropic factor to regulate physiological functions in almost every organ and tissue.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	76-97
28515388-1	2017	Nitric oxide (NO), generated from L-arginine by three different isoforms of nitric oxide synthase (NOS), is a pleiotropic factor to regulate physiological functions in almost every organ and tissue.	Arginine	34-44	nitric oxide synthase 1, neuronal	Mus musculus	76-97
29093670-6	2017	However, the PTZ kindling-induced MAPK, PI3K/AKT signaling activities and the ROS level were attenuated by nNOS gene deficiency, suggesting that nNOS may act through ROS-mediated MAPK and PI3K/AKT signaling pathways to trigger cognition deficit and depressive-like behavior in PTZ-kindled mice.	Pentylenetetrazole	13-16	nitric oxide synthase 1, neuronal	Mus musculus	107-111
29163149-10	2017	Moreover, at this regimen GYY relieved the nitrative stress, as indicated by the decreases in nitric oxide (NO) generation and neuronal NO synthase (nNOS) upregulation elicited by MPTP in the striatum.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	180-184	nitric oxide synthase 1, neuronal	Mus musculus	149-153
29093670-6	2017	However, the PTZ kindling-induced MAPK, PI3K/AKT signaling activities and the ROS level were attenuated by nNOS gene deficiency, suggesting that nNOS may act through ROS-mediated MAPK and PI3K/AKT signaling pathways to trigger cognition deficit and depressive-like behavior in PTZ-kindled mice.	Pentylenetetrazole	13-16	nitric oxide synthase 1, neuronal	Mus musculus	145-149
29093670-6	2017	However, the PTZ kindling-induced MAPK, PI3K/AKT signaling activities and the ROS level were attenuated by nNOS gene deficiency, suggesting that nNOS may act through ROS-mediated MAPK and PI3K/AKT signaling pathways to trigger cognition deficit and depressive-like behavior in PTZ-kindled mice.	Reactive Oxygen Species	78-81	nitric oxide synthase 1, neuronal	Mus musculus	145-149
29093670-6	2017	However, the PTZ kindling-induced MAPK, PI3K/AKT signaling activities and the ROS level were attenuated by nNOS gene deficiency, suggesting that nNOS may act through ROS-mediated MAPK and PI3K/AKT signaling pathways to trigger cognition deficit and depressive-like behavior in PTZ-kindled mice.	Reactive Oxygen Species	166-169	nitric oxide synthase 1, neuronal	Mus musculus	107-111
29093670-6	2017	However, the PTZ kindling-induced MAPK, PI3K/AKT signaling activities and the ROS level were attenuated by nNOS gene deficiency, suggesting that nNOS may act through ROS-mediated MAPK and PI3K/AKT signaling pathways to trigger cognition deficit and depressive-like behavior in PTZ-kindled mice.	Reactive Oxygen Species	166-169	nitric oxide synthase 1, neuronal	Mus musculus	145-149
29093670-6	2017	However, the PTZ kindling-induced MAPK, PI3K/AKT signaling activities and the ROS level were attenuated by nNOS gene deficiency, suggesting that nNOS may act through ROS-mediated MAPK and PI3K/AKT signaling pathways to trigger cognition deficit and depressive-like behavior in PTZ-kindled mice.	Pentylenetetrazole	277-280	nitric oxide synthase 1, neuronal	Mus musculus	107-111
29093670-6	2017	However, the PTZ kindling-induced MAPK, PI3K/AKT signaling activities and the ROS level were attenuated by nNOS gene deficiency, suggesting that nNOS may act through ROS-mediated MAPK and PI3K/AKT signaling pathways to trigger cognition deficit and depressive-like behavior in PTZ-kindled mice.	Pentylenetetrazole	277-280	nitric oxide synthase 1, neuronal	Mus musculus	145-149
28577305-1	2017	Neurons expressing nitric oxide (NO) synthase (nNOS) and thus capable of synthesizing NO play major roles in many aspects of brain function.	Nitric Oxide	19-31	nitric oxide synthase 1, neuronal	Mus musculus	47-51
28476660-10	2017	We conclude that these two independently characterized parallel pathways function mainly via a single series arrangement (beta-AR-cAMP-Epac-PI3K-Akt-NOS1-CaMKII) to mediate increased SR Ca2+ leak.	Cyclic AMP	130-134	nitric oxide synthase 1, neuronal	Mus musculus	149-153
28969637-9	2017	However, these effects were completely abolished by the nitric oxide synthase (NOS) inhibitor N-omega-nitro-L-arginine methyl ester.	NG-Nitroarginine Methyl Ester	94-131	nitric oxide synthase 1, neuronal	Mus musculus	56-77
28690194-2	2017	A hallmark of cardiovascular disease is attenuated NO production, which in part is caused by NO Synthase (NOS) uncoupling, which in turn increases oxidative stress because of superoxide generation.	Superoxides	175-185	nitric oxide synthase 1, neuronal	Mus musculus	93-104
28432455-9	2017	Blockade of nitric oxide synthase (NOS) and indoleamine-pyrrole-2,3-dioxygenase (IDO) improved the activation of CpG-DCs.	cpg-dcs	113-120	nitric oxide synthase 1, neuronal	Mus musculus	12-33
28746839-0	2017	Depletion of 5 hydroxy-triptamine (5-HT) affects the antidepressant-like effect of neuronal nitric oxide synthase inhibitor in mice.	Serotonin	13-33	nitric oxide synthase 1, neuronal	Mus musculus	83-113
28746839-5	2017	We also investigated if the antidepressant-like effect of nNOS inhibitor, 7NI, was dependent on hippocampal serotonin.	7-nitroindazole	74-77	nitric oxide synthase 1, neuronal	Mus musculus	58-62
28746839-5	2017	We also investigated if the antidepressant-like effect of nNOS inhibitor, 7NI, was dependent on hippocampal serotonin.	Serotonin	108-117	nitric oxide synthase 1, neuronal	Mus musculus	58-62
28541476-10	2017	Additionally, 7,8-DHF normalized striatal levels of induced and neuronal nitric oxide synthase (iNOS and nNOS, respectively) and ameliorated the imbalance of p75/TrkB.	6,7-dihydroxyflavone	14-21	nitric oxide synthase 1, neuronal	Mus musculus	64-94
28541476-10	2017	Additionally, 7,8-DHF normalized striatal levels of induced and neuronal nitric oxide synthase (iNOS and nNOS, respectively) and ameliorated the imbalance of p75/TrkB.	6,7-dihydroxyflavone	14-21	nitric oxide synthase 1, neuronal	Mus musculus	105-109
28515175-5	2017	Global NO synthase (NOS) inhibition [NG-nitro-l-arginine methyl ester (l-NAME)] reduced the ET-1 flow response; however, pharmacological inhibition of NOS1 or NOS2, inhibition of NOS3 siRNA, inhibition of arginase inhibition, removal of media l-Arg, or inhibition of NO-dependent signaling pathways (PKG, guanylyl cyclase, or NF-kappaB) did not affect the ET-1 flow response.	NG-Nitroarginine Methyl Ester	37-69	nitric oxide synthase 1, neuronal	Mus musculus	7-18
28515175-5	2017	Global NO synthase (NOS) inhibition [NG-nitro-l-arginine methyl ester (l-NAME)] reduced the ET-1 flow response; however, pharmacological inhibition of NOS1 or NOS2, inhibition of NOS3 siRNA, inhibition of arginase inhibition, removal of media l-Arg, or inhibition of NO-dependent signaling pathways (PKG, guanylyl cyclase, or NF-kappaB) did not affect the ET-1 flow response.	NG-Nitroarginine Methyl Ester	71-77	nitric oxide synthase 1, neuronal	Mus musculus	7-18
28515175-5	2017	Global NO synthase (NOS) inhibition [NG-nitro-l-arginine methyl ester (l-NAME)] reduced the ET-1 flow response; however, pharmacological inhibition of NOS1 or NOS2, inhibition of NOS3 siRNA, inhibition of arginase inhibition, removal of media l-Arg, or inhibition of NO-dependent signaling pathways (PKG, guanylyl cyclase, or NF-kappaB) did not affect the ET-1 flow response.	Arginine	243-248	nitric oxide synthase 1, neuronal	Mus musculus	7-18
28622359-12	2017	However, selective inhibition of beta3-AR by SR59230A abolished the upregulation and activation of nNOS induced NO production.	3-(2-ethylphenoxy)-1-(1,2,3,4-tetrahydronaphth-1-ylamino)-2-propanol oxalate	45-53	nitric oxide synthase 1, neuronal	Mus musculus	99-103
28469071-2	2017	Tetrahydrobiopterin (BH4) is an essential cofactor of tyrosine hydroxylase and nitric oxide synthase (NOS).	sapropterin	0-19	nitric oxide synthase 1, neuronal	Mus musculus	79-100
28469071-2	2017	Tetrahydrobiopterin (BH4) is an essential cofactor of tyrosine hydroxylase and nitric oxide synthase (NOS).	sapropterin	21-24	nitric oxide synthase 1, neuronal	Mus musculus	79-100
28503149-12	2017	Taken together, our findings show that B1- and B2-kinin receptors regulate the endothelium-dependent vasodilation of ACh through nNOS activity and indicate that molecular disturbance of short-range interaction between B1- and B2-kinin receptors with nNOS might be involved in the oxidative pathogenesis of endothelial dysfunction.	Acetylcholine	117-120	nitric oxide synthase 1, neuronal	Mus musculus	129-133
28503149-12	2017	Taken together, our findings show that B1- and B2-kinin receptors regulate the endothelium-dependent vasodilation of ACh through nNOS activity and indicate that molecular disturbance of short-range interaction between B1- and B2-kinin receptors with nNOS might be involved in the oxidative pathogenesis of endothelial dysfunction.	Acetylcholine	117-120	nitric oxide synthase 1, neuronal	Mus musculus	250-254
28105567-8	2017	On the other hand, the anticonvulsant effect of oleuropein (10 mg/kg) was blocked by a non-effective dose of nonspecific inhibitor of nitric oxide synthase (NOS), L-NAME (1 and 10 mg/kg, i.p) and a selective inhibitor of neuronal NOS, 7-nitroindazole (30 mg/kg, i.p.).	oleuropein	48-58	nitric oxide synthase 1, neuronal	Mus musculus	134-155
28213154-2	2017	In the present study, we immunohistochemically analyzed nNOS-positive cells in the mouse BLA by focusing on their density, gamma-Aminobutyric acid (GABA)ergicity, and co-localization with calcium-binding proteins and neuropeptides.	gamma-Aminobutyric Acid	123-146	nitric oxide synthase 1, neuronal	Mus musculus	56-60
28213154-2	2017	In the present study, we immunohistochemically analyzed nNOS-positive cells in the mouse BLA by focusing on their density, gamma-Aminobutyric acid (GABA)ergicity, and co-localization with calcium-binding proteins and neuropeptides.	Calcium	188-195	nitric oxide synthase 1, neuronal	Mus musculus	56-60
27851890-0	2017	Levosimendan exerts anticonvulsant properties against PTZ-induced seizures in mice through activation of nNOS/NO pathway: Role for KATP channel.	Simendan	0-12	nitric oxide synthase 1, neuronal	Mus musculus	105-109
28108357-7	2017	The coupling of nNOS to PSD-95 and nitric oxide (NO) level were reduced in BLA of sigma1R-/- mice, which were recovered by the BLA-injection of NMDAr agonist NMDA.	N-Methylaspartate	144-148	nitric oxide synthase 1, neuronal	Mus musculus	16-20
28108357-8	2017	The bath-application of NMDA in BLA slices from sigma1R-/- mice corrected the reduced fEPSP slopes and increased PPF and PPI and recovered the LTP and LTD induction, which were sensitive to nNOS inhibitor 7-NI.	N-Methylaspartate	24-28	nitric oxide synthase 1, neuronal	Mus musculus	190-194
28108357-8	2017	The bath-application of NMDA in BLA slices from sigma1R-/- mice corrected the reduced fEPSP slopes and increased PPF and PPI and recovered the LTP and LTD induction, which were sensitive to nNOS inhibitor 7-NI.	7-nitroindazole	205-209	nitric oxide synthase 1, neuronal	Mus musculus	190-194
28235709-0	2017	Role of ERK1/2 activation and nNOS uncoupling on endothelial dysfunction induced by lysophosphatidylcholine.	Lysophosphatidylcholines	84-107	nitric oxide synthase 1, neuronal	Mus musculus	30-34
28241801-0	2017	The protective effects of propofol against CoCl2-induced HT22 cell hypoxia injury via PP2A/CAMKIIalpha/nNOS pathway.	Propofol	26-34	nitric oxide synthase 1, neuronal	Mus musculus	103-107
28241801-0	2017	The protective effects of propofol against CoCl2-induced HT22 cell hypoxia injury via PP2A/CAMKIIalpha/nNOS pathway.	cobaltous chloride	43-48	nitric oxide synthase 1, neuronal	Mus musculus	103-107
28241801-9	2017	Further, we found CoCl2 treatment could up-regulate the expression of PP2A, BAX, cleaved caspase three and cause the phosphorylation of nNOS-Ser1412, but it down-regulated the expression of Bcl-2 and the phosphorylation of CAMKIIalpha and nNOS-Ser847.	cobaltous chloride	18-23	nitric oxide synthase 1, neuronal	Mus musculus	136-140
28241801-9	2017	Further, we found CoCl2 treatment could up-regulate the expression of PP2A, BAX, cleaved caspase three and cause the phosphorylation of nNOS-Ser1412, but it down-regulated the expression of Bcl-2 and the phosphorylation of CAMKIIalpha and nNOS-Ser847.	cobaltous chloride	18-23	nitric oxide synthase 1, neuronal	Mus musculus	239-243
28241801-13	2017	CONCLUSION: Our data indicated that propofol could attenuate CoCl2-induced HT22 cells hypoxia injury via PP2A/CAMKIIalpha/nNOS pathway.	Propofol	36-44	nitric oxide synthase 1, neuronal	Mus musculus	122-126
28241801-13	2017	CONCLUSION: Our data indicated that propofol could attenuate CoCl2-induced HT22 cells hypoxia injury via PP2A/CAMKIIalpha/nNOS pathway.	cobaltous chloride	61-66	nitric oxide synthase 1, neuronal	Mus musculus	122-126
28174542-9	2017	In the presence of the NO synthase (NOS) inhibitor L-NAME (100 muM) and/or ODQ to inhibit the guanylyl cyclase, the ATP effect remained unaffected.	NG-Nitroarginine Methyl Ester	51-57	nitric oxide synthase 1, neuronal	Mus musculus	23-34
27921261-0	2017	Attempting to Compensate for Reduced Neuronal Nitric Oxide Synthase Protein with Nitrate Supplementation Cannot Overcome Metabolic Dysfunction but Rather Has Detrimental Effects in Dystrophin-Deficient mdx Muscle.	Nitrates	81-88	nitric oxide synthase 1, neuronal	Mus musculus	37-67
27851890-10	2017	SIGNIFICANCE: Levosimendan has anticonvulsant effects possibly via KATP/nNOS/NO pathway activation in the hippocampus and temporal cortex.	Simendan	14-26	nitric oxide synthase 1, neuronal	Mus musculus	72-76
27710963-7	2017	Both TH and nNOS labeling was co-localized with ~10% of ARN GABA neurons.	gamma-Aminobutyric Acid	60-64	nitric oxide synthase 1, neuronal	Mus musculus	12-16
27820841-0	2016	Metformin Ameliorates Dysfunctional Traits of Glibenclamide- and Glucose-Induced Insulin Secretion by Suppression of Imposed Overactivity of the Islet Nitric Oxide Synthase-NO System.	Metformin	0-9	nitric oxide synthase 1, neuronal	Mus musculus	151-172
28503408-4	2017	We previously reported that in hepatocytes the nNOS (NOS1) inhibitor NANT inhibited APAP toxicity, reactive nitrogen and oxygen species formation, and mitochondrial dysfunction.	N-acetyl-N-nitrosotryptophan	69-73	nitric oxide synthase 1, neuronal	Mus musculus	47-51
28503408-4	2017	We previously reported that in hepatocytes the nNOS (NOS1) inhibitor NANT inhibited APAP toxicity, reactive nitrogen and oxygen species formation, and mitochondrial dysfunction.	N-acetyl-N-nitrosotryptophan	69-73	nitric oxide synthase 1, neuronal	Mus musculus	53-57
28503408-4	2017	We previously reported that in hepatocytes the nNOS (NOS1) inhibitor NANT inhibited APAP toxicity, reactive nitrogen and oxygen species formation, and mitochondrial dysfunction.	Acetaminophen	84-88	nitric oxide synthase 1, neuronal	Mus musculus	47-51
28503408-4	2017	We previously reported that in hepatocytes the nNOS (NOS1) inhibitor NANT inhibited APAP toxicity, reactive nitrogen and oxygen species formation, and mitochondrial dysfunction.	Acetaminophen	84-88	nitric oxide synthase 1, neuronal	Mus musculus	53-57
28503408-4	2017	We previously reported that in hepatocytes the nNOS (NOS1) inhibitor NANT inhibited APAP toxicity, reactive nitrogen and oxygen species formation, and mitochondrial dysfunction.	reactive nitrogen and oxygen species	99-135	nitric oxide synthase 1, neuronal	Mus musculus	47-51
28503408-4	2017	We previously reported that in hepatocytes the nNOS (NOS1) inhibitor NANT inhibited APAP toxicity, reactive nitrogen and oxygen species formation, and mitochondrial dysfunction.	reactive nitrogen and oxygen species	99-135	nitric oxide synthase 1, neuronal	Mus musculus	53-57
28503408-5	2017	In this work we examined the effect of trifluoperazine (TFP), a calmodulin antagonist that inhibits calcium induced nNOS activation, on APAP hepatotoxicity and reactive nitrogen formation in murine hepatocytes and in vivo.	Trifluoperazine	39-54	nitric oxide synthase 1, neuronal	Mus musculus	116-120
28503408-5	2017	In this work we examined the effect of trifluoperazine (TFP), a calmodulin antagonist that inhibits calcium induced nNOS activation, on APAP hepatotoxicity and reactive nitrogen formation in murine hepatocytes and in vivo.	Trifluoperazine	56-59	nitric oxide synthase 1, neuronal	Mus musculus	116-120
28503408-5	2017	In this work we examined the effect of trifluoperazine (TFP), a calmodulin antagonist that inhibits calcium induced nNOS activation, on APAP hepatotoxicity and reactive nitrogen formation in murine hepatocytes and in vivo.	Calcium	100-107	nitric oxide synthase 1, neuronal	Mus musculus	116-120
28503408-10	2017	These data are consistent with a hypothesis that APAP hepatotoxicity occurs with altered calcium metabolism, activation of nNOS leading to increased reactive nitrogen formation, and mitochondrial dysfunction.	Nitrogen	158-166	nitric oxide synthase 1, neuronal	Mus musculus	123-127
27601184-2	2016	However, the potential direct interaction between nNOS-derived nitric oxide (NO) and Nox2-derived reactive oxygen species (ROS) is poorly understood, particularly with respect to the potentiation of N-methyl-D-aspartate (NMDA) receptor activity in the spinal cord associated with the development of central sensitization.	Nitric Oxide	63-75	nitric oxide synthase 1, neuronal	Mus musculus	50-54
27601184-3	2016	Thus, the main purpose of this study was to investigate whether Sig-1R-induced and nNOS-derived NO modulates spinal Nox2 activation leading to an increase in ROS production and ultimately to the potentiation of NMDA receptor activity and pain hypersensitivity.	Reactive Oxygen Species	158-161	nitric oxide synthase 1, neuronal	Mus musculus	83-87
27601184-4	2016	Intrathecal pretreatment with the nNOS inhibitor, 7-nitroindazole or with the Nox inhibitor, apocynin significantly inhibited the mechanical and thermal hypersensitivity induced by intrathecal administration of the Sig-1R agonist, 2-(4-morpholinethyl) 1-phenylcyclohexanecarboxylate hydrochloride (PRE084).	PRE-084 Hydrochloride	231-296	nitric oxide synthase 1, neuronal	Mus musculus	34-38
27601184-4	2016	Intrathecal pretreatment with the nNOS inhibitor, 7-nitroindazole or with the Nox inhibitor, apocynin significantly inhibited the mechanical and thermal hypersensitivity induced by intrathecal administration of the Sig-1R agonist, 2-(4-morpholinethyl) 1-phenylcyclohexanecarboxylate hydrochloride (PRE084).	2-(4-morpholino)ethyl-1-phenylcyclohexane-1-carboxylate	298-304	nitric oxide synthase 1, neuronal	Mus musculus	34-38
27601184-6	2016	Pretreatment with 7-nitroindazole significantly reduced the PRE084-induced increase in Nox2 activity and concomitant ROS production in the lumbar spinal cord dorsal horn, whereas apocynin did not alter the PRE084-induced changes in nNOS phosphorylation.	7-nitroindazole	18-33	nitric oxide synthase 1, neuronal	Mus musculus	232-236
27601184-8	2016	These findings demonstrate that spinal Sig-1R-induced pain hypersensitivity is mediated by nNOS activation, which leads to an increase in Nox2 activity ultimately resulting in a ROS-induced increase in PKC-dependent pGluN1 expression.	Reactive Oxygen Species	178-181	nitric oxide synthase 1, neuronal	Mus musculus	91-95
27601184-8	2016	These findings demonstrate that spinal Sig-1R-induced pain hypersensitivity is mediated by nNOS activation, which leads to an increase in Nox2 activity ultimately resulting in a ROS-induced increase in PKC-dependent pGluN1 expression.	pglun1	216-222	nitric oxide synthase 1, neuronal	Mus musculus	91-95
27671463-9	2016	Expression of NOS (nitric oxide synthase), p47phox and p67phox subunits of NADPH oxidase, catalase or heme oxygenase (HO-1) was associated with HEMA- or LPS-induced apoptosis.	hydroxyethyl methacrylate	144-148	nitric oxide synthase 1, neuronal	Mus musculus	19-40
27875784-2	2016	Some effects of dextrometrophan are associated with alterations in several pathways, such as inhibition of nitric oxide synthase (NOS) enzyme and N-methyl d-aspartate (NMDA) receptors.	dextrometrophan	16-31	nitric oxide synthase 1, neuronal	Mus musculus	107-128
27820841-3	2016	We speculated that metformin might positively influence insulin secretion through impacting the beta-cell nitric oxide synthase (NOS)-NO system, a negative modulator of glucose-stimulated insulin release.	Metformin	19-28	nitric oxide synthase 1, neuronal	Mus musculus	106-127
27820841-3	2016	We speculated that metformin might positively influence insulin secretion through impacting the beta-cell nitric oxide synthase (NOS)-NO system, a negative modulator of glucose-stimulated insulin release.	Glucose	169-176	nitric oxide synthase 1, neuronal	Mus musculus	106-127
27707708-2	2016	Mice with CD-specific knockout (KO) of NO synthase 1 (NOS1) have salt-sensitive hypertension.	Cadmium	10-12	nitric oxide synthase 1, neuronal	Mus musculus	39-52
27707708-2	2016	Mice with CD-specific knockout (KO) of NO synthase 1 (NOS1) have salt-sensitive hypertension.	Cadmium	10-12	nitric oxide synthase 1, neuronal	Mus musculus	54-58
27707708-2	2016	Mice with CD-specific knockout (KO) of NO synthase 1 (NOS1) have salt-sensitive hypertension.	Salts	65-69	nitric oxide synthase 1, neuronal	Mus musculus	39-52
27707708-2	2016	Mice with CD-specific knockout (KO) of NO synthase 1 (NOS1) have salt-sensitive hypertension.	Salts	65-69	nitric oxide synthase 1, neuronal	Mus musculus	54-58
27523033-0	2016	Liposome-entrapped GABA modulates the expression of nNOS in NG108-15 cells.	gamma-Aminobutyric Acid	19-23	nitric oxide synthase 1, neuronal	Mus musculus	52-56
27559013-8	2016	Moreover, trans-astaxanthin at 80mg/kg was demonstrated to effectively antagonize iNOS, nNOS and COX-2 expression, both at mRNA and protein levels, nitric oxide (NO) levels, via regulating NF-kappaB in the hippocampus and PFC.	astaxantin, calcium, citrus bioflavoid, lycopene, vitamin D3 drug combination	10-27	nitric oxide synthase 1, neuronal	Mus musculus	88-92
27523033-3	2016	NEW METHOD: Using GABA-containing liposomes (GL) prepared by the freeze-thawing method, we determined the effect of sustained release of GABA on expression of neuronal nitric oxide synthase (nNOS) and GABAA receptor (GABAAR) in an in vitro neuronal model.	gamma-Aminobutyric Acid	137-141	nitric oxide synthase 1, neuronal	Mus musculus	159-189
27523033-3	2016	NEW METHOD: Using GABA-containing liposomes (GL) prepared by the freeze-thawing method, we determined the effect of sustained release of GABA on expression of neuronal nitric oxide synthase (nNOS) and GABAA receptor (GABAAR) in an in vitro neuronal model.	gamma-Aminobutyric Acid	137-141	nitric oxide synthase 1, neuronal	Mus musculus	191-195
27523033-4	2016	RESULTS: Neuronal cell line NG108-15 treated with different doses of GL during 24h showed an increase in expression of GABAAR (54 and 50% with 10 and 20ng doses, respectively) and nNOS (138, 157 and 165% with 20, 50 and 100ng doses, respectively) compared with cells treated with empty liposomes (EL).	gl	69-71	nitric oxide synthase 1, neuronal	Mus musculus	180-184
27523033-5	2016	Additionally, cells treated with 50ng of GL showed an increase in GABAAR (23%) after 1h followed by an increase in nNOS (55, 46 and 55%) at 8, 12 and 24h time points, respectively.	gl	41-43	nitric oxide synthase 1, neuronal	Mus musculus	115-119
27523033-6	2016	Immunofluorescence experiments confirmed an increase in nNOS (134%) and basal intracellular levels of nitric oxide (84%) after GL treatment.	gl	127-129	nitric oxide synthase 1, neuronal	Mus musculus	56-60
27523033-7	2016	Further, treatment of cells with GL showed a decrease in expression of a protein inhibitor of nNOS (PIN) (26, 66 and 57% with 20, 50 and 100ng doses respectively) compared with control.	gl	33-35	nitric oxide synthase 1, neuronal	Mus musculus	94-98
27523033-9	2016	CONCLUSION: These results suggest that a slow release of GABA can change the expression of nNOS possibly via alteration in PIN levels in neuronal cells.	gamma-Aminobutyric Acid	57-61	nitric oxide synthase 1, neuronal	Mus musculus	91-95
27684214-3	2016	NADPH can produce reactive oxygen species (ROS) and reactive nitrogen species (RNS) mediated by NADPH oxidase (NOX) and nitric oxide synthase (NOS), respectively.	NADP	0-5	nitric oxide synthase 1, neuronal	Mus musculus	120-141
27684214-3	2016	NADPH can produce reactive oxygen species (ROS) and reactive nitrogen species (RNS) mediated by NADPH oxidase (NOX) and nitric oxide synthase (NOS), respectively.	Reactive Oxygen Species	18-41	nitric oxide synthase 1, neuronal	Mus musculus	120-141
27684214-3	2016	NADPH can produce reactive oxygen species (ROS) and reactive nitrogen species (RNS) mediated by NADPH oxidase (NOX) and nitric oxide synthase (NOS), respectively.	Reactive Oxygen Species	43-46	nitric oxide synthase 1, neuronal	Mus musculus	120-141
27684214-3	2016	NADPH can produce reactive oxygen species (ROS) and reactive nitrogen species (RNS) mediated by NADPH oxidase (NOX) and nitric oxide synthase (NOS), respectively.	Reactive Nitrogen Species	52-77	nitric oxide synthase 1, neuronal	Mus musculus	120-141
27684214-3	2016	NADPH can produce reactive oxygen species (ROS) and reactive nitrogen species (RNS) mediated by NADPH oxidase (NOX) and nitric oxide synthase (NOS), respectively.	Reactive Nitrogen Species	79-82	nitric oxide synthase 1, neuronal	Mus musculus	120-141
27296112-0	2016	Disruption of neuronal nitric oxide synthase dimerization contributes to the development of Alzheimer"s disease: Involvement of cyclin-dependent kinase 5-mediated phosphorylation of neuronal nitric oxide synthase at Ser(293).	Serine	216-219	nitric oxide synthase 1, neuronal	Mus musculus	14-44
27822504-7	2016	Consistently, we found that dorsal raphe serotonin [5-hydroxytryptamine (5-HT)] neurons, which are involved in sleep-wake regulation, innervate nNOS+ neurons.	Serotonin	41-50	nitric oxide synthase 1, neuronal	Mus musculus	144-148
27822504-7	2016	Consistently, we found that dorsal raphe serotonin [5-hydroxytryptamine (5-HT)] neurons, which are involved in sleep-wake regulation, innervate nNOS+ neurons.	Serotonin	52-71	nitric oxide synthase 1, neuronal	Mus musculus	144-148
27296112-12	2016	Taken together, our results demonstrate that nNOS dimers are disrupted in the 5 x FAD cortex, and nNOS-Ser(293), a potential site of CDK5 phosphorylation, may be involved in the decrease in nNOS dimerization and NO production, and the development of AD.	Serine	103-106	nitric oxide synthase 1, neuronal	Mus musculus	98-102
27296112-0	2016	Disruption of neuronal nitric oxide synthase dimerization contributes to the development of Alzheimer"s disease: Involvement of cyclin-dependent kinase 5-mediated phosphorylation of neuronal nitric oxide synthase at Ser(293).	Serine	216-219	nitric oxide synthase 1, neuronal	Mus musculus	182-212
27296112-12	2016	Taken together, our results demonstrate that nNOS dimers are disrupted in the 5 x FAD cortex, and nNOS-Ser(293), a potential site of CDK5 phosphorylation, may be involved in the decrease in nNOS dimerization and NO production, and the development of AD.	Serine	103-106	nitric oxide synthase 1, neuronal	Mus musculus	98-102
27296112-4	2016	nNOS dimerization was disrupted in the 5 x FAD cortex, accompanied by an increase in reactive oxygen species (ROS) production.	oxygen species	94-108	nitric oxide synthase 1, neuronal	Mus musculus	0-4
27296112-4	2016	nNOS dimerization was disrupted in the 5 x FAD cortex, accompanied by an increase in reactive oxygen species (ROS) production.	Reactive Oxygen Species	110-113	nitric oxide synthase 1, neuronal	Mus musculus	0-4
27296112-7	2016	In silico analysis revealed that a new nNOS-specific GSP (glycine-serine-proline) motif was well-conserved across species at nNOS-Ser(293), which is located ahead of the N-terminal hook.	Glycine	58-65	nitric oxide synthase 1, neuronal	Mus musculus	39-43
27296112-7	2016	In silico analysis revealed that a new nNOS-specific GSP (glycine-serine-proline) motif was well-conserved across species at nNOS-Ser(293), which is located ahead of the N-terminal hook.	Glycine	58-65	nitric oxide synthase 1, neuronal	Mus musculus	125-129
27296112-7	2016	In silico analysis revealed that a new nNOS-specific GSP (glycine-serine-proline) motif was well-conserved across species at nNOS-Ser(293), which is located ahead of the N-terminal hook.	Serine	66-72	nitric oxide synthase 1, neuronal	Mus musculus	39-43
27296112-7	2016	In silico analysis revealed that a new nNOS-specific GSP (glycine-serine-proline) motif was well-conserved across species at nNOS-Ser(293), which is located ahead of the N-terminal hook.	Serine	66-72	nitric oxide synthase 1, neuronal	Mus musculus	125-129
27296112-7	2016	In silico analysis revealed that a new nNOS-specific GSP (glycine-serine-proline) motif was well-conserved across species at nNOS-Ser(293), which is located ahead of the N-terminal hook.	Proline	73-80	nitric oxide synthase 1, neuronal	Mus musculus	39-43
27296112-7	2016	In silico analysis revealed that a new nNOS-specific GSP (glycine-serine-proline) motif was well-conserved across species at nNOS-Ser(293), which is located ahead of the N-terminal hook.	Proline	73-80	nitric oxide synthase 1, neuronal	Mus musculus	125-129
27296112-7	2016	In silico analysis revealed that a new nNOS-specific GSP (glycine-serine-proline) motif was well-conserved across species at nNOS-Ser(293), which is located ahead of the N-terminal hook.	Serine	130-133	nitric oxide synthase 1, neuronal	Mus musculus	39-43
27296112-7	2016	In silico analysis revealed that a new nNOS-specific GSP (glycine-serine-proline) motif was well-conserved across species at nNOS-Ser(293), which is located ahead of the N-terminal hook.	Serine	130-133	nitric oxide synthase 1, neuronal	Mus musculus	125-129
27296112-9	2016	Motif scan analysis also predicted that CDK5 can phosphorylate nNOS-Ser(293) with a high likelihood.	Serine	68-71	nitric oxide synthase 1, neuronal	Mus musculus	63-67
27296112-10	2016	An in vitro phosphorylation assay clearly showed that CDK5/p25 does indeed phosphorylate nNOS-Ser(293).	Serine	94-97	nitric oxide synthase 1, neuronal	Mus musculus	89-93
27548300-1	2016	Naturally occurring N(omega)-hydroxy-l-arginine (NOHA, 1) is the best substrate of NO synthases (NOS).	N(omega)-hydroxyarginine	20-47	nitric oxide synthase 1, neuronal	Mus musculus	83-95
27548300-1	2016	Naturally occurring N(omega)-hydroxy-l-arginine (NOHA, 1) is the best substrate of NO synthases (NOS).	N(omega)-hydroxyarginine	49-53	nitric oxide synthase 1, neuronal	Mus musculus	83-95
27342567-7	2016	Inhibition of nitric oxide synthase (NOS) in vivo blocked only the beneficial effect of Na2S.	sodium sulfide	88-92	nitric oxide synthase 1, neuronal	Mus musculus	14-35
26381428-0	2016	Neuronal Nitric Oxide Synthase-Mediated Genotoxicity of 2-Methoxyestradiol in Hippocampal HT22 Cell Line.	2-Methoxyestradiol	56-74	nitric oxide synthase 1, neuronal	Mus musculus	0-30
26381428-6	2016	Herein, we demonstrated that 2-methoxyestradiol, at pharmacologically and also physiologically relevant concentrations, increases nuclear localization of neuronal nitric oxide synthase.	2-Methoxyestradiol	29-47	nitric oxide synthase 1, neuronal	Mus musculus	154-184
27317486-4	2016	While neuronal NO synthase (nNOS) in untreated HT22 cells exists mostly as a monomer, glutathione depletion results in increased formation of the dimer nNOS, accompanied by increases in the catalytic activity.	Glutathione	86-97	nitric oxide synthase 1, neuronal	Mus musculus	152-156
27317486-6	2016	Inhibition of PDI"s isomerase activity effectively abrogates glutathione depletion-induced conversion of monomer nNOS into dimer nNOS, accumulation of NO and ROS, and cytotoxicity.	Glutathione	61-72	nitric oxide synthase 1, neuronal	Mus musculus	113-117
27317486-6	2016	Inhibition of PDI"s isomerase activity effectively abrogates glutathione depletion-induced conversion of monomer nNOS into dimer nNOS, accumulation of NO and ROS, and cytotoxicity.	Glutathione	61-72	nitric oxide synthase 1, neuronal	Mus musculus	129-133
27529477-9	2016	Additionally, in isolated mouse cardiomyocytes, NOS-1 inhibition or removal reduced the Ca2+-transient amplitude and sarcomere shortening induced by isoproterenol or by direct PKA activation.	Isoproterenol	149-162	nitric oxide synthase 1, neuronal	Mus musculus	48-53
27282485-1	2016	Previous studies have shown that an enriched environment (EE) has an important effect on brain function via the neuronal nitric oxide synthase/nitric oxide (nNOS/NO) pathway in young and aged animals.	Nitric Oxide	121-133	nitric oxide synthase 1, neuronal	Mus musculus	157-161
26945022-7	2016	Moreover, Hc-TeTx prevented the increase of neuronal nitric oxide synthase but did not affect microglia activation induced by methamphetamine.	hc-tetx	10-17	nitric oxide synthase 1, neuronal	Mus musculus	44-74
27426857-7	2016	Finally, immunohistochemical analysis of neuronal nitric oxide synthase (nNOS; which can mediate EtOH enhancement of GABA release) demonstrated that nNOS expression in the GC layer of PV cerebellum was similar to the levels seen in B6 mice, both being significantly reduced relative to D2 mice and SD rats.	Ethanol	97-101	nitric oxide synthase 1, neuronal	Mus musculus	73-77
27426857-7	2016	Finally, immunohistochemical analysis of neuronal nitric oxide synthase (nNOS; which can mediate EtOH enhancement of GABA release) demonstrated that nNOS expression in the GC layer of PV cerebellum was similar to the levels seen in B6 mice, both being significantly reduced relative to D2 mice and SD rats.	Ethanol	97-101	nitric oxide synthase 1, neuronal	Mus musculus	149-153
27426857-7	2016	Finally, immunohistochemical analysis of neuronal nitric oxide synthase (nNOS; which can mediate EtOH enhancement of GABA release) demonstrated that nNOS expression in the GC layer of PV cerebellum was similar to the levels seen in B6 mice, both being significantly reduced relative to D2 mice and SD rats.	gamma-Aminobutyric Acid	117-121	nitric oxide synthase 1, neuronal	Mus musculus	73-77
27426857-7	2016	Finally, immunohistochemical analysis of neuronal nitric oxide synthase (nNOS; which can mediate EtOH enhancement of GABA release) demonstrated that nNOS expression in the GC layer of PV cerebellum was similar to the levels seen in B6 mice, both being significantly reduced relative to D2 mice and SD rats.	gamma-Aminobutyric Acid	117-121	nitric oxide synthase 1, neuronal	Mus musculus	149-153
27280426-1	2016	The collecting duct endothelin-1 (ET-1), endothelin B (ETB) receptor, and nitric oxide synthase-1 (NOS1) pathways are critical for regulation of fluid-electrolyte balance and blood pressure control during high-salt feeding.	Salts	210-214	nitric oxide synthase 1, neuronal	Mus musculus	74-97
27280426-1	2016	The collecting duct endothelin-1 (ET-1), endothelin B (ETB) receptor, and nitric oxide synthase-1 (NOS1) pathways are critical for regulation of fluid-electrolyte balance and blood pressure control during high-salt feeding.	Salts	210-214	nitric oxide synthase 1, neuronal	Mus musculus	99-103
26647426-2	2016	We recently found that macula densa expresses alpha-, beta-, and gamma-splice variants of neuronal nitric oxide synthase 1 (NOS1), and NOS1beta expression in the macula densa increases on a high-salt diet.	Salts	195-199	nitric oxide synthase 1, neuronal	Mus musculus	99-122
27232376-4	2016	Coadministration of subthreshold doses of lithium (3mg/kg) with nitric oxide synthase (NOS) inhibitors reversed the effect of SIS on seizure susceptibility and decreased hippocampal nitrite levels in IC animals.	Lithium	42-49	nitric oxide synthase 1, neuronal	Mus musculus	64-85
27232376-4	2016	Coadministration of subthreshold doses of lithium (3mg/kg) with nitric oxide synthase (NOS) inhibitors reversed the effect of SIS on seizure susceptibility and decreased hippocampal nitrite levels in IC animals.	Nitrites	182-189	nitric oxide synthase 1, neuronal	Mus musculus	64-85
27239731-1	2016	l-Arginine is the common substrate for nitric oxide synthases (NOS) and arginase.	Arginine	0-10	nitric oxide synthase 1, neuronal	Mus musculus	39-61
27435231-9	2016	Inhibition of NO synthase (NOS) activity or H2O2 decomposition by catalase abolished the differences in the acetylcholine response between the animals.	Acetylcholine	108-121	nitric oxide synthase 1, neuronal	Mus musculus	14-25
26647426-6	2016	Compared with control mice, mice with macula densa-specific knockout of all nitric oxide synthase 1 isoforms (MD-NOS1KO) had a significantly enhanced tubuloglomerular feedback response and after acute volume expansion, significantly reduced GFR, urine flow, and sodium excretion.	Sodium	262-268	nitric oxide synthase 1, neuronal	Mus musculus	76-99
26647426-9	2016	These results indicate that NOS1beta is a primary NOS1 isoform expressed in the macula densa and regulates the tubuloglomerular feedback response, the natriuretic response to acute volume expansion, and the development of salt-sensitive hypertension.	Salts	222-226	nitric oxide synthase 1, neuronal	Mus musculus	28-32
26976926-0	2016	Endothelial dysfunction in DOCA-salt-hypertensive mice: role of neuronal nitric oxide synthase-derived hydrogen peroxide.	Hydrogen Peroxide	103-120	nitric oxide synthase 1, neuronal	Mus musculus	64-94
27445786-1	2016	Nitric oxide (NO) has long been implicated in the generation of long-term potentiation (LTP) and other types of synaptic plasticity, a role for which the intimate coupling between NMDA receptors (NMDARs) and the neuronal isoform of NO synthase (nNOS) is likely to be instrumental in many instances.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	212-243
27445786-1	2016	Nitric oxide (NO) has long been implicated in the generation of long-term potentiation (LTP) and other types of synaptic plasticity, a role for which the intimate coupling between NMDA receptors (NMDARs) and the neuronal isoform of NO synthase (nNOS) is likely to be instrumental in many instances.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	245-249
26976926-10	2016	The expression of both eNOS and nNOS was considerably lower in DOCA-salt-hypertensive mice, whereas phosphorylation of their inhibitory sites was increased.	Desoxycorticosterone Acetate	63-67	nitric oxide synthase 1, neuronal	Mus musculus	32-36
26976926-2	2016	The present study investigated the involvement of nNOS (neuronal nitric oxide synthase) and H2O2 (hydrogen peroxide) in the impaired endothelium-dependent vasodilation of the mesenteric arteries of DOCA (deoxycorticosterone acetate)-salt-hypertensive mice.	Desoxycorticosterone Acetate	198-202	nitric oxide synthase 1, neuronal	Mus musculus	50-54
26976926-10	2016	The expression of both eNOS and nNOS was considerably lower in DOCA-salt-hypertensive mice, whereas phosphorylation of their inhibitory sites was increased.	Salts	68-72	nitric oxide synthase 1, neuronal	Mus musculus	32-36
26976926-2	2016	The present study investigated the involvement of nNOS (neuronal nitric oxide synthase) and H2O2 (hydrogen peroxide) in the impaired endothelium-dependent vasodilation of the mesenteric arteries of DOCA (deoxycorticosterone acetate)-salt-hypertensive mice.	Desoxycorticosterone Acetate	198-202	nitric oxide synthase 1, neuronal	Mus musculus	56-86
26976926-11	2016	The presence of nNOS was confirmed in the endothelial layer of mesenteric arteries from both sham and DOCA-salt-hypertensive mice.	Desoxycorticosterone Acetate	102-106	nitric oxide synthase 1, neuronal	Mus musculus	16-20
26976926-11	2016	The presence of nNOS was confirmed in the endothelial layer of mesenteric arteries from both sham and DOCA-salt-hypertensive mice.	Salts	107-111	nitric oxide synthase 1, neuronal	Mus musculus	16-20
26976926-12	2016	These results demonstrate that endothelial dysfunction in the mesenteric arteries of DOCA-salt-hypertensive mice is associated with reduced expression and functioning of nNOS and impaired production of nNOS-derived H2O2 Such findings offer a new perspective for the understanding of endothelial dysfunction in hypertension.	Desoxycorticosterone Acetate	85-89	nitric oxide synthase 1, neuronal	Mus musculus	170-174
26976926-12	2016	These results demonstrate that endothelial dysfunction in the mesenteric arteries of DOCA-salt-hypertensive mice is associated with reduced expression and functioning of nNOS and impaired production of nNOS-derived H2O2 Such findings offer a new perspective for the understanding of endothelial dysfunction in hypertension.	Desoxycorticosterone Acetate	85-89	nitric oxide synthase 1, neuronal	Mus musculus	202-206
26976926-12	2016	These results demonstrate that endothelial dysfunction in the mesenteric arteries of DOCA-salt-hypertensive mice is associated with reduced expression and functioning of nNOS and impaired production of nNOS-derived H2O2 Such findings offer a new perspective for the understanding of endothelial dysfunction in hypertension.	Salts	90-94	nitric oxide synthase 1, neuronal	Mus musculus	170-174
26976926-12	2016	These results demonstrate that endothelial dysfunction in the mesenteric arteries of DOCA-salt-hypertensive mice is associated with reduced expression and functioning of nNOS and impaired production of nNOS-derived H2O2 Such findings offer a new perspective for the understanding of endothelial dysfunction in hypertension.	Hydrogen Peroxide	215-219	nitric oxide synthase 1, neuronal	Mus musculus	202-206
26976926-8	2016	Selective inhibition of nNOS and catalase led to a higher reduction in the effect of ACh in sham than in DOCA-salt-hypertensive mice.	Acetylcholine	85-88	nitric oxide synthase 1, neuronal	Mus musculus	24-28
26976926-8	2016	Selective inhibition of nNOS and catalase led to a higher reduction in the effect of ACh in sham than in DOCA-salt-hypertensive mice.	doca-salt	105-114	nitric oxide synthase 1, neuronal	Mus musculus	24-28
26976926-9	2016	Production of H2O2 induced by ACh was significantly reduced in vessels from DOCA-salt-hypertensive mice, and it was blunted after nNOS inhibition.	Hydrogen Peroxide	14-18	nitric oxide synthase 1, neuronal	Mus musculus	130-134
26820352-4	2016	In vivo experiments confirmed that PRAM2 could reduce the liver weight, liver index, aspartate transaminase (AST) and alanine aminotransferase (ALT) activities in the serum; meanwhile, PRAM2 could significantly reduce nitric oxide synthase (NOS) activity, and nitric oxide (NO) and malonaldehyde (MDA) contents in the liver tissues, and increase superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities.	Malondialdehyde	282-295	nitric oxide synthase 1, neuronal	Mus musculus	218-239
26820352-4	2016	In vivo experiments confirmed that PRAM2 could reduce the liver weight, liver index, aspartate transaminase (AST) and alanine aminotransferase (ALT) activities in the serum; meanwhile, PRAM2 could significantly reduce nitric oxide synthase (NOS) activity, and nitric oxide (NO) and malonaldehyde (MDA) contents in the liver tissues, and increase superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities.	gsh-px	401-407	nitric oxide synthase 1, neuronal	Mus musculus	218-239
26892297-10	2016	nNOS(+) interneurons in the SP increase from the anterior motor cortex to posterior visual cortex, while CR(+) and CB(+) interneurons the opposite.	sp	28-30	nitric oxide synthase 1, neuronal	Mus musculus	0-4
27026404-5	2016	Tempol and perindopril improved spatial and nonspatial memory in mice without affecting locomotor activity; decreased brain Abeta deposition and BDNF depletion; decreased brain TNF-alpha, NOx, nNOS, iNOS, MDA, and NT levels; and increased brain SOD and GSH contents, parallel to confirmatory histopathological findings.	Perindopril	11-22	nitric oxide synthase 1, neuronal	Mus musculus	193-197
27006199-0	2016	Skeletal muscle glucose uptake during treadmill exercise in neuronal nitric oxide synthase-mu knockout mice.	Glucose	16-23	nitric oxide synthase 1, neuronal	Mus musculus	60-90
27006199-2	2016	The role of the main NO-producing enzyme isoform activated during skeletal muscle contraction, neuronal nitric oxide synthase-mu (nNOSmu), in modulating glucose uptake has not been investigated in a physiological exercise model.	Glucose	153-160	nitric oxide synthase 1, neuronal	Mus musculus	95-125
27025341-1	2016	4-((3,5-Dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid (ZL006, 1) is a small-molecular inhibitor of the nNOS/PSD-95 interaction, that is under preclinical evaluation stage for cerebral ischemia.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	0-61	nitric oxide synthase 1, neuronal	Mus musculus	111-115
27025341-1	2016	4-((3,5-Dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid (ZL006, 1) is a small-molecular inhibitor of the nNOS/PSD-95 interaction, that is under preclinical evaluation stage for cerebral ischemia.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	63-68	nitric oxide synthase 1, neuronal	Mus musculus	111-115
26661936-10	2016	The GPER agonist G-1 caused a concentration-dependent inhibition of carbachol -induced circular muscle strips contraction, which was abolished by tetrodotoxin and the neuronal nitric oxide synthase (nNOS) inhibitor N-propyl-l-arginine.	Carbachol	68-77	nitric oxide synthase 1, neuronal	Mus musculus	167-197
27231671-1	2016	Nitric oxide (NO) is synthesized by a family of NO synthases (NOS), including neuronal, inducible, and endothelial NOS (n/i/eNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	48-60
26791826-1	2016	Nitric oxide synthase 1 (NOS1)-derived nitric oxide (NO) production in collecting ducts is critical for maintaining fluid-electrolyte balance.	Nitric Oxide	39-51	nitric oxide synthase 1, neuronal	Mus musculus	0-23
26791826-1	2016	Nitric oxide synthase 1 (NOS1)-derived nitric oxide (NO) production in collecting ducts is critical for maintaining fluid-electrolyte balance.	Nitric Oxide	39-51	nitric oxide synthase 1, neuronal	Mus musculus	25-29
26883268-2	2016	We have also demonstrated that the mice with deletion of NOS1 specifically from the macula densa developed salt-sensitive hypertension.	Salts	107-111	nitric oxide synthase 1, neuronal	Mus musculus	57-61
26648027-9	2016	These findings indicated that an upregulation of nNOS and iNOS in the spinal cord is associated with bone cancer pain and suggests that exogenously administered L-NMMA may have beneficial effects to alleviate bone cancer pain.	omega-N-Methylarginine	161-167	nitric oxide synthase 1, neuronal	Mus musculus	49-53
26820711-0	2016	Neuronal nitric oxide synthase contributes to pentylenetetrazole-kindling-induced hippocampal neurogenesis.	Pentylenetetrazole	46-64	nitric oxide synthase 1, neuronal	Mus musculus	0-30
26820711-5	2016	The present study, therefore, investigated the role of nNOS in pentylenetetrazole (PTZ)-kindling-induced neurogenesis in hippocampal DG.	Pentylenetetrazole	63-81	nitric oxide synthase 1, neuronal	Mus musculus	55-59
26820711-5	2016	The present study, therefore, investigated the role of nNOS in pentylenetetrazole (PTZ)-kindling-induced neurogenesis in hippocampal DG.	Pentylenetetrazole	83-86	nitric oxide synthase 1, neuronal	Mus musculus	55-59
26820711-6	2016	Our results showed that nNOS expression and enzymatic activity were significantly increased in the hippocampus of PTZ-kindled mice.	Pentylenetetrazole	114-117	nitric oxide synthase 1, neuronal	Mus musculus	24-28
26820711-8	2016	Selective inhibition of nNOS by 7-NI, however, suppressed PTZ-kindling-induced hippocampal DG new born cells proliferation and survival, suggesting that nNOS contributes to PTZ-kindling-induced hippocampal neurogenesis.	7-nitroindazole	32-36	nitric oxide synthase 1, neuronal	Mus musculus	24-28
26820711-8	2016	Selective inhibition of nNOS by 7-NI, however, suppressed PTZ-kindling-induced hippocampal DG new born cells proliferation and survival, suggesting that nNOS contributes to PTZ-kindling-induced hippocampal neurogenesis.	Pentylenetetrazole	58-61	nitric oxide synthase 1, neuronal	Mus musculus	24-28
26820711-8	2016	Selective inhibition of nNOS by 7-NI, however, suppressed PTZ-kindling-induced hippocampal DG new born cells proliferation and survival, suggesting that nNOS contributes to PTZ-kindling-induced hippocampal neurogenesis.	Pentylenetetrazole	58-61	nitric oxide synthase 1, neuronal	Mus musculus	153-157
26820711-8	2016	Selective inhibition of nNOS by 7-NI, however, suppressed PTZ-kindling-induced hippocampal DG new born cells proliferation and survival, suggesting that nNOS contributes to PTZ-kindling-induced hippocampal neurogenesis.	Pentylenetetrazole	173-176	nitric oxide synthase 1, neuronal	Mus musculus	153-157
26806551-1	2016	Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase (NOS) inhibitor, is degraded by dimethylarginine dimethylaminohydrolase 1 (DDAH1).	dimethylarginine	11-27	nitric oxide synthase 1, neuronal	Mus musculus	50-71
26806551-1	2016	Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase (NOS) inhibitor, is degraded by dimethylarginine dimethylaminohydrolase 1 (DDAH1).	N,N-dimethylarginine	29-33	nitric oxide synthase 1, neuronal	Mus musculus	50-71
25316339-0	2016	Substance P Activates Ca2+-Permeable Nonselective Cation Channels through a Phosphatidylcholine-Specific Phospholipase C Signaling Pathway in nNOS-Expressing GABAergic Neurons in Visual Cortex.	Phosphatidylcholines	76-95	nitric oxide synthase 1, neuronal	Mus musculus	142-146
25316339-8	2016	These results suggest that SP regulates nNOS neurons by activating TRP-like Ca(2+)-permeable nonselective cation channels through a PC-PLC-dependent signaling pathway.	Tryptophan	67-70	nitric oxide synthase 1, neuronal	Mus musculus	40-44
26661936-10	2016	The GPER agonist G-1 caused a concentration-dependent inhibition of carbachol -induced circular muscle strips contraction, which was abolished by tetrodotoxin and the neuronal nitric oxide synthase (nNOS) inhibitor N-propyl-l-arginine.	Carbachol	68-77	nitric oxide synthase 1, neuronal	Mus musculus	199-203
26661936-10	2016	The GPER agonist G-1 caused a concentration-dependent inhibition of carbachol -induced circular muscle strips contraction, which was abolished by tetrodotoxin and the neuronal nitric oxide synthase (nNOS) inhibitor N-propyl-l-arginine.	n-propyl-l-arginine	215-234	nitric oxide synthase 1, neuronal	Mus musculus	167-197
26661936-10	2016	The GPER agonist G-1 caused a concentration-dependent inhibition of carbachol -induced circular muscle strips contraction, which was abolished by tetrodotoxin and the neuronal nitric oxide synthase (nNOS) inhibitor N-propyl-l-arginine.	n-propyl-l-arginine	215-234	nitric oxide synthase 1, neuronal	Mus musculus	199-203
26989787-8	2016	Additionally, exposure to PEPs upregulated expression of the Ccl5 (Rantes), Nos1 and Ucp2 genes in the murine lung tissue and modified components of the DNA methylation machinery (Dnmt3a) and expression of transposable element (TE) LINE-1 compared to the control group.	peps	26-30	nitric oxide synthase 1, neuronal	Mus musculus	76-80
26547262-9	2016	CONCLUSIONS &amp; INFERENCES: The results demonstrate that in cisplatin long-term treated mice [Gly(2) ]GLP-2 is able to counteract both the mucosal gastric fundus damage, by preventing the epithelium thickness decrease, and the neuropathy, by protecting the nNOS neurons.	Cisplatin	62-71	nitric oxide synthase 1, neuronal	Mus musculus	259-263
26547262-9	2016	CONCLUSIONS &amp; INFERENCES: The results demonstrate that in cisplatin long-term treated mice [Gly(2) ]GLP-2 is able to counteract both the mucosal gastric fundus damage, by preventing the epithelium thickness decrease, and the neuropathy, by protecting the nNOS neurons.	Glycine	96-99	nitric oxide synthase 1, neuronal	Mus musculus	259-263
26444418-4	2016	As in non-atherosclerotic conditions, the muscarinic receptor agonist acetylcholine (ACh) evoked an endothelium-dependent, COX-mediated contraction following NO synthase (NOS) inhibition in abdominal aortic rings from atherosclerotic apoE(-/-) mice.	Acetylcholine	70-83	nitric oxide synthase 1, neuronal	Mus musculus	158-169
26444418-4	2016	As in non-atherosclerotic conditions, the muscarinic receptor agonist acetylcholine (ACh) evoked an endothelium-dependent, COX-mediated contraction following NO synthase (NOS) inhibition in abdominal aortic rings from atherosclerotic apoE(-/-) mice.	Acetylcholine	85-88	nitric oxide synthase 1, neuronal	Mus musculus	158-169
26547262-6	2016	Immunohistochemistry demonstrated that cisplatin caused a significant decrease in myenteric neurons, mainly those expressing neuronal nitric oxide synthase (nNOS), that was prevented by [Gly(2) ]GLP-2 co-treatment.	Cisplatin	39-48	nitric oxide synthase 1, neuronal	Mus musculus	125-155
26547262-6	2016	Immunohistochemistry demonstrated that cisplatin caused a significant decrease in myenteric neurons, mainly those expressing neuronal nitric oxide synthase (nNOS), that was prevented by [Gly(2) ]GLP-2 co-treatment.	Cisplatin	39-48	nitric oxide synthase 1, neuronal	Mus musculus	157-161
26547262-6	2016	Immunohistochemistry demonstrated that cisplatin caused a significant decrease in myenteric neurons, mainly those expressing neuronal nitric oxide synthase (nNOS), that was prevented by [Gly(2) ]GLP-2 co-treatment.	Glycine	187-190	nitric oxide synthase 1, neuronal	Mus musculus	125-155
26547262-6	2016	Immunohistochemistry demonstrated that cisplatin caused a significant decrease in myenteric neurons, mainly those expressing neuronal nitric oxide synthase (nNOS), that was prevented by [Gly(2) ]GLP-2 co-treatment.	Glycine	187-190	nitric oxide synthase 1, neuronal	Mus musculus	157-161
26427435-4	2016	Although calcium ion influx triggers the neuronal nitric oxide synthase (nNOS) activation, the role of nNOS on photoreceptor cell death by MNU has not been reported yet.	Calcium	9-16	nitric oxide synthase 1, neuronal	Mus musculus	41-71
26427435-4	2016	Although calcium ion influx triggers the neuronal nitric oxide synthase (nNOS) activation, the role of nNOS on photoreceptor cell death by MNU has not been reported yet.	Calcium	9-16	nitric oxide synthase 1, neuronal	Mus musculus	73-77
26427435-4	2016	Although calcium ion influx triggers the neuronal nitric oxide synthase (nNOS) activation, the role of nNOS on photoreceptor cell death by MNU has not been reported yet.	Methylnitrosourea	139-142	nitric oxide synthase 1, neuronal	Mus musculus	103-107
26427435-5	2016	In this study, we investigated the contribution of nNOS on photoreceptor cell death induced by MNU in mice.	Methylnitrosourea	95-98	nitric oxide synthase 1, neuronal	Mus musculus	51-55
26427435-7	2016	Then, we evaluated the effect of nNOS specific inhibitor, ethyl[4-(trifluoromethyl) phenyl]carbamimidothioate (ETPI) on the MNU-induced photoreceptor cell death.	ethyl (4-(trifluoromethyl)phenyl)carbamimidothioate	111-115	nitric oxide synthase 1, neuronal	Mus musculus	33-37
26427435-7	2016	Then, we evaluated the effect of nNOS specific inhibitor, ethyl[4-(trifluoromethyl) phenyl]carbamimidothioate (ETPI) on the MNU-induced photoreceptor cell death.	Methylnitrosourea	124-127	nitric oxide synthase 1, neuronal	Mus musculus	33-37
26427435-9	2016	These data indicate that nNOS is a key molecule for pathogenesis of MNU-induced photoreceptor cell death.	Methylnitrosourea	68-71	nitric oxide synthase 1, neuronal	Mus musculus	25-29
26596859-6	2016	GSNO treatment at 2h after CCI decreased the expression levels of phospho neuronal nitric oxide synthase (pnNOS), alpha II spectrin degraded products, and 3-NT, while also decreasing the activities of nNOS and calpains.	S-Nitrosoglutathione	0-4	nitric oxide synthase 1, neuronal	Mus musculus	107-111
26596859-10	2016	These data indicate that peroxynitrite-mediated activation and GSNO-mediated inhibition of the deleterious nNOS/calpain system play critical roles in the pathobiology of neuronal protection and functional recovery in TBI disease.	S-Nitrosoglutathione	63-67	nitric oxide synthase 1, neuronal	Mus musculus	107-111
28006762-5	2016	Treatment with NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, increased anti-oxidant biomarkers such as thetotal antioxidant capacity (T-AOC) and theactivities of catalase (CAT) and superoxide dismutase (SOD) but decreased a marker of peroxynitrite (ONOO-) action and 3-nitrotyrosine (3-NT) in endotoxemic lung.	NG-Nitroarginine Methyl Ester	15-47	nitric oxide synthase 1, neuronal	Mus musculus	60-81
28006762-5	2016	Treatment with NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, increased anti-oxidant biomarkers such as thetotal antioxidant capacity (T-AOC) and theactivities of catalase (CAT) and superoxide dismutase (SOD) but decreased a marker of peroxynitrite (ONOO-) action and 3-nitrotyrosine (3-NT) in endotoxemic lung.	NG-Nitroarginine Methyl Ester	49-55	nitric oxide synthase 1, neuronal	Mus musculus	60-81
26442661-7	2016	nNOS, IL-1beta, and TNF-alpha were increased by MDMA in CPu of adults, whereas in adolescents, levels were only elevated after combined MDMA plus caffeine.	N-Methyl-3,4-methylenedioxyamphetamine	48-52	nitric oxide synthase 1, neuronal	Mus musculus	0-4
26442661-8	2016	Caffeine alone modified only nNOS.	Caffeine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	29-33
27308186-2	2016	Two reported subtypes of Arg (ArgI and II) compete with nitric oxide synthase (NOS) to use L-arginine as a substrate, and subsequently regulate NOS activity.	Arginine	91-101	nitric oxide synthase 1, neuronal	Mus musculus	56-77
26569535-5	2016	Furthermore, the antidepressant actions of AICAR required endothelial nitric oxide synthase activity with increased NO production in the prefrontal cortex, whereas corticosterone-induced expression of neuronal nitric oxide synthase and NO production may increase the risk of depression.	Corticosterone	164-178	nitric oxide synthase 1, neuronal	Mus musculus	201-231
25956150-7	2015	PCHPs significantly reduced the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) but increased glutathione (GSH) content and anti-oxidant enzymes and nitric oxide synthase (NOS) activities in Pb2+-exposed brain.	pchps	0-5	nitric oxide synthase 1, neuronal	Mus musculus	167-188
26363153-8	2015	Nitric oxide synthase (NOS) inhibition with L-N(G)-nitroarginine methyl ester (1.0muM) blocked neuroprotection by E (0.3muM) or Q (1.0muM).	l-n(g)-nitroarginine methyl ester	44-77	nitric oxide synthase 1, neuronal	Mus musculus	0-21
26454079-0	2015	The neuronal nitric oxide synthase inhibitor NANT blocks acetaminophen toxicity and protein nitration in freshly isolated hepatocytes.	N-acetyl-N-nitrosotryptophan	45-49	nitric oxide synthase 1, neuronal	Mus musculus	4-34
26454079-0	2015	The neuronal nitric oxide synthase inhibitor NANT blocks acetaminophen toxicity and protein nitration in freshly isolated hepatocytes.	Acetaminophen	57-70	nitric oxide synthase 1, neuronal	Mus musculus	4-34
26454079-5	2015	In this work we examined the potential role of nNOS in APAP toxicity in hepatocytes using the specific nNOS inhibitor NANT (10 microM)(N-[(4S)-4-amino-5-[(2-aminoethyl)amino]pentyl]-N"-nitroguanidinetris (trifluoroacetate)).	N-acetyl-N-nitrosotryptophan	118-122	nitric oxide synthase 1, neuronal	Mus musculus	103-107
26483274-12	2015	Together, our results suggest a new role of nNOS at the IDs for the cGMP-dependent NO pathway and the maintenance of ID morphology.	Cyclic GMP	68-72	nitric oxide synthase 1, neuronal	Mus musculus	44-48
25956150-7	2015	PCHPs significantly reduced the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) but increased glutathione (GSH) content and anti-oxidant enzymes and nitric oxide synthase (NOS) activities in Pb2+-exposed brain.	Lead	209-213	nitric oxide synthase 1, neuronal	Mus musculus	167-188
26259139-8	2015	Isoflurane decreased infarct size from 54 +- 10% in control to 36 +- 10% (P &lt; 0.05, n = 8 mice per group), improved cardiac function after reperfusion, and increased the ratios of phosphorylated-Akt/AKT, phosphorylated-eNOS/eNOS, and phosphorylated-nNOS/nNOS in C57BL/6 mice subjected to ischemia-reperfusion injury.	Isoflurane	0-10	nitric oxide synthase 1, neuronal	Mus musculus	252-256
26220904-8	2015	Furthermore, carvacrol significantly inhibited the induction of neuronal nitric oxide synthase (nNOS) after traumatic injury, and treatment with carvacrol and the nNOS inhibitor NLPA together had no extra effect on calcium concentration and neuronal injury.	carvacrol	13-22	nitric oxide synthase 1, neuronal	Mus musculus	64-94
26220904-8	2015	Furthermore, carvacrol significantly inhibited the induction of neuronal nitric oxide synthase (nNOS) after traumatic injury, and treatment with carvacrol and the nNOS inhibitor NLPA together had no extra effect on calcium concentration and neuronal injury.	carvacrol	13-22	nitric oxide synthase 1, neuronal	Mus musculus	96-100
26220904-8	2015	Furthermore, carvacrol significantly inhibited the induction of neuronal nitric oxide synthase (nNOS) after traumatic injury, and treatment with carvacrol and the nNOS inhibitor NLPA together had no extra effect on calcium concentration and neuronal injury.	nlpa	178-182	nitric oxide synthase 1, neuronal	Mus musculus	163-167
26259139-8	2015	Isoflurane decreased infarct size from 54 +- 10% in control to 36 +- 10% (P &lt; 0.05, n = 8 mice per group), improved cardiac function after reperfusion, and increased the ratios of phosphorylated-Akt/AKT, phosphorylated-eNOS/eNOS, and phosphorylated-nNOS/nNOS in C57BL/6 mice subjected to ischemia-reperfusion injury.	Isoflurane	0-10	nitric oxide synthase 1, neuronal	Mus musculus	257-261
26869823-12	2015	L-NG-nitroarginine methyl ester (100muM), which is a nonselective nitric oxide synthase (NOS) inhibitor, blocked the effects of GRe on ICC pacemaker activity and GRe-stimulated cGMP production in ICCs.	NG-Nitroarginine Methyl Ester	0-31	nitric oxide synthase 1, neuronal	Mus musculus	66-87
26269519-9	2015	Inhibition of NOS1 blocked the effect of dextran on TGF response.	Dextrans	41-48	nitric oxide synthase 1, neuronal	Mus musculus	14-18
26235957-0	2015	Striatal NOS1 has dimorphic expression and activity under stress and nicotine sensitization.	Nicotine	69-77	nitric oxide synthase 1, neuronal	Mus musculus	9-13
26241336-8	2015	Ang II (1 muM, 3 h) induced the expression of nNOS and NADPH oxidase, caused NO and superoxide anion accumulation, thus leading to excessive oxidative stress.	Superoxides	84-100	nitric oxide synthase 1, neuronal	Mus musculus	46-50
26241336-11	2015	Importantly, these effects were alleviated by 50 muM propofol, nNOS inhibitor S-methyl-l-thiocitrulline (SMTC) and angiotensin type 1 receptor (AT1R) blocker losartan, but not AT2R blocker PD123319.	S-methylthiocitrulline	78-103	nitric oxide synthase 1, neuronal	Mus musculus	63-67
26241336-11	2015	Importantly, these effects were alleviated by 50 muM propofol, nNOS inhibitor S-methyl-l-thiocitrulline (SMTC) and angiotensin type 1 receptor (AT1R) blocker losartan, but not AT2R blocker PD123319.	S-methylthiocitrulline	105-109	nitric oxide synthase 1, neuronal	Mus musculus	63-67
26324446-0	2015	NOS1-derived nitric oxide promotes NF-kappaB transcriptional activity through inhibition of suppressor of cytokine signaling-1.	Nitric Oxide	13-25	nitric oxide synthase 1, neuronal	Mus musculus	0-4
26192095-13	2015	Related to nitric oxide (NO) metabolism, neuronal nitric oxide synthase (nNOS) protein expression was 52% decreased by the hangover condition compared with control group.	Nitric Oxide	11-23	nitric oxide synthase 1, neuronal	Mus musculus	41-71
26192095-13	2015	Related to nitric oxide (NO) metabolism, neuronal nitric oxide synthase (nNOS) protein expression was 52% decreased by the hangover condition compared with control group.	Nitric Oxide	11-23	nitric oxide synthase 1, neuronal	Mus musculus	73-77
26324446-2	2015	Here, we demonstrate that the low-output nitric oxide (NO) synthase 1 (NOS1 or nNOS) plays a critical role in the inflammatory response by promoting the activity of NF-kappaB.	nitric	41-47	nitric oxide synthase 1, neuronal	Mus musculus	71-75
26324446-2	2015	Here, we demonstrate that the low-output nitric oxide (NO) synthase 1 (NOS1 or nNOS) plays a critical role in the inflammatory response by promoting the activity of NF-kappaB.	nitric	41-47	nitric oxide synthase 1, neuronal	Mus musculus	79-83
26154151-4	2015	Nos1 produces nitric oxide (NO), a major signaling molecule in the CNS implicated in many important functions including neuronal differentiation and memory formation.	Nitric Oxide	14-26	nitric oxide synthase 1, neuronal	Mus musculus	0-4
26332024-0	2015	Modulation of neuronal nitric oxide synthase and apoptosis by the isoflavone genistein in Mdx mice.	isoflavone genistein	66-86	nitric oxide synthase 1, neuronal	Mus musculus	14-44
26332024-8	2015	Our results suggest that this isoflavone might enhance the regenerative spurt in mdx mice muscle restoring nNOS, promoting G1/S phase transition in muscle cell, and inhibiting apoptosis.	Isoflavones	30-40	nitric oxide synthase 1, neuronal	Mus musculus	107-111
26216049-9	2015	L-NAME, as a non-selective nitric oxide synthase (NOS) inhibitor, potentiated the anticonvulsant effects of licofelone.	NG-Nitroarginine Methyl Ester	0-6	nitric oxide synthase 1, neuronal	Mus musculus	27-48
26216049-9	2015	L-NAME, as a non-selective nitric oxide synthase (NOS) inhibitor, potentiated the anticonvulsant effects of licofelone.	licofelone	108-118	nitric oxide synthase 1, neuronal	Mus musculus	27-48
25740549-5	2015	The relaxing effects of acetylcholine (ACh) or sodium nitropurusside (SNP) and effects of NO synthase (NOS) inhibitors on the contractions induced by phenylephrine (PE) were measured in endothelium-intact aortas obtained from both mice.	Phenylephrine	150-163	nitric oxide synthase 1, neuronal	Mus musculus	90-101
26247728-9	2015	These findings suggest that Homer1a may be a key neuroprotective endogenous molecule that protects against NMDA-induced neuronal injury by disassembling NR2B-PSD95-nNOS complexes and reducing the membrane distribution of NMDARs.	N-Methylaspartate	107-111	nitric oxide synthase 1, neuronal	Mus musculus	164-168
24224525-1	2015	AIMS: Inorganic nitrate and nitrite from endogenous and dietary sources have emerged as alternative substrates for nitric oxide (NO) formation in addition to the classic L-arginine NO synthase (NOS)-dependent pathway.	Nitrates	16-23	nitric oxide synthase 1, neuronal	Mus musculus	181-192
24224525-1	2015	AIMS: Inorganic nitrate and nitrite from endogenous and dietary sources have emerged as alternative substrates for nitric oxide (NO) formation in addition to the classic L-arginine NO synthase (NOS)-dependent pathway.	Nitrites	28-35	nitric oxide synthase 1, neuronal	Mus musculus	181-192
25892053-4	2015	Nitric oxide (NO), which is endogenously produced by NO synthases (NOS), is associated with glial tumors.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	53-65
26037847-8	2015	In intraperitoneal administration of pentylenetetrazole, aripiprazole effects on clonic seizure latency were significantly decreased when l-NAME - a nonselective nitric oxide synthase (NOS) inhibitor, 7-nitroindazole - a selective neuronal NOS (nNOS) inhibitor, or aminoguanidine - a selective inducible NOS (iNOS) inhibitor was injected before aripiprazole administration.	Aripiprazole	57-69	nitric oxide synthase 1, neuronal	Mus musculus	162-183
26152695-5	2015	In particular, nNOS(-/-) animals showed decreased S-nitrosylation of proteins that participate in the glutamate/glutamine cycle, a metabolic process by which synaptic glutamate is recycled or oxidized to provide energy.	Glutamic Acid	102-111	nitric oxide synthase 1, neuronal	Mus musculus	15-19
26152695-5	2015	In particular, nNOS(-/-) animals showed decreased S-nitrosylation of proteins that participate in the glutamate/glutamine cycle, a metabolic process by which synaptic glutamate is recycled or oxidized to provide energy.	Glutamine	112-121	nitric oxide synthase 1, neuronal	Mus musculus	15-19
26152695-5	2015	In particular, nNOS(-/-) animals showed decreased S-nitrosylation of proteins that participate in the glutamate/glutamine cycle, a metabolic process by which synaptic glutamate is recycled or oxidized to provide energy.	Glutamic Acid	167-176	nitric oxide synthase 1, neuronal	Mus musculus	15-19
26152695-6	2015	(15)N-glutamine-based metabolomic profiling and enzymatic activity assays indicated that brain extracts from nNOS(-/-) mice converted less glutamate to glutamine and oxidized more glutamate than those from mice of the other genotypes.	n-glutamine	4-15	nitric oxide synthase 1, neuronal	Mus musculus	109-113
26152695-6	2015	(15)N-glutamine-based metabolomic profiling and enzymatic activity assays indicated that brain extracts from nNOS(-/-) mice converted less glutamate to glutamine and oxidized more glutamate than those from mice of the other genotypes.	Glutamic Acid	139-148	nitric oxide synthase 1, neuronal	Mus musculus	109-113
26152695-6	2015	(15)N-glutamine-based metabolomic profiling and enzymatic activity assays indicated that brain extracts from nNOS(-/-) mice converted less glutamate to glutamine and oxidized more glutamate than those from mice of the other genotypes.	Glutamine	6-15	nitric oxide synthase 1, neuronal	Mus musculus	109-113
26152695-6	2015	(15)N-glutamine-based metabolomic profiling and enzymatic activity assays indicated that brain extracts from nNOS(-/-) mice converted less glutamate to glutamine and oxidized more glutamate than those from mice of the other genotypes.	Glutamic Acid	180-189	nitric oxide synthase 1, neuronal	Mus musculus	109-113
26152695-9	2015	Thus, NO modulates glutamatergic neurotransmission through the selective, nNOS-dependent S-nitrosylation of proteins that govern glutamate transport and metabolism.	Glutamic Acid	19-28	nitric oxide synthase 1, neuronal	Mus musculus	74-78
26037847-8	2015	In intraperitoneal administration of pentylenetetrazole, aripiprazole effects on clonic seizure latency were significantly decreased when l-NAME - a nonselective nitric oxide synthase (NOS) inhibitor, 7-nitroindazole - a selective neuronal NOS (nNOS) inhibitor, or aminoguanidine - a selective inducible NOS (iNOS) inhibitor was injected before aripiprazole administration.	Aripiprazole	57-69	nitric oxide synthase 1, neuronal	Mus musculus	231-243
26037847-8	2015	In intraperitoneal administration of pentylenetetrazole, aripiprazole effects on clonic seizure latency were significantly decreased when l-NAME - a nonselective nitric oxide synthase (NOS) inhibitor, 7-nitroindazole - a selective neuronal NOS (nNOS) inhibitor, or aminoguanidine - a selective inducible NOS (iNOS) inhibitor was injected before aripiprazole administration.	Aripiprazole	57-69	nitric oxide synthase 1, neuronal	Mus musculus	245-249
26037847-8	2015	In intraperitoneal administration of pentylenetetrazole, aripiprazole effects on clonic seizure latency were significantly decreased when l-NAME - a nonselective nitric oxide synthase (NOS) inhibitor, 7-nitroindazole - a selective neuronal NOS (nNOS) inhibitor, or aminoguanidine - a selective inducible NOS (iNOS) inhibitor was injected before aripiprazole administration.	NG-Nitroarginine Methyl Ester	138-144	nitric oxide synthase 1, neuronal	Mus musculus	162-183
26037847-8	2015	In intraperitoneal administration of pentylenetetrazole, aripiprazole effects on clonic seizure latency were significantly decreased when l-NAME - a nonselective nitric oxide synthase (NOS) inhibitor, 7-nitroindazole - a selective neuronal NOS (nNOS) inhibitor, or aminoguanidine - a selective inducible NOS (iNOS) inhibitor was injected before aripiprazole administration.	NG-Nitroarginine Methyl Ester	138-144	nitric oxide synthase 1, neuronal	Mus musculus	231-243
26037847-8	2015	In intraperitoneal administration of pentylenetetrazole, aripiprazole effects on clonic seizure latency were significantly decreased when l-NAME - a nonselective nitric oxide synthase (NOS) inhibitor, 7-nitroindazole - a selective neuronal NOS (nNOS) inhibitor, or aminoguanidine - a selective inducible NOS (iNOS) inhibitor was injected before aripiprazole administration.	NG-Nitroarginine Methyl Ester	138-144	nitric oxide synthase 1, neuronal	Mus musculus	245-249
26037847-13	2015	In conclusion, the release of nitric oxide via iNOS or nNOS may be involved in anticonvulsant properties of aripiprazole.	Nitric Oxide	30-42	nitric oxide synthase 1, neuronal	Mus musculus	55-59
26037847-13	2015	In conclusion, the release of nitric oxide via iNOS or nNOS may be involved in anticonvulsant properties of aripiprazole.	Aripiprazole	108-120	nitric oxide synthase 1, neuronal	Mus musculus	55-59
25913572-1	2015	There is increasing evidence that the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethyl-arginine (ADMA) is involved in the pathogenesis of chronic lung diseases.	dimethylarginine	98-115	nitric oxide synthase 1, neuronal	Mus musculus	49-70
25913572-1	2015	There is increasing evidence that the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethyl-arginine (ADMA) is involved in the pathogenesis of chronic lung diseases.	N,N-dimethylarginine	117-121	nitric oxide synthase 1, neuronal	Mus musculus	49-70
26111153-12	2015	This suggests that a polybacterial infection can cause significant changes in the vascular and colonic BH4/nNOS/NRF2 pathways which might lead to impaired vascular relaxation and colonic motility.	sapropterin	103-106	nitric oxide synthase 1, neuronal	Mus musculus	107-111
25913075-2	2015	In the vasodegenerative phase, during hyperoxia, defective endothelial nitric oxide synthase (NOS) produces reactive oxygen and nitrogen free radicals rather than vasoprotective nitric oxide for unclear reasons.	reactive oxygen and nitrogen free radicals	108-150	nitric oxide synthase 1, neuronal	Mus musculus	71-92
25749441-0	2015	Glucose uptake during contraction in isolated skeletal muscles from neuronal nitric oxide synthase mu knockout mice.	Glucose	0-7	nitric oxide synthase 1, neuronal	Mus musculus	77-98
25748602-5	2015	Tingenone (200 microg/paw) administered into the right hind paw induced a local antinociceptive effect, that was antagonized by l-NOArg, nonselective nitric oxide synthase (NOS) inhibitor and by L-NPA, selective neuronal NOS (nNOS) inhibitor.	tingenone	0-9	nitric oxide synthase 1, neuronal	Mus musculus	150-171
25748602-5	2015	Tingenone (200 microg/paw) administered into the right hind paw induced a local antinociceptive effect, that was antagonized by l-NOArg, nonselective nitric oxide synthase (NOS) inhibitor and by L-NPA, selective neuronal NOS (nNOS) inhibitor.	tingenone	0-9	nitric oxide synthase 1, neuronal	Mus musculus	212-224
25748602-5	2015	Tingenone (200 microg/paw) administered into the right hind paw induced a local antinociceptive effect, that was antagonized by l-NOArg, nonselective nitric oxide synthase (NOS) inhibitor and by L-NPA, selective neuronal NOS (nNOS) inhibitor.	tingenone	0-9	nitric oxide synthase 1, neuronal	Mus musculus	226-230
25959785-10	2015	These alterations may be mediated by the reduction of NO levels in trophoblastic cells, due to the inhibitory effect of L-NAME on nitric oxide synthase (NOS) synthesis.	NG-Nitroarginine Methyl Ester	120-126	nitric oxide synthase 1, neuronal	Mus musculus	130-151
25749441-1	2015	Inhibition of nitric oxide synthase (NOS) significantly attenuates the increase in skeletal muscle glucose uptake during contraction/exercise, and a greater attenuation is observed in individuals with Type 2 diabetes compared with healthy individuals.	Glucose	99-106	nitric oxide synthase 1, neuronal	Mus musculus	14-35
25727730-9	2015	Nitrate levels in skeletal muscle and blood in nNOS(-/-) mice were dramatically lower when compared with controls, which support further our hypothesis.	Nitrates	0-7	nitric oxide synthase 1, neuronal	Mus musculus	47-51
25373868-10	2015	This decline was accompanied by an increase in reactive oxygen species (ROS) and a decrease in nitric oxide (NO) production by neuronal nitric oxide synthase (nNOS).	Nitric Oxide	95-107	nitric oxide synthase 1, neuronal	Mus musculus	127-157
25926464-9	2015	This is accompanied by increased nNOS levels in the AD mice and is reversed upon normalization of RyR-evoked calcium release with chronic dantrolene treatment.	Dantrolene	138-148	nitric oxide synthase 1, neuronal	Mus musculus	33-37
25900831-6	2015	In carotid bodies from mice lacking HO-2, compensatory increased abundance of nNOS (neuronal nitric oxide synthase) mediated O2 sensing through PKG-dependent regulation of H2S by nitric oxide.	Oxygen	125-127	nitric oxide synthase 1, neuronal	Mus musculus	78-82
25900831-6	2015	In carotid bodies from mice lacking HO-2, compensatory increased abundance of nNOS (neuronal nitric oxide synthase) mediated O2 sensing through PKG-dependent regulation of H2S by nitric oxide.	Oxygen	125-127	nitric oxide synthase 1, neuronal	Mus musculus	84-114
25900831-6	2015	In carotid bodies from mice lacking HO-2, compensatory increased abundance of nNOS (neuronal nitric oxide synthase) mediated O2 sensing through PKG-dependent regulation of H2S by nitric oxide.	Hydrogen Sulfide	172-175	nitric oxide synthase 1, neuronal	Mus musculus	78-82
25900831-6	2015	In carotid bodies from mice lacking HO-2, compensatory increased abundance of nNOS (neuronal nitric oxide synthase) mediated O2 sensing through PKG-dependent regulation of H2S by nitric oxide.	Hydrogen Sulfide	172-175	nitric oxide synthase 1, neuronal	Mus musculus	84-114
25900831-6	2015	In carotid bodies from mice lacking HO-2, compensatory increased abundance of nNOS (neuronal nitric oxide synthase) mediated O2 sensing through PKG-dependent regulation of H2S by nitric oxide.	Nitric Oxide	93-105	nitric oxide synthase 1, neuronal	Mus musculus	78-82
25373868-10	2015	This decline was accompanied by an increase in reactive oxygen species (ROS) and a decrease in nitric oxide (NO) production by neuronal nitric oxide synthase (nNOS).	Nitric Oxide	95-107	nitric oxide synthase 1, neuronal	Mus musculus	159-163
25855188-9	2015	Consistent with these observations, studies in neuronal NO synthase (nNOS) knock-out (KO) mice confirmed that PDE10A operates downstream of nNOS to limit cGMP production and excitatory corticostriatal transmission.	Cyclic GMP	154-158	nitric oxide synthase 1, neuronal	Mus musculus	140-144
25892862-0	2015	Thalidomide ameliorates portal hypertension via nitric oxide synthase independent reduced systolic blood pressure.	Thalidomide	0-11	nitric oxide synthase 1, neuronal	Mus musculus	48-69
25892862-4	2015	One hypothesis is that thalidomide destabilizes tumor necrosis factor alpha (TNFalpha) mRNA and therefore diminishes TNFalpha induction of nitric oxide synthase (NOS) and the production of nitric oxide (NO).	Thalidomide	23-34	nitric oxide synthase 1, neuronal	Mus musculus	139-160
25786132-3	2015	We have previously reported that LPS-mediated nitric oxide synthase (NOS) uncoupling, through increases in asymmetric dimethylarginine (ADMA), plays an important role in the development of ALI through the generation of reactive oxygen and nitrogen species.	dimethylarginine	118-134	nitric oxide synthase 1, neuronal	Mus musculus	46-67
25822458-1	2015	Nitric-Oxide Synthase (NOS), that produces the biological signal molecule Nitric-Oxide (NO), exists in three different isoforms called, neuronal (nNOS), endothelial (eNOS) and inducible (iNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	146-150
25786132-3	2015	We have previously reported that LPS-mediated nitric oxide synthase (NOS) uncoupling, through increases in asymmetric dimethylarginine (ADMA), plays an important role in the development of ALI through the generation of reactive oxygen and nitrogen species.	N,N-dimethylarginine	136-140	nitric oxide synthase 1, neuronal	Mus musculus	46-67
25786132-3	2015	We have previously reported that LPS-mediated nitric oxide synthase (NOS) uncoupling, through increases in asymmetric dimethylarginine (ADMA), plays an important role in the development of ALI through the generation of reactive oxygen and nitrogen species.	reactive oxygen and nitrogen	219-247	nitric oxide synthase 1, neuronal	Mus musculus	46-67
25451109-0	2015	Differential effects of corticosterone on the colocalization of reelin and neuronal nitric oxide synthase in the adult hippocampus in wild type and heterozygous reeler mice.	Corticosterone	24-38	nitric oxide synthase 1, neuronal	Mus musculus	75-105
25837940-0	2015	Involvement of neuronal nitric oxide synthase in N-methyl-N-nitrosourea-induced retinal degeneration in mice.	Methylnitrosourea	49-71	nitric oxide synthase 1, neuronal	Mus musculus	15-45
25837940-3	2015	We hypothesized that nitric oxide synthase (NOS)/NO are involved in photoreceptor cell death by MNU.	Methylnitrosourea	96-99	nitric oxide synthase 1, neuronal	Mus musculus	21-42
25391901-5	2015	We determined that nitric oxide synthase 1 (NOS1) and NOS3 contribute to shear stress-mediated NO production in the CD, that is attenuated by low doses of the ENaC inhibitors amiloride and benzamil.	Cadmium	116-118	nitric oxide synthase 1, neuronal	Mus musculus	19-42
25391901-5	2015	We determined that nitric oxide synthase 1 (NOS1) and NOS3 contribute to shear stress-mediated NO production in the CD, that is attenuated by low doses of the ENaC inhibitors amiloride and benzamil.	Cadmium	116-118	nitric oxide synthase 1, neuronal	Mus musculus	44-48
25391901-5	2015	We determined that nitric oxide synthase 1 (NOS1) and NOS3 contribute to shear stress-mediated NO production in the CD, that is attenuated by low doses of the ENaC inhibitors amiloride and benzamil.	Amiloride	175-184	nitric oxide synthase 1, neuronal	Mus musculus	19-42
25391901-5	2015	We determined that nitric oxide synthase 1 (NOS1) and NOS3 contribute to shear stress-mediated NO production in the CD, that is attenuated by low doses of the ENaC inhibitors amiloride and benzamil.	Amiloride	175-184	nitric oxide synthase 1, neuronal	Mus musculus	44-48
25391901-5	2015	We determined that nitric oxide synthase 1 (NOS1) and NOS3 contribute to shear stress-mediated NO production in the CD, that is attenuated by low doses of the ENaC inhibitors amiloride and benzamil.	benzamil	189-197	nitric oxide synthase 1, neuronal	Mus musculus	19-42
25391901-5	2015	We determined that nitric oxide synthase 1 (NOS1) and NOS3 contribute to shear stress-mediated NO production in the CD, that is attenuated by low doses of the ENaC inhibitors amiloride and benzamil.	benzamil	189-197	nitric oxide synthase 1, neuronal	Mus musculus	44-48
25391901-7	2015	We further elucidated whether mice lacking NOS1 in the collecting duct (CDNOS1KO) have an impaired renal ET-1 system in the CD.	Cadmium	72-74	nitric oxide synthase 1, neuronal	Mus musculus	43-47
25664654-0	2015	Genetic absence of nNOS worsens fetal alcohol effects in mice.	Alcohols	38-45	nitric oxide synthase 1, neuronal	Mus musculus	19-23
25664654-9	2015	The purpose of this study was to determine whether mutation of nNOS can likewise worsen alcohol-induced microencephaly and lead to permanent neuronal deficits.	Alcohols	88-95	nitric oxide synthase 1, neuronal	Mus musculus	63-67
25664654-13	2015	RESULTS: Alcohol caused dose-dependent microencephaly, but only in the nNOS(-/-) mice and not in wild-type mice.	Alcohols	9-16	nitric oxide synthase 1, neuronal	Mus musculus	71-75
25664654-14	2015	Alcohol-induced neuronal losses were more severe in the nNOS(-/-) mice than in the wild-type mice in all of the brain regions examined, including the cerebral cortex, hippocampal CA3 subregion, hippocampal CA1 subregion, and dentate gyrus.	Alcohols	0-7	nitric oxide synthase 1, neuronal	Mus musculus	56-60
25664654-15	2015	CONCLUSIONS: Targeted mutation of the nNOS gene increases the vulnerability of the developing brain to alcohol-induced growth restriction and neuronal losses.	Alcohols	103-110	nitric oxide synthase 1, neuronal	Mus musculus	38-42
25684045-0	2015	Genetic absence of nNOS worsens fetal alcohol effects in mice.	Alcohols	38-45	nitric oxide synthase 1, neuronal	Mus musculus	19-23
25684045-10	2015	In this study, we examined whether homozygous mutation of the nNOS gene in mice worsens the behavioral deficits of developmental alcohol exposure.	Alcohols	129-136	nitric oxide synthase 1, neuronal	Mus musculus	62-66
25684045-15	2015	Furthermore, the nNOS(-/-) mice were substantially more impaired than wild-type mice in their performance on all 3 of the behavioral tests and at both the low (2.2) and high (4.4) doses of alcohol.	Alcohols	189-196	nitric oxide synthase 1, neuronal	Mus musculus	17-21
25684045-16	2015	CONCLUSIONS: Targeted disruption of the nNOS gene worsens the behavioral impact of developmental alcohol exposure and allows alcohol-induced learning problems to emerge that are not seen in wild type.	Alcohols	97-104	nitric oxide synthase 1, neuronal	Mus musculus	40-44
25684045-16	2015	CONCLUSIONS: Targeted disruption of the nNOS gene worsens the behavioral impact of developmental alcohol exposure and allows alcohol-induced learning problems to emerge that are not seen in wild type.	Alcohols	125-132	nitric oxide synthase 1, neuronal	Mus musculus	40-44
25967872-10	2015	Also, L-NAME (100 muM), a non-selective NO synthase (NOS) inhibitor, blocked the effects of quercetin on pacemaker activity and quercetin stimulated cGMP production.	NG-Nitroarginine Methyl Ester	6-12	nitric oxide synthase 1, neuronal	Mus musculus	40-51
25326127-7	2015	Oxypurinol and Tempol diminished the leak in NOS1(-/-) cardiomyocytes.	Oxypurinol	0-10	nitric oxide synthase 1, neuronal	Mus musculus	45-49
25326127-12	2015	CONCLUSIONS: Ca(2+) leak and temperature are normally inversely proportional, whereas NOS1 deficiency reverses this effect, increasing leak and elevating reactive oxygen species production because temperature increases.	Reactive Oxygen Species	154-177	nitric oxide synthase 1, neuronal	Mus musculus	86-90
25359537-11	2014	We conclude that ROS-induced upregulation of ROCK-2 expression accounts for the increased pyloric sphincter tone and nNOS downregulation in the newborn hph-1 mice.	Reactive Oxygen Species	17-20	nitric oxide synthase 1, neuronal	Mus musculus	117-121
25511929-0	2015	Importance of genetics in fetal alcohol effects: null mutation of the nNOS gene worsens alcohol-induced cerebellar neuronal losses and behavioral deficits.	Alcohols	32-39	nitric oxide synthase 1, neuronal	Mus musculus	70-74
25511929-0	2015	Importance of genetics in fetal alcohol effects: null mutation of the nNOS gene worsens alcohol-induced cerebellar neuronal losses and behavioral deficits.	Alcohols	88-95	nitric oxide synthase 1, neuronal	Mus musculus	70-74
25511929-6	2015	Previous studies have revealed that mice carrying a homozygous mutation of the gene for neuronal nitric oxide synthase (nNOS-/- mice) have more severe acute alcohol-induced neuronal losses from the cerebellum than wild type mice.	Alcohols	157-164	nitric oxide synthase 1, neuronal	Mus musculus	88-118
25511929-6	2015	Previous studies have revealed that mice carrying a homozygous mutation of the gene for neuronal nitric oxide synthase (nNOS-/- mice) have more severe acute alcohol-induced neuronal losses from the cerebellum than wild type mice.	Alcohols	157-164	nitric oxide synthase 1, neuronal	Mus musculus	120-124
25511929-10	2015	Alcohol caused dose-related deficits in rotarod and balance beam performance in both nNOS-/- and wild type mice.	Alcohols	0-7	nitric oxide synthase 1, neuronal	Mus musculus	85-89
25511929-11	2015	However, the alcohol-induced behavioral deficits were substantially worse in the nNOS-/- mice than in wild type.	Alcohols	13-20	nitric oxide synthase 1, neuronal	Mus musculus	81-85
25511929-12	2015	Likewise, alcohol exposure led to losses of Purkinje cells and cerebellar granule cells in mice of both genotypes, but the cell losses were more severe in the nNOS-/- mice than in wild type.	Alcohols	10-17	nitric oxide synthase 1, neuronal	Mus musculus	159-163
25511929-14	2015	Thus, homozygous mutation of the nNOS gene increases vulnerability to alcohol-induced cerebellar dysfunction and neuronal loss.	Alcohols	70-77	nitric oxide synthase 1, neuronal	Mus musculus	33-37
25511929-15	2015	nNOS is the first gene identified whose mutation worsens alcohol-induced cerebellar behavioral deficits.	Alcohols	57-64	nitric oxide synthase 1, neuronal	Mus musculus	0-4
25042931-3	2014	In mice lacking dystrophin, restoration of nNOS effects by a phosphodiesterase 5 (PDE5) inhibitor (sildenafil) improves skeletal and cardiac muscle performance.	Sildenafil Citrate	99-109	nitric oxide synthase 1, neuronal	Mus musculus	43-47
25457840-8	2014	The retinal-protective effect of ABT-702 was demonstrated by significant reduction of Iba-1, ENT1, TNF-alpha, IL-6, and iNOS/nNOS protein or mRNA expression in TON as revealed by western blot and real time PCR.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	33-36	nitric oxide synthase 1, neuronal	Mus musculus	125-129
25344365-5	2014	Swelling-induced NO release was also prevented by the nitric oxide synthase 1 (NOS1) inhibitor, nitroguanidine, and significantly reduced in NOS1 knockout mice.	nitroguanidine	96-110	nitric oxide synthase 1, neuronal	Mus musculus	54-77
25344365-5	2014	Swelling-induced NO release was also prevented by the nitric oxide synthase 1 (NOS1) inhibitor, nitroguanidine, and significantly reduced in NOS1 knockout mice.	nitroguanidine	96-110	nitric oxide synthase 1, neuronal	Mus musculus	79-83
25454121-3	2014	Nitric oxide (NO) signaling has been involved in both memory development through neuronal NO synthase (nNOS), and neuroinflammation through inducible NO synthase (iNOS) which mediates CNS inflammatory processes.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	103-107
25281315-0	2015	Nitric oxide synthase inhibition decreases l-DOPA-induced dyskinesia and the expression of striatal molecular markers in Pitx3(-/-) aphakia mice.	Levodopa	43-49	nitric oxide synthase 1, neuronal	Mus musculus	0-21
25281315-1	2015	Nitric oxide (NO), a gaseous messenger molecule synthesized by nitric oxide synthase (NOS), plays a pivotal role in integrating dopamine transmission in the basal ganglia and has been implicated in the pathogenesis of Parkinson disease (PD).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	63-84
25281315-1	2015	Nitric oxide (NO), a gaseous messenger molecule synthesized by nitric oxide synthase (NOS), plays a pivotal role in integrating dopamine transmission in the basal ganglia and has been implicated in the pathogenesis of Parkinson disease (PD).	Dopamine	128-136	nitric oxide synthase 1, neuronal	Mus musculus	63-84
25192731-3	2014	Although there have been some discrepant results, it has been consistently demonstrated that inhibition of NO synthase (NOS) attenuates the increase in skeletal muscle glucose uptake during contraction in mouse and rat muscle ex vivo, during in situ contraction in rats and during exercise in humans.	Glucose	168-175	nitric oxide synthase 1, neuronal	Mus musculus	107-118
25195695-2	2014	Since NO synthase (NOS) and arginase compete for the same substrate l-arginine, limiting arginase activity may provide more NO and thus be a beneficial therapeutic approach to erectile dysfunction (ED).	Arginine	68-78	nitric oxide synthase 1, neuronal	Mus musculus	6-17
25025574-1	2014	Neuronal NO synthase (nNOS)-mediated cGMP accumulation has been shown to affect a variety of neuronal cell activities, regardless of whether they are detrimental or beneficial, depending on the amount of their levels, under the physiological and pathological situations.	Cyclic GMP	37-41	nitric oxide synthase 1, neuronal	Mus musculus	22-26
25025574-2	2014	In the present study, we examined the role of proton-sensing G protein-coupled receptors (GPCRs), which have been identified as new pH sensors, in the acidic pH-induced nNOS/cGMP activity in N1E-115 neuronal cells.	Cyclic GMP	174-178	nitric oxide synthase 1, neuronal	Mus musculus	169-173
25025574-4	2014	An extracellular acidic pH increased cGMP accumulation, which was inhibited by nNOS-specific inhibitors.	Cyclic GMP	37-41	nitric oxide synthase 1, neuronal	Mus musculus	79-83
25025574-7	2014	Moreover cGMP accumulation was inhibited by 2-aminoethoxydiphenyl borate, an inhibitor of inositol 1,4,5-trisphosphate channel; however, it was not by wortmannin, a phosphatidylinositol 3-kinase inhibitor, which inhibited Akt/nNOS phosphorylation.	Cyclic GMP	9-13	nitric oxide synthase 1, neuronal	Mus musculus	226-230
25025574-7	2014	Moreover cGMP accumulation was inhibited by 2-aminoethoxydiphenyl borate, an inhibitor of inositol 1,4,5-trisphosphate channel; however, it was not by wortmannin, a phosphatidylinositol 3-kinase inhibitor, which inhibited Akt/nNOS phosphorylation.	2-aminoethoxydiphenyl borate	44-72	nitric oxide synthase 1, neuronal	Mus musculus	226-230
25025574-8	2014	In conclusion, acidic pH stimulates cGMP accumulation preferentially through the OGR1/Gq/11 proteins/phospholipase C/Ca(2+)/nNOS in N1E-115 neuronal cells.	Cyclic GMP	36-40	nitric oxide synthase 1, neuronal	Mus musculus	124-128
25173990-9	2014	Both anti- and proconvulsant effects of D-pen were blocked by a single dose of a nonspecific inhibitor of nitric oxide synthase (NOS), L-NAME (10 mg/kg, i.p.	Penicillamine	40-45	nitric oxide synthase 1, neuronal	Mus musculus	106-127
25149996-10	2014	Pre-treatment with aminoguanidine (50mg/kg, ip), an inducible nitric oxide synthase (NOS) inhibitor, significantly potentiated the anxiolytic-like activity of piperine, as compared to piperine and aminoguanidine alone in stressed mice.	piperine	159-167	nitric oxide synthase 1, neuronal	Mus musculus	62-83
25271439-9	2014	Moreover, pretreatment with tempol notably inhibited cisplatin-induced oxidative stress and disruption of mitochondrial function by restoring mitochondrial oxidative phosphorylation, complexes I and III activities, mNOS protein expression and ATP content.	tempol	28-34	nitric oxide synthase 1, neuronal	Mus musculus	215-219
25271439-9	2014	Moreover, pretreatment with tempol notably inhibited cisplatin-induced oxidative stress and disruption of mitochondrial function by restoring mitochondrial oxidative phosphorylation, complexes I and III activities, mNOS protein expression and ATP content.	Cisplatin	53-62	nitric oxide synthase 1, neuronal	Mus musculus	215-219
25149996-10	2014	Pre-treatment with aminoguanidine (50mg/kg, ip), an inducible nitric oxide synthase (NOS) inhibitor, significantly potentiated the anxiolytic-like activity of piperine, as compared to piperine and aminoguanidine alone in stressed mice.	pimagedine	19-33	nitric oxide synthase 1, neuronal	Mus musculus	62-83
25170949-0	2014	Neuronal nitric oxide synthase induction in the antitumorigenic and neurotoxic effects of 2-methoxyestradiol.	2-Methoxyestradiol	90-108	nitric oxide synthase 1, neuronal	Mus musculus	0-30
25113933-2	2014	Results revealed that all the synthesized analogs of oleanolic acid inhibit NO production with an IC50 of 2.66-41.7 muM as compared to the specific nitric oxide synthase (NOS) inhibitor, L-NAME (IC50=69.21 and 73.18 muM on RAW 264.7 and J774A.1 cells, respectively) without affecting the cell viability when tested at their half maximal concentration.	Oleanolic Acid	53-67	nitric oxide synthase 1, neuronal	Mus musculus	148-169
25113933-2	2014	Results revealed that all the synthesized analogs of oleanolic acid inhibit NO production with an IC50 of 2.66-41.7 muM as compared to the specific nitric oxide synthase (NOS) inhibitor, L-NAME (IC50=69.21 and 73.18 muM on RAW 264.7 and J774A.1 cells, respectively) without affecting the cell viability when tested at their half maximal concentration.	NG-Nitroarginine Methyl Ester	187-193	nitric oxide synthase 1, neuronal	Mus musculus	148-169
25170949-10	2014	We presented evidence that 2-methoxyestradiol, in contrast to 17beta-estradiol, specifically affects neuronal nitric oxide synthase and augments 3-nitrotyrosine level leading to osteosarcoma and immortalized hippocampal cell death.	2-Methoxyestradiol	27-45	nitric oxide synthase 1, neuronal	Mus musculus	101-131
24846012-5	2014	These data indicate that the co-administration of morphine with CORM-2 or CoPP produced remarkable local antinociceptive effects in WT and nNOS-KO mice and reveal that a significant interaction between carbon monoxide and nitric oxide systems occurs on the local antinociceptive effects produced by morphine during acute thermal nociception.	Morphine	50-58	nitric oxide synthase 1, neuronal	Mus musculus	139-143
24513083-6	2014	Furthermore, ICA-treated mice showed an increased expression of three nitric oxide synthase (NOS) isoforms at both mRNA and protein levels, together with increased NO and cGMP levels in the hippocampus and cortex of mice.	icarrin	13-16	nitric oxide synthase 1, neuronal	Mus musculus	70-91
24463882-4	2014	A PDZ domain-deleted nNOS gene (DeltaPDZ nNOS) was packaged into tyrosine mutant AAV-9 and delivered to the heart of ~14-month-old female mdx mice, a phenotypic model of Duchenne cardiomyopathy.	Tyrosine	65-73	nitric oxide synthase 1, neuronal	Mus musculus	21-25
24803306-14	2014	Our results suggest that agomelatine has anticonvulsant activity in intravenous penthylenetetrazol-induced seizure in acute therapy and this effect can be at least in part due to iNOS or nNOS induction.	agomelatine	25-36	nitric oxide synthase 1, neuronal	Mus musculus	187-191
24803306-14	2014	Our results suggest that agomelatine has anticonvulsant activity in intravenous penthylenetetrazol-induced seizure in acute therapy and this effect can be at least in part due to iNOS or nNOS induction.	penthylenetetrazol	80-98	nitric oxide synthase 1, neuronal	Mus musculus	187-191
25033204-1	2014	AIM: Argininosuccinate synthetase (ASS) is essential for recycling L-citrulline, the by-product of NO synthase (NOS), to the NOS substrate L-arginine.	Citrulline	67-79	nitric oxide synthase 1, neuronal	Mus musculus	99-110
25033204-1	2014	AIM: Argininosuccinate synthetase (ASS) is essential for recycling L-citrulline, the by-product of NO synthase (NOS), to the NOS substrate L-arginine.	Arginine	139-149	nitric oxide synthase 1, neuronal	Mus musculus	99-110
24760996-2	2014	Severe anemia activates hypoxia-inducible factor (HIF) signaling by hypoxic- and neuronal nitric oxide (NO) synthase- (nNOS) dependent mechanisms.	Nitric Oxide	90-102	nitric oxide synthase 1, neuronal	Mus musculus	119-123
24713372-12	2014	Melatonin alone and as a pretreatment before ethanol hangover significantly increased NO production by nNOS and iNOS as compared with control groups.	Melatonin	0-9	nitric oxide synthase 1, neuronal	Mus musculus	103-107
24782615-1	2014	AIM: To investigate the relationship between neuronal nitric oxide synthase (nNOS) expression and the natriuretic peptide signaling pathway in the gastric fundus of streptozotocin (STZ)-induced diabetic mice.	Streptozocin	181-184	nitric oxide synthase 1, neuronal	Mus musculus	77-81
24353182-8	2014	Correspondingly, pharmacological (methyl-beta-cyclodextrin) or genetic disruption of caveolae (Cav-1 knockout mice) abolished coronary FMD, which was rescued by sepiapterin, the stable precursor of NO synthase (NOS) cofactor, tetrahydrobiopterin.	sepiapterin	161-172	nitric oxide synthase 1, neuronal	Mus musculus	198-209
24622771-6	2014	The nitric oxide synthase (NOS) inhibitor L-NAME abolished the differences in phenylephrine response between the groups, suggesting that ISO impaired basal NO availability in the aorta of WT and beta1KO mice.	NG-Nitroarginine Methyl Ester	42-48	nitric oxide synthase 1, neuronal	Mus musculus	4-25
24657074-1	2014	Nitric oxide is a gaseous molecule associated with many distinct physiological functions, and is derived from L-arginine catalyzed by nitric oxide synthase (NOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	134-155
24657074-1	2014	Nitric oxide is a gaseous molecule associated with many distinct physiological functions, and is derived from L-arginine catalyzed by nitric oxide synthase (NOS).	Arginine	110-120	nitric oxide synthase 1, neuronal	Mus musculus	134-155
24690995-1	2014	The purpose of the work was to study the impact of the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA) and its degrading enzyme, dimethylarginine dimethylaminohydrolase (DDAH1), on atherosclerosis in subtotally nephrectomized (SNX) ApoE-deficient mice.	dimethylarginine	115-131	nitric oxide synthase 1, neuronal	Mus musculus	66-87
24690995-1	2014	The purpose of the work was to study the impact of the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA) and its degrading enzyme, dimethylarginine dimethylaminohydrolase (DDAH1), on atherosclerosis in subtotally nephrectomized (SNX) ApoE-deficient mice.	N,N-dimethylarginine	133-137	nitric oxide synthase 1, neuronal	Mus musculus	66-87
24782615-1	2014	AIM: To investigate the relationship between neuronal nitric oxide synthase (nNOS) expression and the natriuretic peptide signaling pathway in the gastric fundus of streptozotocin (STZ)-induced diabetic mice.	Streptozocin	165-179	nitric oxide synthase 1, neuronal	Mus musculus	45-75
24782615-1	2014	AIM: To investigate the relationship between neuronal nitric oxide synthase (nNOS) expression and the natriuretic peptide signaling pathway in the gastric fundus of streptozotocin (STZ)-induced diabetic mice.	Streptozocin	165-179	nitric oxide synthase 1, neuronal	Mus musculus	77-81
24782615-1	2014	AIM: To investigate the relationship between neuronal nitric oxide synthase (nNOS) expression and the natriuretic peptide signaling pathway in the gastric fundus of streptozotocin (STZ)-induced diabetic mice.	Streptozocin	181-184	nitric oxide synthase 1, neuronal	Mus musculus	45-75
24671193-7	2014	L-NIO (an endothelial NOS (eNOS) inhibitor) significantly attenuated cerebral vasodilation but not BBB disruption, whereas L-NPA and 7-NI (neuronal NOS (nNOS) inhibitors) significantly reduced BBB disruption but not cerebral vasodilation.	7-nitroindazole	133-137	nitric oxide synthase 1, neuronal	Mus musculus	139-151
24671193-7	2014	L-NIO (an endothelial NOS (eNOS) inhibitor) significantly attenuated cerebral vasodilation but not BBB disruption, whereas L-NPA and 7-NI (neuronal NOS (nNOS) inhibitors) significantly reduced BBB disruption but not cerebral vasodilation.	7-nitroindazole	133-137	nitric oxide synthase 1, neuronal	Mus musculus	153-157
24622771-6	2014	The nitric oxide synthase (NOS) inhibitor L-NAME abolished the differences in phenylephrine response between the groups, suggesting that ISO impaired basal NO availability in the aorta of WT and beta1KO mice.	Phenylephrine	78-91	nitric oxide synthase 1, neuronal	Mus musculus	4-25
24607683-3	2014	Compared to the sham operated group, castration and testosterone induced BPH, indicated by increased penile erection latency; decreased penis nitric oxide synthase (NOS) activity; reduced serum acid phosphatase (ACP) activity; increased prostate index; and epithelial thickening, increased glandular perimeter, increased proliferating cell nuclear antigen (PCNA) index and upregulation of basic fibroblast growth factor (bFGF) in the prostate.	Testosterone	52-64	nitric oxide synthase 1, neuronal	Mus musculus	142-163
24406719-6	2014	Additionally, we examined the effects of the combined administration of sub-effective doses of agmatine with antidepressants, the NMDA receptor antagonist MK-801 and the neuronal nitric oxide synthase inhibitor 7-nitroindazole (7-NI) in mice exposed to either TNF-alpha or saline.	7-nitroindazole	211-226	nitric oxide synthase 1, neuronal	Mus musculus	170-200
24406719-6	2014	Additionally, we examined the effects of the combined administration of sub-effective doses of agmatine with antidepressants, the NMDA receptor antagonist MK-801 and the neuronal nitric oxide synthase inhibitor 7-nitroindazole (7-NI) in mice exposed to either TNF-alpha or saline.	7-nitroindazole	228-232	nitric oxide synthase 1, neuronal	Mus musculus	170-200
24366262-6	2014	However, in preparations pretreated with the nitric oxide synthase inhibitor N-nitro-l-arginine (l-NNA, 200 mum) and in nNOS-knockout (KO) mouse preparations, PAG shifted the transwall gradient in the depolarizing direction.	propargylglycine	159-162	nitric oxide synthase 1, neuronal	Mus musculus	120-124
24366262-12	2014	Our results suggest that endogenously generated H2S acts as a stealth hyperpolarizing factor on smooth muscle cells to maintain the CO-dependent transwall gradient and inhibits NO production from nNOS.	Hydrogen Sulfide	48-51	nitric oxide synthase 1, neuronal	Mus musculus	196-200
24114430-8	2014	An interaction between HO-1/carbon monoxide and NOS1/nitric oxide systems was also demonstrated.	Carbon Monoxide	28-43	nitric oxide synthase 1, neuronal	Mus musculus	48-52
24114430-8	2014	An interaction between HO-1/carbon monoxide and NOS1/nitric oxide systems was also demonstrated.	Nitric Oxide	53-65	nitric oxide synthase 1, neuronal	Mus musculus	48-52
24744897-1	2014	Earlier, we demonstrated that the inhibition of nitric oxide synthase (NOS) by nitro-l-arginine methyl ester (l-NAME) infusion increases the endogenous production of proinflammatory cytokine, tumor necrosis factor (TNF-alpha).	nitro-l-arginine methyl ester	79-108	nitric oxide synthase 1, neuronal	Mus musculus	48-69
24744897-1	2014	Earlier, we demonstrated that the inhibition of nitric oxide synthase (NOS) by nitro-l-arginine methyl ester (l-NAME) infusion increases the endogenous production of proinflammatory cytokine, tumor necrosis factor (TNF-alpha).	NG-Nitroarginine Methyl Ester	110-116	nitric oxide synthase 1, neuronal	Mus musculus	48-69
24081550-1	2014	RATIONALE: Nitric oxide (NO) is a messenger synthesized in both the neuronal and glial populations by nitric oxide synthase type 1 (NOS1).	Nitric Oxide	11-23	nitric oxide synthase 1, neuronal	Mus musculus	102-130
24081550-1	2014	RATIONALE: Nitric oxide (NO) is a messenger synthesized in both the neuronal and glial populations by nitric oxide synthase type 1 (NOS1).	Nitric Oxide	11-23	nitric oxide synthase 1, neuronal	Mus musculus	132-136
24081550-8	2014	Control NOS1-/- males exhibited an exacerbated anxiety-related response in relation to control NOS1-/- females and control wild-type (WT) males; these differences disappeared in the nicotine-administered NOS1-/- males.	Nicotine	182-190	nitric oxide synthase 1, neuronal	Mus musculus	8-12
24081550-9	2014	Additionally, nicotine administration differentially affected the horizontal movements of NOS1-/- females with respect to WT animals.	Nicotine	14-22	nitric oxide synthase 1, neuronal	Mus musculus	90-94
24145125-6	2014	Inhibitors of NOS and the cystic fibrosis transmembrane conductance regulator (CFTR) prevented a decrease in AgRP secretion with glucose, suggesting a pivotal role for nNOS and the CFTR in glucose-sensing.	Glucose	189-196	nitric oxide synthase 1, neuronal	Mus musculus	168-172
24305053-8	2014	This anti-angiogenic effect was prevented by administration of the nitric oxide synthase (NOS) inhibitor L-NAME and in mice with neuronal and inducible NOS deficiency, suggesting that excessive nitric oxide released from hyperactive interneurons and glia inhibited vessel growth.	NG-Nitroarginine Methyl Ester	105-111	nitric oxide synthase 1, neuronal	Mus musculus	67-88
24240125-9	2014	Our results identify NO produced by NOS-I as a key messenger in the early phase of embryonic development of chicken, acting as a critical determinant of myogenesis through its physiological cGMP/PKG pathway.	Cyclic GMP	190-194	nitric oxide synthase 1, neuronal	Mus musculus	36-41
23820268-0	2013	Folic acid reverses nitric oxide synthase uncoupling and prevents cardiac dysfunction in insulin resistance: role of Ca2+/calmodulin-activated protein kinase II.	Folic Acid	0-10	nitric oxide synthase 1, neuronal	Mus musculus	20-41
24502594-1	2014	Nitric oxide (NO), generated by NO synthase (NOS) enzymes, is an important bioactive molecule involved in the regulation of several biological phenomena that are crucial for organogenesis, including gene expression, cell growth, matrix remolding, proliferation, differentiation and apoptosis.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	32-43
24145125-5	2014	Increasing glucose concentrations elicited a rise in Akt and neuronal nitric oxide synthase (nNOS) phosphorylation, CaMKKbeta levels, and a reduction of AMP-kinase alpha phosphorylation.	Glucose	11-18	nitric oxide synthase 1, neuronal	Mus musculus	61-91
24145125-5	2014	Increasing glucose concentrations elicited a rise in Akt and neuronal nitric oxide synthase (nNOS) phosphorylation, CaMKKbeta levels, and a reduction of AMP-kinase alpha phosphorylation.	Glucose	11-18	nitric oxide synthase 1, neuronal	Mus musculus	93-97
24145125-6	2014	Inhibitors of NOS and the cystic fibrosis transmembrane conductance regulator (CFTR) prevented a decrease in AgRP secretion with glucose, suggesting a pivotal role for nNOS and the CFTR in glucose-sensing.	Glucose	129-136	nitric oxide synthase 1, neuronal	Mus musculus	168-172
24117944-0	2014	The beneficial effects of melatonin against heart mitochondrial impairment during sepsis: inhibition of iNOS and preservation of nNOS.	Melatonin	26-35	nitric oxide synthase 1, neuronal	Mus musculus	129-133
24117944-8	2014	Melatonin administration inhibited iNOS/i-mtNOS induction, restored mitochondrial homeostasis in septic mice, and preserved the activity of nNOS/c-mtNOS.	Melatonin	0-9	nitric oxide synthase 1, neuronal	Mus musculus	140-144
23820268-1	2013	Nitric oxide synthase (NOS) may be uncoupled to produce superoxide rather than nitric oxide (NO) under pathological conditions such as diabetes mellitus and insulin resistance, leading to cardiac contractile anomalies.	Superoxides	56-66	nitric oxide synthase 1, neuronal	Mus musculus	0-21
24162656-0	2013	Opposite actions of alcohol on tonic GABA(A) receptor currents mediated by nNOS and PKC activity.	Alcohols	20-27	nitric oxide synthase 1, neuronal	Mus musculus	75-79
24162656-3	2013	The effect of alcohol on granule cell GABA(A)R inhibition was determined by a balance between two opposing effects: enhanced presynaptic vesicular release of GABA via alcohol inhibition of nitric oxide synthase (NOS) and a direct suppression of the activity of postsynaptic GABA(A)Rs.	Alcohols	14-21	nitric oxide synthase 1, neuronal	Mus musculus	189-210
24162656-3	2013	The effect of alcohol on granule cell GABA(A)R inhibition was determined by a balance between two opposing effects: enhanced presynaptic vesicular release of GABA via alcohol inhibition of nitric oxide synthase (NOS) and a direct suppression of the activity of postsynaptic GABA(A)Rs.	gamma-Aminobutyric Acid	158-162	nitric oxide synthase 1, neuronal	Mus musculus	189-210
24008126-1	2013	Nitric oxide which is synthesised by nitric oxide synthase (NOS) is involved in processes related to regeneration after nerve injury and neuropathic pain.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	37-58
24008126-7	2013	Significant differences between CCI and sham-operated animals were found in nNOS-/- after day 6, in WT mice after day 10, and in iNOS-/- after day 17 post surgery.	CCI	32-35	nitric oxide synthase 1, neuronal	Mus musculus	76-80
24133409-3	2013	In this study, we investigated whether mice with a life long genetic deletion of the neuronal nitric oxide synthase (nNOS) gene would show similar CMMC characteristics as wild type mice that have endogenous NO production acutely inhibited.	7-(chlorocarbonylmethoxy)-4-methylcoumarin	147-151	nitric oxide synthase 1, neuronal	Mus musculus	117-121
24096211-9	2013	Furthermore, the protective effects of NaHS were associated with its ability to repress the hypoxia-induced nitric oxide synthase (NOS) activity and nitric oxide production in the hippocampus of mice brain.	sodium bisulfide	39-43	nitric oxide synthase 1, neuronal	Mus musculus	108-129
23948215-1	2013	Both nitric oxide (NO) and reactive oxygen species (ROS) generated by nNOS and NADPH oxidase (NOX), respectively, in the brain have been implicated in an array of behaviors ranging from learning and memory to social interactions.	Nitric Oxide	5-17	nitric oxide synthase 1, neuronal	Mus musculus	70-74
23948215-1	2013	Both nitric oxide (NO) and reactive oxygen species (ROS) generated by nNOS and NADPH oxidase (NOX), respectively, in the brain have been implicated in an array of behaviors ranging from learning and memory to social interactions.	Reactive Oxygen Species	27-50	nitric oxide synthase 1, neuronal	Mus musculus	70-74
23948215-1	2013	Both nitric oxide (NO) and reactive oxygen species (ROS) generated by nNOS and NADPH oxidase (NOX), respectively, in the brain have been implicated in an array of behaviors ranging from learning and memory to social interactions.	Reactive Oxygen Species	52-55	nitric oxide synthase 1, neuronal	Mus musculus	70-74
23499699-3	2013	This increased GluN receptor activity opposes MOP receptor signalling, and via neural nitric oxide synthase (nNOS) and calcium and calmodulin regulated kinase II (CaMKII) induces the phosphorylation and uncoupling of the opioid receptor, which results in the development of morphine analgesic tolerance.	Morphine	274-282	nitric oxide synthase 1, neuronal	Mus musculus	79-107
23831997-10	2013	These results suggest that nNOS-derived excess NO in the glutamatergic pathway plays a key role in the failure of the BBB during PTZ-induced GCS.	Pentylenetetrazole	129-132	nitric oxide synthase 1, neuronal	Mus musculus	27-31
23831997-7	2013	PTZ activates the glutamatergic pathway via the NMDA receptor, then nitric oxide (NO) is generated by NMDA receptor-coupled neuronal NO synthase (nNOS).	Pentylenetetrazole	0-3	nitric oxide synthase 1, neuronal	Mus musculus	146-150
23831997-7	2013	PTZ activates the glutamatergic pathway via the NMDA receptor, then nitric oxide (NO) is generated by NMDA receptor-coupled neuronal NO synthase (nNOS).	Nitric Oxide	68-80	nitric oxide synthase 1, neuronal	Mus musculus	146-150
23831997-8	2013	To examine the influence of nNOS-derived NO induced by PTZ on the increases of the BBB permeability, GdET1WI was performed using conventional nNOS gene-deficient mice with or without PTZ injection.	Pentylenetetrazole	55-58	nitric oxide synthase 1, neuronal	Mus musculus	28-32
23831997-9	2013	The failure of the BBB induced by PTZ was completely protected by nNOS deficiency in the brain.	Pentylenetetrazole	34-37	nitric oxide synthase 1, neuronal	Mus musculus	66-70
24040016-2	2013	The neuronal nitric oxide synthase/3",5"-cyclic guanosine monophosphate (nNOS/cGMP) pathway is implicated in synaptic plasticity, and in learning and memory processes.	Nitric Oxide	13-25	nitric oxide synthase 1, neuronal	Mus musculus	73-77
24040016-2	2013	The neuronal nitric oxide synthase/3",5"-cyclic guanosine monophosphate (nNOS/cGMP) pathway is implicated in synaptic plasticity, and in learning and memory processes.	3",5"-cyclic guanosine monophosphate	35-71	nitric oxide synthase 1, neuronal	Mus musculus	73-77
24040016-2	2013	The neuronal nitric oxide synthase/3",5"-cyclic guanosine monophosphate (nNOS/cGMP) pathway is implicated in synaptic plasticity, and in learning and memory processes.	Cyclic GMP	78-82	nitric oxide synthase 1, neuronal	Mus musculus	73-77
23499699-3	2013	This increased GluN receptor activity opposes MOP receptor signalling, and via neural nitric oxide synthase (nNOS) and calcium and calmodulin regulated kinase II (CaMKII) induces the phosphorylation and uncoupling of the opioid receptor, which results in the development of morphine analgesic tolerance.	Morphine	274-282	nitric oxide synthase 1, neuronal	Mus musculus	109-113
23499699-8	2013	Treatments that rescue morphine from analgesic tolerance, such as GluN receptor antagonism or PKC, nNOS and CaMKII inhibitors, all induce MOP receptor-GluN receptor re-association and reduce GluN receptor/CaMKII activity.	Morphine	23-31	nitric oxide synthase 1, neuronal	Mus musculus	99-103
23955171-1	2013	Experience-induced changes associated with odor learning are mediated by a number of signaling molecules, including nitric oxide (NO), which is predominantly synthesized by neuronal nitric oxide synthase (nNOS) in the brain.	Nitric Oxide	116-128	nitric oxide synthase 1, neuronal	Mus musculus	173-203
23955171-1	2013	Experience-induced changes associated with odor learning are mediated by a number of signaling molecules, including nitric oxide (NO), which is predominantly synthesized by neuronal nitric oxide synthase (nNOS) in the brain.	Nitric Oxide	116-128	nitric oxide synthase 1, neuronal	Mus musculus	205-209
23955171-6	2013	In wild-type mice, pretraining systemic injections of L-NAME, a nonspecific nNOS blocker, disrupted odor-CS fear retention in a dose-dependent manner.	NG-Nitroarginine Methyl Ester	54-60	nitric oxide synthase 1, neuronal	Mus musculus	76-80
23955171-6	2013	In wild-type mice, pretraining systemic injections of L-NAME, a nonspecific nNOS blocker, disrupted odor-CS fear retention in a dose-dependent manner.	odor-cs	100-107	nitric oxide synthase 1, neuronal	Mus musculus	76-80
23469860-7	2013	In addition, treatment with IL1ra plus L-NAME produced an additive inhibition of LPS-induced vascular hyporeactivity, suggesting different signalling pathways between IL-1beta and NOS (NO synthase).	NG-Nitroarginine Methyl Ester	39-45	nitric oxide synthase 1, neuronal	Mus musculus	185-196
23831468-6	2013	Immunohistochemical analysis using two different hypoxic probes showed that IR decreased hypoxic regions in tumors; treatment with a nitric oxide synthase (NOS) inhibitor, L-NAME, abrogated the effects of IR.	NG-Nitroarginine Methyl Ester	172-178	nitric oxide synthase 1, neuronal	Mus musculus	133-154
23709593-4	2013	Dilation to acetylcholine at P7 was abolished by inhibition of NO synthase (NOS) (l-NAME) or of phosphoinositide-3-kinase (PI3K) (wortmannin, LY294002).	Acetylcholine	12-25	nitric oxide synthase 1, neuronal	Mus musculus	63-74
23709593-4	2013	Dilation to acetylcholine at P7 was abolished by inhibition of NO synthase (NOS) (l-NAME) or of phosphoinositide-3-kinase (PI3K) (wortmannin, LY294002).	NG-Nitroarginine Methyl Ester	82-88	nitric oxide synthase 1, neuronal	Mus musculus	63-74
23603358-17	2013	The results showed that repeated administration of ketamine increased nitric oxide (NO) and nitric oxide synthase (NOS) in prefrontal cortex, hippocampus and serum, while decreased SOD in hippocampus and serum.	Ketamine	51-59	nitric oxide synthase 1, neuronal	Mus musculus	92-113
23665290-0	2013	Curcumin ameliorates memory deficits via neuronal nitric oxide synthase in aged mice.	Curcumin	0-8	nitric oxide synthase 1, neuronal	Mus musculus	41-71
23665290-3	2013	The present study attempts to investigate the effects of curcumin on memory decline of aged mice with a focus upon the possible contribution of the neuronal nitric oxide synthase (nNOS)/nitric oxide (NO) pathway in the memory amelioration effect of curcumin.	Nitric Oxide	157-169	nitric oxide synthase 1, neuronal	Mus musculus	180-184
23665290-3	2013	The present study attempts to investigate the effects of curcumin on memory decline of aged mice with a focus upon the possible contribution of the neuronal nitric oxide synthase (nNOS)/nitric oxide (NO) pathway in the memory amelioration effect of curcumin.	Curcumin	249-257	nitric oxide synthase 1, neuronal	Mus musculus	148-178
23665290-3	2013	The present study attempts to investigate the effects of curcumin on memory decline of aged mice with a focus upon the possible contribution of the neuronal nitric oxide synthase (nNOS)/nitric oxide (NO) pathway in the memory amelioration effect of curcumin.	Curcumin	249-257	nitric oxide synthase 1, neuronal	Mus musculus	180-184
23665290-5	2013	Immunoblotting revealed that chronic treatment of curcumin increased nNOS expression in the prefrontal cortex, amygdala and hippocampus, as well as the enhancement of nNOS activity and NO concentration.	Curcumin	50-58	nitric oxide synthase 1, neuronal	Mus musculus	69-73
23665290-5	2013	Immunoblotting revealed that chronic treatment of curcumin increased nNOS expression in the prefrontal cortex, amygdala and hippocampus, as well as the enhancement of nNOS activity and NO concentration.	Curcumin	50-58	nitric oxide synthase 1, neuronal	Mus musculus	167-171
23665290-6	2013	This enhancement was suppressed by pre-treatment with 7-nitroindazole (7-NI), a specific inhibitor of neuronal nitric oxide synthase (nNOS).	7-nitroindazole	54-69	nitric oxide synthase 1, neuronal	Mus musculus	102-132
23665290-6	2013	This enhancement was suppressed by pre-treatment with 7-nitroindazole (7-NI), a specific inhibitor of neuronal nitric oxide synthase (nNOS).	7-nitroindazole	54-69	nitric oxide synthase 1, neuronal	Mus musculus	134-138
23665290-6	2013	This enhancement was suppressed by pre-treatment with 7-nitroindazole (7-NI), a specific inhibitor of neuronal nitric oxide synthase (nNOS).	7-nitroindazole	71-75	nitric oxide synthase 1, neuronal	Mus musculus	102-132
23665290-6	2013	This enhancement was suppressed by pre-treatment with 7-nitroindazole (7-NI), a specific inhibitor of neuronal nitric oxide synthase (nNOS).	7-nitroindazole	71-75	nitric oxide synthase 1, neuronal	Mus musculus	134-138
23665290-7	2013	Furthermore, inhibition of nNOS synthase by 7-NI also prevented the memory improvement effects of curcumin in aged mice.	7-nitroindazole	44-48	nitric oxide synthase 1, neuronal	Mus musculus	27-31
23665290-7	2013	Furthermore, inhibition of nNOS synthase by 7-NI also prevented the memory improvement effects of curcumin in aged mice.	Curcumin	98-106	nitric oxide synthase 1, neuronal	Mus musculus	27-31
23665290-8	2013	Taken together, the results of the present study suggest that the amelioration of memory deficits by curcumin in aged mice was mediated, at least in part, by activating the nNOS activity in specific brain regions.	Curcumin	101-109	nitric oxide synthase 1, neuronal	Mus musculus	173-177
23880066-10	2013	RESULTS: Pretreatment with co-ultraPEALut significantly reduced cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression in a concentration-dependent manner, restored neuronal nitric oxide synthase (nNOS) expression at all three tested concentrations, and protected cells by cell death (MTT assay) in spinal cord organotypic cultures.	monooxyethylene trimethylolpropane tristearate	309-312	nitric oxide synthase 1, neuronal	Mus musculus	189-219
23880066-10	2013	RESULTS: Pretreatment with co-ultraPEALut significantly reduced cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression in a concentration-dependent manner, restored neuronal nitric oxide synthase (nNOS) expression at all three tested concentrations, and protected cells by cell death (MTT assay) in spinal cord organotypic cultures.	monooxyethylene trimethylolpropane tristearate	309-312	nitric oxide synthase 1, neuronal	Mus musculus	221-225
23483201-5	2013	RESULTS: While nitric oxide, synthetized by NOS1 and/or NOS2, increased the local antinociceptive effects of morphine during acute and chronic pain, it decreased the inhibitory effects of morphine after visceral pain.	Nitric Oxide	15-27	nitric oxide synthase 1, neuronal	Mus musculus	44-48
23483201-5	2013	RESULTS: While nitric oxide, synthetized by NOS1 and/or NOS2, increased the local antinociceptive effects of morphine during acute and chronic pain, it decreased the inhibitory effects of morphine after visceral pain.	Morphine	109-117	nitric oxide synthase 1, neuronal	Mus musculus	44-48
23483201-7	2013	CONCLUSIONS: CORM-2 and CoPP treatments improved the local antinociceptive effects of morphine during chronic inflammatory and neuropathic pain by interaction with nitric oxide synthetized by NOS1 and NOS2 isoforms.	Morphine	86-94	nitric oxide synthase 1, neuronal	Mus musculus	192-196
23483201-7	2013	CONCLUSIONS: CORM-2 and CoPP treatments improved the local antinociceptive effects of morphine during chronic inflammatory and neuropathic pain by interaction with nitric oxide synthetized by NOS1 and NOS2 isoforms.	Nitric Oxide	164-176	nitric oxide synthase 1, neuronal	Mus musculus	192-196
23639814-6	2013	Gastric tissue neuronal nitric oxide synthase (nNOS) protein expression was upregulated in both newborn and adult hph-1 mice, but in the former there was evidence of enzyme uncoupling and higher tissue superoxide generation when compared with same age-matched animals.	Superoxides	202-212	nitric oxide synthase 1, neuronal	Mus musculus	47-51
23812222-3	2013	MATERIALS AND METHODS: On gestation day 8, mice were injected with a non-teratogenic dose (20 mg/kg) of the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl esther (L-NAME).	Nitroarginine	146-167	nitric oxide synthase 1, neuronal	Mus musculus	108-129
23399681-2	2013	Nitric oxide synthase (NOS) expression could be modified by simulation of PPARgamma which in turn activates nitric oxide (NO)/soluble guanylyl-cyclase (sGC)/cyclic guanosine mono phosphate (cGMP) pathway.	Nitric Oxide	108-120	nitric oxide synthase 1, neuronal	Mus musculus	0-21
23624088-8	2013	Surprisingly, inhibition of NOS1 did not affect contraction but reduced peak [Ca(2+)]i transient; prevented faster relaxation without affecting the tau of [Ca(2+)]i transient or PLN-Ser(16)/PLN in HP, suggesting myofilament Ca(2+) desensitization by NOS1.	Serine	182-185	nitric oxide synthase 1, neuronal	Mus musculus	28-32
23064802-4	2013	Both systemic administration of 7-Nitroindazole (7-NI), a selective nNOS activity inhibitor, and selective infusion of 7-NI into the hippocampus resulted in an increase in GR expression in the hippocampus.	7-nitroindazole	32-47	nitric oxide synthase 1, neuronal	Mus musculus	68-72
23064802-5	2013	Moreover, KCl exposure, which can induce overexpression of nNOS, resulted in a decrease in GR protein level in cultured hippocampal neurons.	Potassium Chloride	10-13	nitric oxide synthase 1, neuronal	Mus musculus	59-63
23064802-6	2013	Moreover, blockade of nNOS activity in the hippocampus leads to decreased corticosterone (CORT, glucocorticoids in rodents) concentration in the plasma and reduced corticotrophin-releasing factor expression in the hypothalamus.	Corticosterone	74-88	nitric oxide synthase 1, neuronal	Mus musculus	22-26
23064802-6	2013	Moreover, blockade of nNOS activity in the hippocampus leads to decreased corticosterone (CORT, glucocorticoids in rodents) concentration in the plasma and reduced corticotrophin-releasing factor expression in the hypothalamus.	Corticosterone	90-94	nitric oxide synthase 1, neuronal	Mus musculus	22-26
23504347-3	2013	AIMS: The purpose of this study was to investigate whether reduced levels of estradiol-17beta (E2) down-regulates tetrahydrobiopterin (BH4, a cofactor for nNOS dimerization and enzyme activity) biosynthesis and therefore nNOS mediated gastric motility would be impaired in a mouse model of chronic estrogen deficiency, follicle stimulating hormone receptor knock-out female mice (FORKO).	Estradiol	77-93	nitric oxide synthase 1, neuronal	Mus musculus	155-159
23504347-3	2013	AIMS: The purpose of this study was to investigate whether reduced levels of estradiol-17beta (E2) down-regulates tetrahydrobiopterin (BH4, a cofactor for nNOS dimerization and enzyme activity) biosynthesis and therefore nNOS mediated gastric motility would be impaired in a mouse model of chronic estrogen deficiency, follicle stimulating hormone receptor knock-out female mice (FORKO).	Estradiol	77-93	nitric oxide synthase 1, neuronal	Mus musculus	221-225
23504347-3	2013	AIMS: The purpose of this study was to investigate whether reduced levels of estradiol-17beta (E2) down-regulates tetrahydrobiopterin (BH4, a cofactor for nNOS dimerization and enzyme activity) biosynthesis and therefore nNOS mediated gastric motility would be impaired in a mouse model of chronic estrogen deficiency, follicle stimulating hormone receptor knock-out female mice (FORKO).	sapropterin	114-133	nitric oxide synthase 1, neuronal	Mus musculus	155-159
23504347-3	2013	AIMS: The purpose of this study was to investigate whether reduced levels of estradiol-17beta (E2) down-regulates tetrahydrobiopterin (BH4, a cofactor for nNOS dimerization and enzyme activity) biosynthesis and therefore nNOS mediated gastric motility would be impaired in a mouse model of chronic estrogen deficiency, follicle stimulating hormone receptor knock-out female mice (FORKO).	sapropterin	114-133	nitric oxide synthase 1, neuronal	Mus musculus	221-225
23504347-3	2013	AIMS: The purpose of this study was to investigate whether reduced levels of estradiol-17beta (E2) down-regulates tetrahydrobiopterin (BH4, a cofactor for nNOS dimerization and enzyme activity) biosynthesis and therefore nNOS mediated gastric motility would be impaired in a mouse model of chronic estrogen deficiency, follicle stimulating hormone receptor knock-out female mice (FORKO).	sapropterin	135-138	nitric oxide synthase 1, neuronal	Mus musculus	155-159
23504347-3	2013	AIMS: The purpose of this study was to investigate whether reduced levels of estradiol-17beta (E2) down-regulates tetrahydrobiopterin (BH4, a cofactor for nNOS dimerization and enzyme activity) biosynthesis and therefore nNOS mediated gastric motility would be impaired in a mouse model of chronic estrogen deficiency, follicle stimulating hormone receptor knock-out female mice (FORKO).	sapropterin	135-138	nitric oxide synthase 1, neuronal	Mus musculus	221-225
23608660-3	2013	The collecting duct (CD) is the site of daily fine-tune regulation of sodium balance, and led us to hypothesize that a CD-specific deletion of NOS1 would result in an impaired ability to excrete a sodium load leading to a salt-sensitive blood pressure phenotype.	Cadmium	21-23	nitric oxide synthase 1, neuronal	Mus musculus	143-147
23608660-3	2013	The collecting duct (CD) is the site of daily fine-tune regulation of sodium balance, and led us to hypothesize that a CD-specific deletion of NOS1 would result in an impaired ability to excrete a sodium load leading to a salt-sensitive blood pressure phenotype.	Sodium	70-76	nitric oxide synthase 1, neuronal	Mus musculus	143-147
23608660-3	2013	The collecting duct (CD) is the site of daily fine-tune regulation of sodium balance, and led us to hypothesize that a CD-specific deletion of NOS1 would result in an impaired ability to excrete a sodium load leading to a salt-sensitive blood pressure phenotype.	Cadmium	119-121	nitric oxide synthase 1, neuronal	Mus musculus	143-147
23608660-3	2013	The collecting duct (CD) is the site of daily fine-tune regulation of sodium balance, and led us to hypothesize that a CD-specific deletion of NOS1 would result in an impaired ability to excrete a sodium load leading to a salt-sensitive blood pressure phenotype.	Sodium	197-203	nitric oxide synthase 1, neuronal	Mus musculus	143-147
23608660-3	2013	The collecting duct (CD) is the site of daily fine-tune regulation of sodium balance, and led us to hypothesize that a CD-specific deletion of NOS1 would result in an impaired ability to excrete a sodium load leading to a salt-sensitive blood pressure phenotype.	Salts	222-226	nitric oxide synthase 1, neuronal	Mus musculus	143-147
23608660-4	2013	We bred AQP2-CRE mice with NOS1 floxed mice to produce flox control and CD-specific NOS1 knockout (CDNOS1KO) littermates.	Cadmium	72-74	nitric oxide synthase 1, neuronal	Mus musculus	84-88
23608660-8	2013	These findings reveal that NOS1 in the CD is critical in the regulation of fluid-electrolyte balance, and this new genetic model of CD NOS1 gene deletion will be a valuable tool to study salt-dependent blood pressure mechanisms.	Cadmium	39-41	nitric oxide synthase 1, neuronal	Mus musculus	27-31
23608660-8	2013	These findings reveal that NOS1 in the CD is critical in the regulation of fluid-electrolyte balance, and this new genetic model of CD NOS1 gene deletion will be a valuable tool to study salt-dependent blood pressure mechanisms.	Salts	187-191	nitric oxide synthase 1, neuronal	Mus musculus	135-139
23639802-10	2013	Interestingly, the nNOS-selective inhibitor S-methyl-L-thiocitrulline significantly increased the EC50 value by  60% in tissues from C57BL/6 mice but reduced the maximum response by  80% in those from nNOS(-/-) mice.	S-methylthiocitrulline	44-69	nitric oxide synthase 1, neuronal	Mus musculus	19-23
23639802-10	2013	Interestingly, the nNOS-selective inhibitor S-methyl-L-thiocitrulline significantly increased the EC50 value by  60% in tissues from C57BL/6 mice but reduced the maximum response by  80% in those from nNOS(-/-) mice.	S-methylthiocitrulline	44-69	nitric oxide synthase 1, neuronal	Mus musculus	201-205
23500667-0	2013	Curcumin ameliorates ethanol-induced memory deficits and enhanced brain nitric oxide synthase activity in mice.	Curcumin	0-8	nitric oxide synthase 1, neuronal	Mus musculus	72-93
23558387-8	2013	Genetic nNOS deficiency replicated L-NAME effects on TNF-treated muscle, diminishing NO activity (-80%; P &lt; 0.05) and preventing the decrement in specific force (P &lt; 0.05).	NG-Nitroarginine Methyl Ester	35-41	nitric oxide synthase 1, neuronal	Mus musculus	8-12
23534354-12	2013	nNOS inhibition by 7-NI had no impact on vaginal lubrication.	7-nitroindazole	19-23	nitric oxide synthase 1, neuronal	Mus musculus	0-4
23399681-2	2013	Nitric oxide synthase (NOS) expression could be modified by simulation of PPARgamma which in turn activates nitric oxide (NO)/soluble guanylyl-cyclase (sGC)/cyclic guanosine mono phosphate (cGMP) pathway.	Cyclic GMP	157-188	nitric oxide synthase 1, neuronal	Mus musculus	0-21
23399681-2	2013	Nitric oxide synthase (NOS) expression could be modified by simulation of PPARgamma which in turn activates nitric oxide (NO)/soluble guanylyl-cyclase (sGC)/cyclic guanosine mono phosphate (cGMP) pathway.	Cyclic GMP	190-194	nitric oxide synthase 1, neuronal	Mus musculus	0-21
23399681-5	2013	While selective inhibition of PPARgamma, neuronal NOS or GC could reverse the pioglitazone-induced potentiation of morphine withdrawal signs; sildenafil, a phosphodiesterase-5 inhibitor amplified its effect.	Pioglitazone	78-90	nitric oxide synthase 1, neuronal	Mus musculus	41-53
23399681-5	2013	While selective inhibition of PPARgamma, neuronal NOS or GC could reverse the pioglitazone-induced potentiation of morphine withdrawal signs; sildenafil, a phosphodiesterase-5 inhibitor amplified its effect.	Morphine	115-123	nitric oxide synthase 1, neuronal	Mus musculus	41-53
23805518-1	2013	OBJECTIVE: Effects of neurophathologic changes and expression of Glu and 60 nNOS were observed in acute isocarbophos and phoxim poisoning in mice.	isocarbophos	104-116	nitric oxide synthase 1, neuronal	Mus musculus	76-80
23396146-1	2013	The aim of the present study was to examine the effects of nitric oxide synthase (NOS) inhibitors on responses, elicited by benzodiazepines (BZs) in a modified elevated plus-maze task in mice.	Benzodiazepines	124-139	nitric oxide synthase 1, neuronal	Mus musculus	59-80
23396146-1	2013	The aim of the present study was to examine the effects of nitric oxide synthase (NOS) inhibitors on responses, elicited by benzodiazepines (BZs) in a modified elevated plus-maze task in mice.	Benzodiazepines	141-144	nitric oxide synthase 1, neuronal	Mus musculus	59-80
23501611-9	2013	Western blot analysis showed that puerarin dramatically increased the expression levels of nNOS, eNOS and phosphor-Akt in brains of Pb-treated mice.	puerarin	34-42	nitric oxide synthase 1, neuronal	Mus musculus	91-95
23501611-9	2013	Western blot analysis showed that puerarin dramatically increased the expression levels of nNOS, eNOS and phosphor-Akt in brains of Pb-treated mice.	Lead	132-134	nitric oxide synthase 1, neuronal	Mus musculus	91-95
23805518-11	2013	The statistically reduced of the expression of Glu (P&lt;0.01), the elevation of nNOS (P&lt;0.01), after Isocarbophos intoxication were observed.	isocarbophos	105-117	nitric oxide synthase 1, neuronal	Mus musculus	81-85
23203546-7	2013	PFF increased NO production by approximately fourfold in WT and eNOS-/- osteoblasts and significantly stimulated NO production in iNOS-/- and nNOS-/- osteoblasts.	p-Fluorophenylalanine	0-3	nitric oxide synthase 1, neuronal	Mus musculus	142-146
23486839-3	2013	In this study, neuronal loss and changes to the structure and immunoreactivity of myenteric neuronal nitric oxide synthase (nNOS) neurons were examined in colonic segments from mice following exposure to oxaliplatin ex vivo and following repeated intraperitoneal injections of oxaliplatin over 3 weeks in vivo, using immunohistochemistry and confocal microscopy.	Oxaliplatin	204-215	nitric oxide synthase 1, neuronal	Mus musculus	124-128
23331097-4	2013	We hypothesized that NOS1 splice variant expression and NO production in the inner medullary collecting duct (IMCD) are regulated differently in mice and rats by high dietary sodium.	Sodium	175-181	nitric oxide synthase 1, neuronal	Mus musculus	21-25
23262264-16	2013	The present findings suggest that suppression of the NO synthase/NO/cGMP pathway may be involved in the antidepressant-like effects of estradiol in OVX mice.	Cyclic GMP	68-72	nitric oxide synthase 1, neuronal	Mus musculus	53-64
23160444-7	2013	As well, genetic deletion of NOS1 splice variants in the collecting duct results in a salt-sensitive hypertensive phenotype in mice, much like the collecting duct ET1 and collecting duct ETB knockout mice.	Salts	86-90	nitric oxide synthase 1, neuronal	Mus musculus	29-33
23215832-1	2013	Nitric oxide (NO) is produced from the conversion of L-arginine by NO synthase (NOS) and regulates a variety of processes in the gastrointestinal tract.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	67-78
23215832-1	2013	Nitric oxide (NO) is produced from the conversion of L-arginine by NO synthase (NOS) and regulates a variety of processes in the gastrointestinal tract.	Arginine	53-63	nitric oxide synthase 1, neuronal	Mus musculus	67-78
23269673-1	2013	Nitric-oxide synthase (NOS) catalyzes nitric oxide (NO) synthesis via a two-step process: L-arginine (L-Arg)   N-hydroxy-L-arginine   citrulline + NO.	Nitric Oxide	38-50	nitric oxide synthase 1, neuronal	Mus musculus	0-21
23269673-1	2013	Nitric-oxide synthase (NOS) catalyzes nitric oxide (NO) synthesis via a two-step process: L-arginine (L-Arg)   N-hydroxy-L-arginine   citrulline + NO.	Arginine	90-100	nitric oxide synthase 1, neuronal	Mus musculus	0-21
23269673-1	2013	Nitric-oxide synthase (NOS) catalyzes nitric oxide (NO) synthesis via a two-step process: L-arginine (L-Arg)   N-hydroxy-L-arginine   citrulline + NO.	Arginine	102-107	nitric oxide synthase 1, neuronal	Mus musculus	0-21
23269673-1	2013	Nitric-oxide synthase (NOS) catalyzes nitric oxide (NO) synthesis via a two-step process: L-arginine (L-Arg)   N-hydroxy-L-arginine   citrulline + NO.	n-hydroxy-l-arginine   citrulline	111-144	nitric oxide synthase 1, neuronal	Mus musculus	0-21
23247392-2	2013	Evidence indicates that cardiac relaxation may depend on nitric oxide (NO), generated by NO synthase (NOS) requiring the co-factor tetrahydrobiopterin (BH(4)).	Nitric Oxide	57-69	nitric oxide synthase 1, neuronal	Mus musculus	89-100
23247392-2	2013	Evidence indicates that cardiac relaxation may depend on nitric oxide (NO), generated by NO synthase (NOS) requiring the co-factor tetrahydrobiopterin (BH(4)).	sapropterin	131-150	nitric oxide synthase 1, neuronal	Mus musculus	89-100
23399148-3	2013	The content of malondialdehyde (MDA), nitric oxide (NO) production, and the activity of NO synthase (NOS), inducible NOS (iNOS) decreased significantly when the cells were incubated with MT-alpha-glucan.	mt-alpha-glucan	187-202	nitric oxide synthase 1, neuronal	Mus musculus	88-99
23167744-8	2013	This downregulation also occludes the ability of cannabinoid agonists to activate the pro-survival signaling molecule cAMP response element-binding protein in NPY/nNOS-expressing interneurons.	Cannabinoids	49-60	nitric oxide synthase 1, neuronal	Mus musculus	163-167
23167744-8	2013	This downregulation also occludes the ability of cannabinoid agonists to activate the pro-survival signaling molecule cAMP response element-binding protein in NPY/nNOS-expressing interneurons.	Cyclic AMP	118-122	nitric oxide synthase 1, neuronal	Mus musculus	163-167
21788124-8	2013	In addition, MPTP-treated BALB/c mice showed a more significant increase of MAO-B expression than MPTP-treated C57BL/6 mice at 12 h. The increase of nNOS and iNOS protein expressions in MPTP-treated BALB/c mice was more pronounced in the striatum and midbrain than in MPTP-treated C57BL/6 mice at 12 h and 2 d. These results indicate that MAO-B, DAT, nNOS or iNOS expression levels do not influence the different strain susceptibility to MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	13-17	nitric oxide synthase 1, neuronal	Mus musculus	149-153
21788124-8	2013	In addition, MPTP-treated BALB/c mice showed a more significant increase of MAO-B expression than MPTP-treated C57BL/6 mice at 12 h. The increase of nNOS and iNOS protein expressions in MPTP-treated BALB/c mice was more pronounced in the striatum and midbrain than in MPTP-treated C57BL/6 mice at 12 h and 2 d. These results indicate that MAO-B, DAT, nNOS or iNOS expression levels do not influence the different strain susceptibility to MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	13-17	nitric oxide synthase 1, neuronal	Mus musculus	351-355
21788124-8	2013	In addition, MPTP-treated BALB/c mice showed a more significant increase of MAO-B expression than MPTP-treated C57BL/6 mice at 12 h. The increase of nNOS and iNOS protein expressions in MPTP-treated BALB/c mice was more pronounced in the striatum and midbrain than in MPTP-treated C57BL/6 mice at 12 h and 2 d. These results indicate that MAO-B, DAT, nNOS or iNOS expression levels do not influence the different strain susceptibility to MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	nitric oxide synthase 1, neuronal	Mus musculus	149-153
21788124-8	2013	In addition, MPTP-treated BALB/c mice showed a more significant increase of MAO-B expression than MPTP-treated C57BL/6 mice at 12 h. The increase of nNOS and iNOS protein expressions in MPTP-treated BALB/c mice was more pronounced in the striatum and midbrain than in MPTP-treated C57BL/6 mice at 12 h and 2 d. These results indicate that MAO-B, DAT, nNOS or iNOS expression levels do not influence the different strain susceptibility to MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	nitric oxide synthase 1, neuronal	Mus musculus	351-355
21788124-8	2013	In addition, MPTP-treated BALB/c mice showed a more significant increase of MAO-B expression than MPTP-treated C57BL/6 mice at 12 h. The increase of nNOS and iNOS protein expressions in MPTP-treated BALB/c mice was more pronounced in the striatum and midbrain than in MPTP-treated C57BL/6 mice at 12 h and 2 d. These results indicate that MAO-B, DAT, nNOS or iNOS expression levels do not influence the different strain susceptibility to MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	nitric oxide synthase 1, neuronal	Mus musculus	149-153
21788124-8	2013	In addition, MPTP-treated BALB/c mice showed a more significant increase of MAO-B expression than MPTP-treated C57BL/6 mice at 12 h. The increase of nNOS and iNOS protein expressions in MPTP-treated BALB/c mice was more pronounced in the striatum and midbrain than in MPTP-treated C57BL/6 mice at 12 h and 2 d. These results indicate that MAO-B, DAT, nNOS or iNOS expression levels do not influence the different strain susceptibility to MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	nitric oxide synthase 1, neuronal	Mus musculus	351-355
21788124-8	2013	In addition, MPTP-treated BALB/c mice showed a more significant increase of MAO-B expression than MPTP-treated C57BL/6 mice at 12 h. The increase of nNOS and iNOS protein expressions in MPTP-treated BALB/c mice was more pronounced in the striatum and midbrain than in MPTP-treated C57BL/6 mice at 12 h and 2 d. These results indicate that MAO-B, DAT, nNOS or iNOS expression levels do not influence the different strain susceptibility to MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	nitric oxide synthase 1, neuronal	Mus musculus	149-153
21788124-8	2013	In addition, MPTP-treated BALB/c mice showed a more significant increase of MAO-B expression than MPTP-treated C57BL/6 mice at 12 h. The increase of nNOS and iNOS protein expressions in MPTP-treated BALB/c mice was more pronounced in the striatum and midbrain than in MPTP-treated C57BL/6 mice at 12 h and 2 d. These results indicate that MAO-B, DAT, nNOS or iNOS expression levels do not influence the different strain susceptibility to MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	nitric oxide synthase 1, neuronal	Mus musculus	351-355
21788124-8	2013	In addition, MPTP-treated BALB/c mice showed a more significant increase of MAO-B expression than MPTP-treated C57BL/6 mice at 12 h. The increase of nNOS and iNOS protein expressions in MPTP-treated BALB/c mice was more pronounced in the striatum and midbrain than in MPTP-treated C57BL/6 mice at 12 h and 2 d. These results indicate that MAO-B, DAT, nNOS or iNOS expression levels do not influence the different strain susceptibility to MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	nitric oxide synthase 1, neuronal	Mus musculus	149-153
23262264-16	2013	The present findings suggest that suppression of the NO synthase/NO/cGMP pathway may be involved in the antidepressant-like effects of estradiol in OVX mice.	Estradiol	135-144	nitric oxide synthase 1, neuronal	Mus musculus	53-64
23091050-4	2012	LV superoxide (O(2)( -)) production was increased in nNOS(-/-) mice and reduced by L-N(omega)-nitroarginine methyl ester (L-NAME), indicating uncoupling of eNOS activity.	Superoxides	3-13	nitric oxide synthase 1, neuronal	Mus musculus	53-57
21788124-8	2013	In addition, MPTP-treated BALB/c mice showed a more significant increase of MAO-B expression than MPTP-treated C57BL/6 mice at 12 h. The increase of nNOS and iNOS protein expressions in MPTP-treated BALB/c mice was more pronounced in the striatum and midbrain than in MPTP-treated C57BL/6 mice at 12 h and 2 d. These results indicate that MAO-B, DAT, nNOS or iNOS expression levels do not influence the different strain susceptibility to MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	nitric oxide synthase 1, neuronal	Mus musculus	351-355
23818850-4	2013	We show that pial arteriolar responses to endothelial NOS (eNOS) and neuronal NOS (nNOS) agonists (Acetylcholine (ACh) and N-Methyl-D-Aspartate (NMDA)) were blunted in mice with ECM, and could be partially recovered by exogenous supplementation of tetrahydrobiopterin (BH4).	Acetylcholine	99-112	nitric oxide synthase 1, neuronal	Mus musculus	83-87
23818850-4	2013	We show that pial arteriolar responses to endothelial NOS (eNOS) and neuronal NOS (nNOS) agonists (Acetylcholine (ACh) and N-Methyl-D-Aspartate (NMDA)) were blunted in mice with ECM, and could be partially recovered by exogenous supplementation of tetrahydrobiopterin (BH4).	N-Methylaspartate	123-143	nitric oxide synthase 1, neuronal	Mus musculus	69-81
23091050-3	2012	We evaluated whether nNOS also plays a role in beta(3)-AR signaling and found that the beta(3)-AR-mediated reduction in cell shortening and [Ca(2+)](i) transient amplitude was abolished both in eNOS(-/-) and nNOS(-/-) left ventricular (LV) myocytes and in wild type LV myocytes after nNOS inhibition with S-methyl-L-thiocitrulline.	S-methylthiocitrulline	305-330	nitric oxide synthase 1, neuronal	Mus musculus	21-25
23091050-4	2012	LV superoxide (O(2)( -)) production was increased in nNOS(-/-) mice and reduced by L-N(omega)-nitroarginine methyl ester (L-NAME), indicating uncoupling of eNOS activity.	Superoxides	15-20	nitric oxide synthase 1, neuronal	Mus musculus	53-57
23091050-5	2012	eNOS S-glutathionylation and Ser-1177 phosphorylation were significantly increased in nNOS(-/-) myocytes, whereas myocardial tetrahydrobiopterin, eNOS Thr-495 phosphorylation, and arginase activity did not differ between genotypes.	Serine	29-32	nitric oxide synthase 1, neuronal	Mus musculus	86-90
23091050-7	2012	In summary, our data show that increased O(2)( -) production by XOR selectively uncouples eNOS activity and abolishes the negative inotropic effect of beta(3)-AR stimulation in nNOS(-/-) myocytes.	Superoxides	41-45	nitric oxide synthase 1, neuronal	Mus musculus	177-181
23443130-3	2012	The content of malondialdehyde (MDA), nitric oxide (NO) production, and the activity of NO synthase (NOS), inducible NOS (iNOS), decreased significantly when incubated with SES.	sesamin	173-176	nitric oxide synthase 1, neuronal	Mus musculus	88-99
23033162-1	2012	Nitric oxide (NO), synthesized as needed by NO synthase (NOS), is involved in spinogenesis and synaptogenesis.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	44-55
23516890-3	2012	This fact allowed us to assume that the radioprotective effect of S-substituted ITU caused inhibition of the endogenous synthesis of NO, which promotes the development of circulatory hypoxia, and that a further search for the radioprotective agents in this class of chemicals should be considered as the search for effective inhibitors of NO-synthase (NOS).	Sulfur	66-67	nitric oxide synthase 1, neuronal	Mus musculus	339-350
22960186-0	2012	Relationship of nitric oxide synthase induction to peroxynitrite-mediated oxidative damage during the first week after experimental traumatic brain injury.	Peroxynitrous Acid	51-64	nitric oxide synthase 1, neuronal	Mus musculus	16-37
22960186-2	2012	Nitric oxide is produced by at least three isoforms of the enzyme nitric oxide synthase (NOS) including: endothelial NOS (eNOS) in the CNS vasculature, neuronal NOS (nNOS), and inducible NOS (iNOS) in macrophages/microglia.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	66-87
22960186-2	2012	Nitric oxide is produced by at least three isoforms of the enzyme nitric oxide synthase (NOS) including: endothelial NOS (eNOS) in the CNS vasculature, neuronal NOS (nNOS), and inducible NOS (iNOS) in macrophages/microglia.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	152-164
22960186-2	2012	Nitric oxide is produced by at least three isoforms of the enzyme nitric oxide synthase (NOS) including: endothelial NOS (eNOS) in the CNS vasculature, neuronal NOS (nNOS), and inducible NOS (iNOS) in macrophages/microglia.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	166-170
22943535-1	2012	We investigated the anticonvulsant and neurobiological effects of a highly selective neuronal nitric oxide synthase (nNOS) inhibitor, N (w) -propyl-l-arginine (L-NPA), on kainic acid (KA)-induced status epilepticus (SE) and early epileptogenesis in C57BL/6J mice.	n (w) -propyl-l-arginine	134-158	nitric oxide synthase 1, neuronal	Mus musculus	85-115
23516890-3	2012	This fact allowed us to assume that the radioprotective effect of S-substituted ITU caused inhibition of the endogenous synthesis of NO, which promotes the development of circulatory hypoxia, and that a further search for the radioprotective agents in this class of chemicals should be considered as the search for effective inhibitors of NO-synthase (NOS).	substituted itu	68-83	nitric oxide synthase 1, neuronal	Mus musculus	339-350
22985517-1	2012	Nicotine, an active tobacco derived alkaloid, regulates the activity of the neuronal nitric oxide synthase (nNOS) as well as the release of nitric oxide (NO) in the nervous system.	Nicotine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	108-112
22985517-1	2012	Nicotine, an active tobacco derived alkaloid, regulates the activity of the neuronal nitric oxide synthase (nNOS) as well as the release of nitric oxide (NO) in the nervous system.	Nitric Oxide	85-97	nitric oxide synthase 1, neuronal	Mus musculus	108-112
23012472-0	2012	Cyclic AMP-dependent phosphorylation of neuronal nitric oxide synthase mediates penile erection.	Cyclic AMP	0-10	nitric oxide synthase 1, neuronal	Mus musculus	40-70
23018244-8	2012	Mesterolone administered to exercised mice (Ex-C x Ex-M) upregulated NOS I in all three muscles and NOS III in TA and SOL.	Mesterolone	0-11	nitric oxide synthase 1, neuronal	Mus musculus	69-74
23018244-9	2012	The exercise to mesterolone-treated mice (Sed-M x Ex-M) produced a strong increase in NOS I expression in GAS; in contrast it antagonized the mesterolone-induced upregulation of NOS I in TA muscle and NOS III in SOL and GAS.	Mesterolone	16-27	nitric oxide synthase 1, neuronal	Mus musculus	86-91
23044319-4	2012	METHODS: Wild-type (WT) mice were injected subcutaneously with nitric oxide synthase (NOS) inhibitor L-arginine methyl ester (L-NAME, 50 mgxkg(-1)xd(-1)) to establish PE-like model (L-NAME group) at early-, mid-, and late-pregnant periods respectively; simultaneously, the control mice were injected with normal saline (NS group).	arginine methyl ester	101-124	nitric oxide synthase 1, neuronal	Mus musculus	63-84
22943535-1	2012	We investigated the anticonvulsant and neurobiological effects of a highly selective neuronal nitric oxide synthase (nNOS) inhibitor, N (w) -propyl-l-arginine (L-NPA), on kainic acid (KA)-induced status epilepticus (SE) and early epileptogenesis in C57BL/6J mice.	n (w) -propyl-l-arginine	134-158	nitric oxide synthase 1, neuronal	Mus musculus	117-121
22943535-1	2012	We investigated the anticonvulsant and neurobiological effects of a highly selective neuronal nitric oxide synthase (nNOS) inhibitor, N (w) -propyl-l-arginine (L-NPA), on kainic acid (KA)-induced status epilepticus (SE) and early epileptogenesis in C57BL/6J mice.	Kainic Acid	171-182	nitric oxide synthase 1, neuronal	Mus musculus	117-121
23012472-1	2012	Nitric oxide (NO) generated by neuronal NO synthase (nNOS) initiates penile erection, but has not been thought to participate in the sustained erection required for normal sexual performance.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	53-57
23012472-2	2012	We now show that cAMP-dependent phosphorylation of nNOS mediates erectile physiology, including sustained erection.	Cyclic AMP	17-21	nitric oxide synthase 1, neuronal	Mus musculus	51-55
23012472-3	2012	nNOS is phosphorylated by cAMP-dependent protein kinase (PKA) at serine(S)1412.	Cyclic AMP	26-30	nitric oxide synthase 1, neuronal	Mus musculus	0-4
23012472-3	2012	nNOS is phosphorylated by cAMP-dependent protein kinase (PKA) at serine(S)1412.	Serine	65-71	nitric oxide synthase 1, neuronal	Mus musculus	0-4
23012472-5	2012	Stimulation of cAMP formation by forskolin also activates nNOS phosphorylation.	Cyclic AMP	15-19	nitric oxide synthase 1, neuronal	Mus musculus	58-62
23012472-5	2012	Stimulation of cAMP formation by forskolin also activates nNOS phosphorylation.	Colforsin	33-42	nitric oxide synthase 1, neuronal	Mus musculus	58-62
23012472-6	2012	Sustained penile erection elicited by either intracavernous forskolin injection, or augmented by forskolin during cavernous nerve electrical stimulation, is prevented by the NOS inhibitor L-NAME or in nNOS-deleted mice.	Colforsin	60-69	nitric oxide synthase 1, neuronal	Mus musculus	201-205
23012472-6	2012	Sustained penile erection elicited by either intracavernous forskolin injection, or augmented by forskolin during cavernous nerve electrical stimulation, is prevented by the NOS inhibitor L-NAME or in nNOS-deleted mice.	Colforsin	97-106	nitric oxide synthase 1, neuronal	Mus musculus	201-205
22573263-8	2012	Treatment with MK801, an NMDAR inhibitor, inhibited mechanical allodynia, ERK1/2 phosphorylation, and nNOS and iNOS upregulation in diabetic mice.	Dizocilpine Maleate	15-20	nitric oxide synthase 1, neuronal	Mus musculus	102-106
22821418-10	2012	7-Nitroindazole [a neuronal nitric oxide synthase (NOS) inhibitor] and aminoguanidine (an inducible NOS inhibitor) significantly enhanced memory improving activity and brain nitrite decreasing effect of naringin in unstressed and stressed mice respectively.	7-nitroindazole	0-15	nitric oxide synthase 1, neuronal	Mus musculus	19-49
22821418-10	2012	7-Nitroindazole [a neuronal nitric oxide synthase (NOS) inhibitor] and aminoguanidine (an inducible NOS inhibitor) significantly enhanced memory improving activity and brain nitrite decreasing effect of naringin in unstressed and stressed mice respectively.	naringin	203-211	nitric oxide synthase 1, neuronal	Mus musculus	19-49
22789621-7	2012	Neuronal nitric oxide synthase (nNOS) activity was higher in PMCA2(+/-) cerebella and inhibition of nNOS or the soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) pathway, which mediates nitric oxide (NO) signaling, reduced the amplitude of Ca(2+) transients in PMCA2(+/-) PCs, in vitro.	Cyclic GMP	144-174	nitric oxide synthase 1, neuronal	Mus musculus	32-36
22789621-7	2012	Neuronal nitric oxide synthase (nNOS) activity was higher in PMCA2(+/-) cerebella and inhibition of nNOS or the soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) pathway, which mediates nitric oxide (NO) signaling, reduced the amplitude of Ca(2+) transients in PMCA2(+/-) PCs, in vitro.	Cyclic GMP	176-180	nitric oxide synthase 1, neuronal	Mus musculus	0-30
22789621-7	2012	Neuronal nitric oxide synthase (nNOS) activity was higher in PMCA2(+/-) cerebella and inhibition of nNOS or the soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) pathway, which mediates nitric oxide (NO) signaling, reduced the amplitude of Ca(2+) transients in PMCA2(+/-) PCs, in vitro.	Cyclic GMP	176-180	nitric oxide synthase 1, neuronal	Mus musculus	32-36
22610171-5	2012	Capsaicin (1-100 mug kg(-1) min(-1)) dose dependently increased coronary blood flow in control mice, which was inhibited by the TRPV1 antagonist capsazepine or the nitric oxide synthase (NOS) inhibitor N-nitro-l-arginine methyl ester (L-NAME).	Capsaicin	0-9	nitric oxide synthase 1, neuronal	Mus musculus	164-185
22610171-5	2012	Capsaicin (1-100 mug kg(-1) min(-1)) dose dependently increased coronary blood flow in control mice, which was inhibited by the TRPV1 antagonist capsazepine or the nitric oxide synthase (NOS) inhibitor N-nitro-l-arginine methyl ester (L-NAME).	n-nitro-l-arginine methyl ester	202-233	nitric oxide synthase 1, neuronal	Mus musculus	164-185
22580898-5	2012	Leptin also sensitized aortae from eNOS(-/-) mice to acetylcholine, an effect blocked by neuronal NOS (nNOS) inhibition and not observed in eNOS-nNOS double(-/-) mice.	Acetylcholine	53-66	nitric oxide synthase 1, neuronal	Mus musculus	89-101
22763878-4	2012	NADPH-d histochemistry and nNOS immunohistochemistry showed that high concentrations of silicon in drinking water were able to minimize the impairment of the function of nitrergic neurons induced by aluminium administration.	Silicon	88-95	nitric oxide synthase 1, neuronal	Mus musculus	27-31
22763878-4	2012	NADPH-d histochemistry and nNOS immunohistochemistry showed that high concentrations of silicon in drinking water were able to minimize the impairment of the function of nitrergic neurons induced by aluminium administration.	Water	108-113	nitric oxide synthase 1, neuronal	Mus musculus	27-31
22484619-3	2012	Here, we examine whether nNOS is regulated by Ang II and affects NADPH oxidase production of intracellular reactive oxygen species (ROS(i)) and contractile function in left ventricular (LV) myocytes.	Reactive Oxygen Species	107-130	nitric oxide synthase 1, neuronal	Mus musculus	25-29
22789621-7	2012	Neuronal nitric oxide synthase (nNOS) activity was higher in PMCA2(+/-) cerebella and inhibition of nNOS or the soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) pathway, which mediates nitric oxide (NO) signaling, reduced the amplitude of Ca(2+) transients in PMCA2(+/-) PCs, in vitro.	Nitric Oxide	9-21	nitric oxide synthase 1, neuronal	Mus musculus	32-36
22484619-3	2012	Here, we examine whether nNOS is regulated by Ang II and affects NADPH oxidase production of intracellular reactive oxygen species (ROS(i)) and contractile function in left ventricular (LV) myocytes.	Reactive Oxygen Species	132-135	nitric oxide synthase 1, neuronal	Mus musculus	25-29
22484619-7	2012	Indeed, n(omega)-nitro-l-arginine methyl ester (l-NAME) or a selective nNOS inhibitor, S-methyl-l-thiocitrulline (SMTC) increased NADPH oxidase production of superoxide/ROS(i) and abolished faster myocyte relaxation induced by Ang II.	NG-Nitroarginine Methyl Ester	48-54	nitric oxide synthase 1, neuronal	Mus musculus	71-75
22484619-7	2012	Indeed, n(omega)-nitro-l-arginine methyl ester (l-NAME) or a selective nNOS inhibitor, S-methyl-l-thiocitrulline (SMTC) increased NADPH oxidase production of superoxide/ROS(i) and abolished faster myocyte relaxation induced by Ang II.	S-methylthiocitrulline	87-112	nitric oxide synthase 1, neuronal	Mus musculus	71-75
22484619-7	2012	Indeed, n(omega)-nitro-l-arginine methyl ester (l-NAME) or a selective nNOS inhibitor, S-methyl-l-thiocitrulline (SMTC) increased NADPH oxidase production of superoxide/ROS(i) and abolished faster myocyte relaxation induced by Ang II.	Superoxides	158-168	nitric oxide synthase 1, neuronal	Mus musculus	71-75
22484619-7	2012	Indeed, n(omega)-nitro-l-arginine methyl ester (l-NAME) or a selective nNOS inhibitor, S-methyl-l-thiocitrulline (SMTC) increased NADPH oxidase production of superoxide/ROS(i) and abolished faster myocyte relaxation induced by Ang II.	Reactive Oxygen Species	169-172	nitric oxide synthase 1, neuronal	Mus musculus	71-75
22406306-1	2012	Nitric oxide (NO) production involves four different NO-synthases (NOSs) that are either constitutive (neuronal, nNOS; endothelial, eNOS; mitochondrial, mNOS) or inducible (iNOS) in nature.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	113-117
22175298-3	2012	Intriguingly, supplementation of irradiated cells with L-arginine results in decreased production of peroxynitrite, suggesting that suppression of superoxide generation by nitric oxide synthase in one or more microenvironments is an important factor in the observed radioprotection.	Arginine	55-65	nitric oxide synthase 1, neuronal	Mus musculus	172-193
22175298-3	2012	Intriguingly, supplementation of irradiated cells with L-arginine results in decreased production of peroxynitrite, suggesting that suppression of superoxide generation by nitric oxide synthase in one or more microenvironments is an important factor in the observed radioprotection.	Peroxynitrous Acid	101-114	nitric oxide synthase 1, neuronal	Mus musculus	172-193
22175298-3	2012	Intriguingly, supplementation of irradiated cells with L-arginine results in decreased production of peroxynitrite, suggesting that suppression of superoxide generation by nitric oxide synthase in one or more microenvironments is an important factor in the observed radioprotection.	Superoxides	147-157	nitric oxide synthase 1, neuronal	Mus musculus	172-193
22624839-8	2012	However, nNOS protein expression was up-regulated 2-fold by BRL, and the suppressive effect of BRL on superoxide generation was abrogated by acute nNOS inhibition.	Superoxides	102-112	nitric oxide synthase 1, neuronal	Mus musculus	147-151
22258323-6	2012	Other major control mechanisms include COX-2 and nNOS affecting renin through PGE2, PGI2, and nitric oxide.	Dinoprostone	78-82	nitric oxide synthase 1, neuronal	Mus musculus	49-53
22541557-1	2012	Argininosuccinate lyase (ASL) is required for the synthesis and channeling of L-arginine to nitric oxide synthase (NOS) for nitric oxide (NO) production.	Arginine	78-88	nitric oxide synthase 1, neuronal	Mus musculus	92-113
22378773-5	2012	In the presence of the AT(1)R antagonist losartan, ANG II increased NO production in isolated mNTS neurons, an effect blocked by the AT(2)R antagonist PD123319, but not the angiotensin (1-7) antagonist D-Ala. Studies in mNTS neurons of nNOS-null or endothelial NOS (eNOS)-null mice established nNOS as the source of NO.	Losartan	41-49	nitric oxide synthase 1, neuronal	Mus musculus	236-240
22378773-5	2012	In the presence of the AT(1)R antagonist losartan, ANG II increased NO production in isolated mNTS neurons, an effect blocked by the AT(2)R antagonist PD123319, but not the angiotensin (1-7) antagonist D-Ala. Studies in mNTS neurons of nNOS-null or endothelial NOS (eNOS)-null mice established nNOS as the source of NO.	Losartan	41-49	nitric oxide synthase 1, neuronal	Mus musculus	294-298
22378773-5	2012	In the presence of the AT(1)R antagonist losartan, ANG II increased NO production in isolated mNTS neurons, an effect blocked by the AT(2)R antagonist PD123319, but not the angiotensin (1-7) antagonist D-Ala. Studies in mNTS neurons of nNOS-null or endothelial NOS (eNOS)-null mice established nNOS as the source of NO.	PD 123319	151-159	nitric oxide synthase 1, neuronal	Mus musculus	236-240
22378773-5	2012	In the presence of the AT(1)R antagonist losartan, ANG II increased NO production in isolated mNTS neurons, an effect blocked by the AT(2)R antagonist PD123319, but not the angiotensin (1-7) antagonist D-Ala. Studies in mNTS neurons of nNOS-null or endothelial NOS (eNOS)-null mice established nNOS as the source of NO.	PD 123319	151-159	nitric oxide synthase 1, neuronal	Mus musculus	294-298
22378773-6	2012	ANG II-induced ROS production was enhanced by PD123319, the NOS inhibitor N(G)-nitro-l-arginine (LNNA), or in nNOS-null mice.	Reactive Oxygen Species	15-18	nitric oxide synthase 1, neuronal	Mus musculus	110-114
22450373-1	2012	The anxiogenic and antinociceptive effects produced by glutamate N-methyl-D-aspartate receptor activation within the dorsal periaqueductal gray (dPAG) matter have been related to nitric oxide (NO) production, since injection of NO synthase (NOS) inhibitors reverses these effects.	Nitric Oxide	179-191	nitric oxide synthase 1, neuronal	Mus musculus	228-239
22258323-6	2012	Other major control mechanisms include COX-2 and nNOS affecting renin through PGE2, PGI2, and nitric oxide.	Nitric Oxide	94-106	nitric oxide synthase 1, neuronal	Mus musculus	49-53
22384812-4	2012	SVZ-derived aNSCs were protected from DNA damage by the treatment of Nomega-nitro-L-arginine methyl ester (L-NAME), a NO synthase (NOS) inhibitor, both in vitro and in vivo.	NG-Nitroarginine Methyl Ester	69-105	nitric oxide synthase 1, neuronal	Mus musculus	118-129
22384812-4	2012	SVZ-derived aNSCs were protected from DNA damage by the treatment of Nomega-nitro-L-arginine methyl ester (L-NAME), a NO synthase (NOS) inhibitor, both in vitro and in vivo.	NG-Nitroarginine Methyl Ester	107-113	nitric oxide synthase 1, neuronal	Mus musculus	118-129
22258323-6	2012	Other major control mechanisms include COX-2 and nNOS affecting renin through PGE2, PGI2, and nitric oxide.	Epoprostenol	84-88	nitric oxide synthase 1, neuronal	Mus musculus	49-53
22033862-14	2012	Thus, gallic acid showed antianxiety-like activity in unstressed mice probably by inhibition of nNOS.	Gallic Acid	6-17	nitric oxide synthase 1, neuronal	Mus musculus	96-100
22349394-3	2012	Carbon monoxide (CO) and nitric oxide (NO), generated by heme oxygenase-2 (HO-2) and neuronal nitric oxide synthase (nNOS), respectively, inhibit carotid body activity.	Carbon Monoxide	0-15	nitric oxide synthase 1, neuronal	Mus musculus	85-115
22349394-3	2012	Carbon monoxide (CO) and nitric oxide (NO), generated by heme oxygenase-2 (HO-2) and neuronal nitric oxide synthase (nNOS), respectively, inhibit carotid body activity.	Carbon Monoxide	0-15	nitric oxide synthase 1, neuronal	Mus musculus	117-121
22209711-11	2012	Nitrite measurements, electron paramagnetic resonance spectroscopy and immunohistochemistry indicated that glutamate was a potent inducer of NO production via activation of nNOS in the cortical layer VI.	Glutamic Acid	107-116	nitric oxide synthase 1, neuronal	Mus musculus	173-177
22349394-3	2012	Carbon monoxide (CO) and nitric oxide (NO), generated by heme oxygenase-2 (HO-2) and neuronal nitric oxide synthase (nNOS), respectively, inhibit carotid body activity.	Carbon Monoxide	17-19	nitric oxide synthase 1, neuronal	Mus musculus	85-115
22349394-3	2012	Carbon monoxide (CO) and nitric oxide (NO), generated by heme oxygenase-2 (HO-2) and neuronal nitric oxide synthase (nNOS), respectively, inhibit carotid body activity.	Carbon Monoxide	17-19	nitric oxide synthase 1, neuronal	Mus musculus	117-121
22349394-3	2012	Carbon monoxide (CO) and nitric oxide (NO), generated by heme oxygenase-2 (HO-2) and neuronal nitric oxide synthase (nNOS), respectively, inhibit carotid body activity.	Nitric Oxide	25-37	nitric oxide synthase 1, neuronal	Mus musculus	85-115
22349394-3	2012	Carbon monoxide (CO) and nitric oxide (NO), generated by heme oxygenase-2 (HO-2) and neuronal nitric oxide synthase (nNOS), respectively, inhibit carotid body activity.	Nitric Oxide	25-37	nitric oxide synthase 1, neuronal	Mus musculus	117-121
22209711-12	2012	In vivo administration of nNOS siRNA promoted excitotoxicity and mimicked the effects of L-NAME, LNIO and NPLA.	NG-Nitroarginine Methyl Ester	89-95	nitric oxide synthase 1, neuronal	Mus musculus	26-30
22209711-12	2012	In vivo administration of nNOS siRNA promoted excitotoxicity and mimicked the effects of L-NAME, LNIO and NPLA.	N(G)-iminoethylornithine	97-101	nitric oxide synthase 1, neuronal	Mus musculus	26-30
22209711-13	2012	A short-term glutamate treatment increased nNOS Ser1412 phosphorylation, while a long-term exposure inhibited nNOS/NR2B protein-protein interactions.	Glutamic Acid	13-22	nitric oxide synthase 1, neuronal	Mus musculus	43-47
22209711-14	2012	Altogether, these findings indicate that, in deep cortical layers of mice neonates, glutamate stimulates nNOS activity.	Glutamic Acid	84-93	nitric oxide synthase 1, neuronal	Mus musculus	105-109
22145776-9	2012	nNOS inhibition by 7-NI reduced the number of micturitions and increased residual volume and leak point pressure.	7-nitroindazole	19-23	nitric oxide synthase 1, neuronal	Mus musculus	0-4
22120830-1	2012	Production of nitric oxide through the action of nitric oxide synthase (NOS) has been detected in the islets of Langerhans.	Nitric Oxide	14-26	nitric oxide synthase 1, neuronal	Mus musculus	49-70
22116513-8	2012	An intravenous bolus injection of ascorbate (200 mg/kg body wt), given 30 min prior to CLP, prevented eNOS uncoupling, attenuated the increases in iNOS and nNOS activity, decreased 3-nitrotyrosine formation and PP2A activity, preserved the phosphorylation state of occludin, and completely inhibited the vascular leakage of dextran and Evans blue.	Ascorbic Acid	34-43	nitric oxide synthase 1, neuronal	Mus musculus	156-160
22316281-7	2012	This effect was reversed by treating animals with L-NMMA or N-propyl-L-arginine (a selective inhibitor of neuronal nitric oxide synthase, nNOS), suggesting involvement of the nNOS/NO pathway.	omega-N-Methylarginine	50-56	nitric oxide synthase 1, neuronal	Mus musculus	138-142
22316281-7	2012	This effect was reversed by treating animals with L-NMMA or N-propyl-L-arginine (a selective inhibitor of neuronal nitric oxide synthase, nNOS), suggesting involvement of the nNOS/NO pathway.	omega-N-Methylarginine	50-56	nitric oxide synthase 1, neuronal	Mus musculus	175-179
22316281-7	2012	This effect was reversed by treating animals with L-NMMA or N-propyl-L-arginine (a selective inhibitor of neuronal nitric oxide synthase, nNOS), suggesting involvement of the nNOS/NO pathway.	n-propyl-l-arginine	60-79	nitric oxide synthase 1, neuronal	Mus musculus	138-142
22316281-7	2012	This effect was reversed by treating animals with L-NMMA or N-propyl-L-arginine (a selective inhibitor of neuronal nitric oxide synthase, nNOS), suggesting involvement of the nNOS/NO pathway.	n-propyl-l-arginine	60-79	nitric oxide synthase 1, neuronal	Mus musculus	175-179
21945464-5	2012	Conversely, nNOS-derived NO regulates basal myocardial inotropy and relaxation by inhibiting the sarcolemmal Ca(2+) current (I(Ca)) and promoting protein kinase A-dependent phospholamban (PLN) phosphorylation, independent of cGMP.	Cyclic GMP	225-229	nitric oxide synthase 1, neuronal	Mus musculus	12-16
22145776-12	2012	CONCLUSIONS: Irrespective of the hormonal status, sildenafil decreased leak point pressure by a nNOS-mediated mechanism.	Sildenafil Citrate	50-60	nitric oxide synthase 1, neuronal	Mus musculus	96-100
22262891-6	2012	The activation of kisspeptin signaling in preoptic neurons promotes the activation of nNOS through its phosphorylation on serine 1412 via the AKT pathway and mimics the positive feedback effects of estrogens.	Serine	122-128	nitric oxide synthase 1, neuronal	Mus musculus	86-90
22948718-5	2012	Renal NO synthase (NOS) activity was determined by measuring the rate of formation of L-[(14)C]citruline from L-[(14)C]arginine.	l-[(14)c]citruline	86-104	nitric oxide synthase 1, neuronal	Mus musculus	6-17
22182498-1	2012	The overproduction of nitric oxide during the biological response to inflammation by the nitric oxide synthase (NOS) enzymes have been implicated in the pathology of many diseases.	Nitric Oxide	22-34	nitric oxide synthase 1, neuronal	Mus musculus	89-110
21874230-8	2012	Both cytocidal effect and NO             production were significantly inhibited by L-NAME, an inhibitor of NO synthase             (NOS).	NG-Nitroarginine Methyl Ester	84-90	nitric oxide synthase 1, neuronal	Mus musculus	108-119
22058155-12	2012	Mice deficient in nNOS demonstrate increased Bsl LTCC function and an attenuated contractile reserve to Dob, whereas eNOS(-/-) mice demonstrate normal LTCC and contractile function under all conditions.	Dobutamine	104-107	nitric oxide synthase 1, neuronal	Mus musculus	18-22
22007835-6	2012	Treatment of N(G) -nitro-L-arginine methyl ester [L-NAME, a non-selective nitric oxide synthase (NOS) inhibitor] reserved the expression of cav-1, inhibited MMPs activity, and reduced BBB permeability.	NG-Nitroarginine Methyl Ester	13-48	nitric oxide synthase 1, neuronal	Mus musculus	74-95
22007835-6	2012	Treatment of N(G) -nitro-L-arginine methyl ester [L-NAME, a non-selective nitric oxide synthase (NOS) inhibitor] reserved the expression of cav-1, inhibited MMPs activity, and reduced BBB permeability.	NG-Nitroarginine Methyl Ester	50-56	nitric oxide synthase 1, neuronal	Mus musculus	74-95
22948718-5	2012	Renal NO synthase (NOS) activity was determined by measuring the rate of formation of L-[(14)C]citruline from L-[(14)C]arginine.	l-[(14)c]arginine	110-127	nitric oxide synthase 1, neuronal	Mus musculus	6-17
22912680-8	2012	Treatment with PEA reduced MPTP-induced microglial activation, the number of GFAP-positive astrocytes and S100beta overexpression, and protected against the alterations of microtubule-associated protein 2a,b-, dopamine transporter-, nNOS- positive cells in the substantia nigra.	palmidrol	15-18	nitric oxide synthase 1, neuronal	Mus musculus	233-237
22001257-0	2012	Acetaminophen-induced hepatotoxicity and protein nitration in neuronal nitric-oxide synthase knockout mice.	Acetaminophen	0-13	nitric oxide synthase 1, neuronal	Mus musculus	62-92
22001257-11	2012	These data indicate a role for nNOS with inactivation of MnSOD and ALT release during APAP toxicity.	Acetaminophen	86-90	nitric oxide synthase 1, neuronal	Mus musculus	31-35
21879311-0	2012	Nitric oxide synthase inhibition abrogates hydrogen sulfide-induced cardioprotection in mice.	Hydrogen Sulfide	43-59	nitric oxide synthase 1, neuronal	Mus musculus	0-21
21879311-7	2012	However, co-administration of N-nitro-L-arginine methyl ester, a nitric oxide synthase (NOS) inhibitor, and Celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor along with NaHS and ISO abrogated the beneficial effect of H(2)S differentially.	n-nitro-l-arginine methyl ester	30-61	nitric oxide synthase 1, neuronal	Mus musculus	65-86
21939674-7	2012	1400W but not NPA, when administered at equivalent doses considering the magnitude of their Ki values for iNOS and nNOS, respectively, reduced the IT, thus suggesting that aminoguanidine-induced effects would be due to selective iNOS inhibition.	N-((3-(aminomethyl)phenyl)methyl)ethanimidamide	0-5	nitric oxide synthase 1, neuronal	Mus musculus	115-119
23226517-4	2012	Loss of neuronal nitric oxide synthase (nNOS) expression and impaired nonadrenergic, noncholinergic (NANC) relaxations in diabetic mice were relieved by long-term preventive treatment with THSG.	thsg	189-193	nitric oxide synthase 1, neuronal	Mus musculus	8-38
23226517-4	2012	Loss of neuronal nitric oxide synthase (nNOS) expression and impaired nonadrenergic, noncholinergic (NANC) relaxations in diabetic mice were relieved by long-term preventive treatment with THSG.	thsg	189-193	nitric oxide synthase 1, neuronal	Mus musculus	40-44
22912680-8	2012	Treatment with PEA reduced MPTP-induced microglial activation, the number of GFAP-positive astrocytes and S100beta overexpression, and protected against the alterations of microtubule-associated protein 2a,b-, dopamine transporter-, nNOS- positive cells in the substantia nigra.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	27-31	nitric oxide synthase 1, neuronal	Mus musculus	233-237
22389692-4	2012	Slices were incubated with the inhibitor of neuronal nitric oxide synthase (nNOS) 7-nitroindazole (10 microM) and pharmacological blockers used to isolate Ca(2+) current subtypes.	7-nitroindazole	82-97	nitric oxide synthase 1, neuronal	Mus musculus	44-74
22479635-10	2012	Anti-bacteria by the antibiotic cefotaxime and/or the immunosuppressant rapamycin or artesunate that also inhibits nitric oxide synthase (NOS) can abrogate NO production, mitigate hypoxia, and considerably ameliorate or even completely abort synovitis, hence highlighting that NO may serve as an initiator of inflammatory arthritis.	Cefotaxime	32-42	nitric oxide synthase 1, neuronal	Mus musculus	115-136
22479635-10	2012	Anti-bacteria by the antibiotic cefotaxime and/or the immunosuppressant rapamycin or artesunate that also inhibits nitric oxide synthase (NOS) can abrogate NO production, mitigate hypoxia, and considerably ameliorate or even completely abort synovitis, hence highlighting that NO may serve as an initiator of inflammatory arthritis.	Artesunate	85-95	nitric oxide synthase 1, neuronal	Mus musculus	115-136
22389692-4	2012	Slices were incubated with the inhibitor of neuronal nitric oxide synthase (nNOS) 7-nitroindazole (10 microM) and pharmacological blockers used to isolate Ca(2+) current subtypes.	7-nitroindazole	82-97	nitric oxide synthase 1, neuronal	Mus musculus	76-80
21849632-1	2011	Nitric oxide (NO) is an important signaling molecule produced in skeletal muscle primarily via the neuronal subtype of NO synthase (NOS1, or nNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	132-136
21983297-2	2011	We have previously reported that ileal P-gp expression levels decrease via a nitric oxide synthase (NOS)-mediated pathway in a streptozotocin (STZ)-induced type 1 diabetic mouse model.	Streptozocin	127-141	nitric oxide synthase 1, neuronal	Mus musculus	77-98
21983297-2	2011	We have previously reported that ileal P-gp expression levels decrease via a nitric oxide synthase (NOS)-mediated pathway in a streptozotocin (STZ)-induced type 1 diabetic mouse model.	Streptozocin	143-146	nitric oxide synthase 1, neuronal	Mus musculus	77-98
22152956-9	2011	Nebivolol and CL 316243 significantly increased myocardial nNOS expression.	Nebivolol	0-9	nitric oxide synthase 1, neuronal	Mus musculus	59-63
28510048-1	2011	Neuronal nitric oxide synthases (nNOS) are Ca2+/calmodulin-activated enzymes that synthesize the gaseous messenger nitric oxide (NO).	Nitric Oxide	9-21	nitric oxide synthase 1, neuronal	Mus musculus	33-37
21849632-1	2011	Nitric oxide (NO) is an important signaling molecule produced in skeletal muscle primarily via the neuronal subtype of NO synthase (NOS1, or nNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	141-145
21615722-2	2011	We previously reported that neuronal NOS (nNOS)-derived H(2)O(2) is an important endothelium-derived relaxant factor in the mouse aorta.	Hydrogen Peroxide	56-64	nitric oxide synthase 1, neuronal	Mus musculus	42-46
21890687-4	2011	iNOS and nNOS expressions were increased after MI associated with an increase in nitrotyrosine formation.	3-nitrotyrosine	81-94	nitric oxide synthase 1, neuronal	Mus musculus	9-13
21890687-10	2011	Sepiapterin increased capillary density and prevented LV remodeling and dysfunction after MI in wild-type, eNOS(-/-), and nNOS(-/-) but not iNOS(-/-) mice.	sepiapterin	0-11	nitric oxide synthase 1, neuronal	Mus musculus	122-126
21615722-0	2011	Decreased production of neuronal NOS-derived hydrogen peroxide contributes to endothelial dysfunction in atherosclerosis.	Hydrogen Peroxide	45-62	nitric oxide synthase 1, neuronal	Mus musculus	24-36
21615722-2	2011	We previously reported that neuronal NOS (nNOS)-derived H(2)O(2) is an important endothelium-derived relaxant factor in the mouse aorta.	Hydrogen Peroxide	56-64	nitric oxide synthase 1, neuronal	Mus musculus	28-40
21529143-5	2011	RESULTS: A remarkable three- to fourfold increase in neuronal nitric oxide synthase (nNOS) expression and activity was detected by western blot, citrulline assay, electronic and confocal microscopy, flow cytometry, and NO electrode sensor in mitochondria from ob/ob mice.	Citrulline	145-155	nitric oxide synthase 1, neuronal	Mus musculus	53-83
21529143-5	2011	RESULTS: A remarkable three- to fourfold increase in neuronal nitric oxide synthase (nNOS) expression and activity was detected by western blot, citrulline assay, electronic and confocal microscopy, flow cytometry, and NO electrode sensor in mitochondria from ob/ob mice.	Citrulline	145-155	nitric oxide synthase 1, neuronal	Mus musculus	85-89
21529143-7	2011	Low metabolic status restricted beta-oxidation in obese mitochondria and displaced acetyl-CoA to fat synthesis; instead, small interference RNA nNOS caused a phenotype change with fat reduction in ob/ob adipocytes.	Acetyl Coenzyme A	83-93	nitric oxide synthase 1, neuronal	Mus musculus	144-148
21615722-4	2011	We hypothesized that a decrease in nNOS-derived H(2)O(2) contributes to the impaired vasodilatation in apolipoprotein E-deficient mice (ApoE(-/-)).	Water	48-53	nitric oxide synthase 1, neuronal	Mus musculus	35-39
21615722-6	2011	Antisense oligodeoxynucleotides were used to knockdown eNOS and nNOS in vivo.	Oligodeoxyribonucleotides	10-31	nitric oxide synthase 1, neuronal	Mus musculus	64-68
21615722-9	2011	Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice.	l-arg(no2) -l-dbu	24-41	nitric oxide synthase 1, neuronal	Mus musculus	14-18
21615722-9	2011	Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice.	Hydrogen Peroxide	92-100	nitric oxide synthase 1, neuronal	Mus musculus	14-18
21615722-9	2011	Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice.	Hydrogen Peroxide	92-100	nitric oxide synthase 1, neuronal	Mus musculus	56-60
21615722-9	2011	Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice.	Oxygen	106-112	nitric oxide synthase 1, neuronal	Mus musculus	14-18
21615722-9	2011	Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice.	Oxygen	106-112	nitric oxide synthase 1, neuronal	Mus musculus	56-60
21615722-9	2011	Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice.	Water	117-122	nitric oxide synthase 1, neuronal	Mus musculus	14-18
21615722-9	2011	Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice.	Water	117-122	nitric oxide synthase 1, neuronal	Mus musculus	56-60
21615722-9	2011	Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice.	Acetylcholine	134-137	nitric oxide synthase 1, neuronal	Mus musculus	14-18
21615722-9	2011	Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice.	Acetylcholine	134-137	nitric oxide synthase 1, neuronal	Mus musculus	56-60
21615722-9	2011	Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice.	Hydrogen Peroxide	225-233	nitric oxide synthase 1, neuronal	Mus musculus	14-18
21615722-9	2011	Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice.	Hydrogen Peroxide	225-233	nitric oxide synthase 1, neuronal	Mus musculus	56-60
21615722-12	2011	CONCLUSIONS AND IMPLICATIONS: Our data show that endothelial nNOS-derived H(2)O(2) production is impaired and contributes to endothelial dysfunction in ApoE(-/-) aorta.	Hydrogen Peroxide	74-82	nitric oxide synthase 1, neuronal	Mus musculus	61-65
21777607-5	2011	In this study, we tested whether early life environmental complexity impacts affective responses, aggressive behaviors, and expression of neuronal nitric oxide synthase (nNOS), the synthetic enzyme for nitric oxide, in adulthood.	Nitric Oxide	147-159	nitric oxide synthase 1, neuronal	Mus musculus	170-174
21767657-1	2011	Although all three nitric oxide (NO) synthases (nNOS, iNOS, and eNOS) are expressed in injured arteries, it remains to be elucidated the role of the NOSs in their entirety in the vascular lesion formation.	Nitric Oxide	19-31	nitric oxide synthase 1, neuronal	Mus musculus	48-52
21875647-6	2011	In contrast, pretreatment with methylene blue (a soluble guanlyate cyclase inhibitor and nitric oxide synthase (NOS) inhibitor) or 7-nitroindazole (a specific neuronal NOS inhibitor) potentiated the antidepressant-like effect of sub-effective dose of 1-(7-methoxy-2-methyl-1,2,3,4-tetrahydro-isoquinolin-4-YL)-cyclohexanol (2mg/kg, i.p.)	Methylene Blue	31-45	nitric oxide synthase 1, neuronal	Mus musculus	89-110
21719758-1	2011	RATIONALE: Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor that competes with L-arginine for binding to NOS.	dimethylarginine	22-38	nitric oxide synthase 1, neuronal	Mus musculus	63-84
21719758-1	2011	RATIONALE: Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor that competes with L-arginine for binding to NOS.	N,N-dimethylarginine	40-44	nitric oxide synthase 1, neuronal	Mus musculus	63-84
21719758-1	2011	RATIONALE: Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor that competes with L-arginine for binding to NOS.	Arginine	120-130	nitric oxide synthase 1, neuronal	Mus musculus	63-84
22040569-0	2011	Inhibition of nitric oxide synthase lowers fatty acid oxidation in preeclampsia-like mice at early gestational stage.	Fatty Acids	43-53	nitric oxide synthase 1, neuronal	Mus musculus	14-35
22040569-5	2011	The aim of this research was to investigate whether the nitric oxide synthase (NOS) inhibitor L-NAME may cause down-regulation of LCHAD in the pathogenesis of preeclampsia.	NG-Nitroarginine Methyl Ester	94-100	nitric oxide synthase 1, neuronal	Mus musculus	56-77
21896719-3	2011	Using a recently developed NO chemical sensor [Cu(2)(FL2E)] to study adult cardiac myocytes from wild-type, eNOS(null), and nNOS(null) mice, we discovered that physiological concentrations of H(2)O(2) activate eNOS but not nNOS.	h(2)	192-196	nitric oxide synthase 1, neuronal	Mus musculus	124-128
21651902-9	2011	NOS-1(-/-) mice injected with LPS exhibited smaller increase in plasma NOx, no NOS-2 and COX-2 expression and reduced mortality.	nicotine 1-N-oxide	71-74	nitric oxide synthase 1, neuronal	Mus musculus	0-5
21825026-7	2011	The same was found when SMTC was combined with angiotensin II to reproduce the hypertension and vasoconstriction seen with l-NAME (58 +- 3 vs. 54 +- 7 units, l-NAME 81 +- 2 units), or when SMTC was replaced by the nNOS inhibitor NPA (57 +- 5 vs. 56 +- 7 units, l-NAME 79 +- 4 units) or by the iNOS inhibitor 1400W (50 +- 1 vs. 55 +- 4 units, l-NAME 81 +- 3 units).	smtc	24-28	nitric oxide synthase 1, neuronal	Mus musculus	214-218
21515310-1	2011	Previous behavioral studies have manipulated nitric oxide (NO) production either by pharmacological inhibition of its synthetic enzyme, nitric oxide synthase (NOS), or by deletion of the genes that code for NOS.	Nitric Oxide	45-57	nitric oxide synthase 1, neuronal	Mus musculus	136-157
21515310-4	2011	In the brain L-arginine is converted into NO and citrulline by the enzyme, neuronal NOS (nNOS).	Arginine	13-23	nitric oxide synthase 1, neuronal	Mus musculus	75-87
21515310-4	2011	In the brain L-arginine is converted into NO and citrulline by the enzyme, neuronal NOS (nNOS).	Arginine	13-23	nitric oxide synthase 1, neuronal	Mus musculus	89-93
21515310-4	2011	In the brain L-arginine is converted into NO and citrulline by the enzyme, neuronal NOS (nNOS).	Citrulline	49-59	nitric oxide synthase 1, neuronal	Mus musculus	75-87
21515310-4	2011	In the brain L-arginine is converted into NO and citrulline by the enzyme, neuronal NOS (nNOS).	Citrulline	49-59	nitric oxide synthase 1, neuronal	Mus musculus	89-93
21896719-3	2011	Using a recently developed NO chemical sensor [Cu(2)(FL2E)] to study adult cardiac myocytes from wild-type, eNOS(null), and nNOS(null) mice, we discovered that physiological concentrations of H(2)O(2) activate eNOS but not nNOS.	h(2)	192-196	nitric oxide synthase 1, neuronal	Mus musculus	223-227
22321750-2	2011	METHODS: Wild-type (WT) mice were injected subcutaneously with nitric oxide synthase (NOS) inhibitor L-arginine methyl ester (L-NAME, 50 mgxkg(-1)xd(-1)) to establish PE-like model (L-NAME group) at early, middle and late pregnant periods respectively.	arginine methyl ester	101-124	nitric oxide synthase 1, neuronal	Mus musculus	63-84
21788351-7	2011	Components of oxidative phosphorylation complexes, mitofilin, porin, nNOS, p-nNOS, and Tfam as well as mitochondrial volume and cristae abundance were significantly higher with (-)-epicatechin treatment for hindlimb and cardiac muscles than exercise alone.	Catechin	177-192	nitric oxide synthase 1, neuronal	Mus musculus	69-73
21788351-7	2011	Components of oxidative phosphorylation complexes, mitofilin, porin, nNOS, p-nNOS, and Tfam as well as mitochondrial volume and cristae abundance were significantly higher with (-)-epicatechin treatment for hindlimb and cardiac muscles than exercise alone.	Catechin	177-192	nitric oxide synthase 1, neuronal	Mus musculus	77-81
21443684-8	2011	Inhibition of NOS did not affect DHE oxidation in fibers from WT or Sod1(-/-) mice at rest or during contractions, but transgenic mice overexpressing nNOS showed increased DAF-FM fluorescence and reduced DHE oxidation in resting muscle fibers.	Dihydroergotamine	204-207	nitric oxide synthase 1, neuronal	Mus musculus	150-154
21680773-1	2011	Nitrergic neurotransmission at the smooth muscle neuromuscular junctions requires nitric oxide (NO) release that is dependent on the transport and docking of neuronal NO synthase (nNOS) alpha to the membrane of nerve terminals.	Nitric Oxide	82-94	nitric oxide synthase 1, neuronal	Mus musculus	180-184
23554705-2	2011	Lung concentrations of NO and its amino acid precursor, L-arginine, are regulated by the relative expressions of the NO synthase (NOS) and arginase isoforms.	Arginine	56-66	nitric oxide synthase 1, neuronal	Mus musculus	117-128
21348811-1	2011	UNLABELLED: Morphine increases the production of nitric oxide (NO) via the phosphoinositide 3-kinase/Akt/neural nitric oxide synthase (nNOS) pathway.	Morphine	12-20	nitric oxide synthase 1, neuronal	Mus musculus	135-139
21348811-1	2011	UNLABELLED: Morphine increases the production of nitric oxide (NO) via the phosphoinositide 3-kinase/Akt/neural nitric oxide synthase (nNOS) pathway.	Nitric Oxide	49-61	nitric oxide synthase 1, neuronal	Mus musculus	135-139
21348811-4	2011	AIMS: Here, we examined how nNOS/NO signaling is downregulated by the morphine-activated MOR and how this regulation affects antinociception.	Morphine	70-78	nitric oxide synthase 1, neuronal	Mus musculus	28-32
21348811-7	2011	INNOVATION: Indeed, in RGSZ2-deficient mice morphine over-stimulates the nNOS/NO/NMDAR/CaMKII pathway, causing analgesic tolerance to develop rapidly.	Morphine	44-52	nitric oxide synthase 1, neuronal	Mus musculus	73-77
21733493-0	2011	Synergic effects of estradiol and progesterone on regulation of the hypothalamic neuronal nitric oxide synthase expression in ovariectomized mice.	Estradiol	20-29	nitric oxide synthase 1, neuronal	Mus musculus	81-111
21733493-0	2011	Synergic effects of estradiol and progesterone on regulation of the hypothalamic neuronal nitric oxide synthase expression in ovariectomized mice.	Progesterone	34-46	nitric oxide synthase 1, neuronal	Mus musculus	81-111
21737065-4	2011	Inhibition of endogenously expressed nNOS by 7-NI and ARR17477 enhanced the toxicity of MPP(+) and MG-132 in N1E-115 cells, whereas in transfected SH-SY5Y cells overexpressing nNOS, ARR17477 and 7-NI protected against MPP(+)- and MG-132-induced cell death.	7-nitroindazole	45-49	nitric oxide synthase 1, neuronal	Mus musculus	37-41
21737065-4	2011	Inhibition of endogenously expressed nNOS by 7-NI and ARR17477 enhanced the toxicity of MPP(+) and MG-132 in N1E-115 cells, whereas in transfected SH-SY5Y cells overexpressing nNOS, ARR17477 and 7-NI protected against MPP(+)- and MG-132-induced cell death.	N-(4-(2-((3-chlorophenylmethyl)amino)ethyl)phenyl)-2-thiophenecarboxamide	54-62	nitric oxide synthase 1, neuronal	Mus musculus	37-41
21737065-4	2011	Inhibition of endogenously expressed nNOS by 7-NI and ARR17477 enhanced the toxicity of MPP(+) and MG-132 in N1E-115 cells, whereas in transfected SH-SY5Y cells overexpressing nNOS, ARR17477 and 7-NI protected against MPP(+)- and MG-132-induced cell death.	mangion-purified polysaccharide (Candida albicans)	88-91	nitric oxide synthase 1, neuronal	Mus musculus	37-41
21737065-4	2011	Inhibition of endogenously expressed nNOS by 7-NI and ARR17477 enhanced the toxicity of MPP(+) and MG-132 in N1E-115 cells, whereas in transfected SH-SY5Y cells overexpressing nNOS, ARR17477 and 7-NI protected against MPP(+)- and MG-132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	nitric oxide synthase 1, neuronal	Mus musculus	37-41
21737065-4	2011	Inhibition of endogenously expressed nNOS by 7-NI and ARR17477 enhanced the toxicity of MPP(+) and MG-132 in N1E-115 cells, whereas in transfected SH-SY5Y cells overexpressing nNOS, ARR17477 and 7-NI protected against MPP(+)- and MG-132-induced cell death.	7-nitroindazole	195-199	nitric oxide synthase 1, neuronal	Mus musculus	37-41
21737065-4	2011	Inhibition of endogenously expressed nNOS by 7-NI and ARR17477 enhanced the toxicity of MPP(+) and MG-132 in N1E-115 cells, whereas in transfected SH-SY5Y cells overexpressing nNOS, ARR17477 and 7-NI protected against MPP(+)- and MG-132-induced cell death.	mangion-purified polysaccharide (Candida albicans)	218-221	nitric oxide synthase 1, neuronal	Mus musculus	37-41
21737065-4	2011	Inhibition of endogenously expressed nNOS by 7-NI and ARR17477 enhanced the toxicity of MPP(+) and MG-132 in N1E-115 cells, whereas in transfected SH-SY5Y cells overexpressing nNOS, ARR17477 and 7-NI protected against MPP(+)- and MG-132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	230-236	nitric oxide synthase 1, neuronal	Mus musculus	37-41
21602468-1	2011	Nitric oxide (NO) is an important vasoactive molecule produced by three NO synthase (NOS) enzymes: neuronal (nNOS), inducible (iNOS), and endothelial NOS (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	72-83
21602468-1	2011	Nitric oxide (NO) is an important vasoactive molecule produced by three NO synthase (NOS) enzymes: neuronal (nNOS), inducible (iNOS), and endothelial NOS (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	109-113
22053696-6	2011	In summary, our data provide evidence that nNOS is not constitutively expressed, but is induced during arteriogenesis, playing a role in supplying reactive oxygen species such as H2O2 and low levels of NO.	Reactive Oxygen Species	147-170	nitric oxide synthase 1, neuronal	Mus musculus	43-47
22053696-6	2011	In summary, our data provide evidence that nNOS is not constitutively expressed, but is induced during arteriogenesis, playing a role in supplying reactive oxygen species such as H2O2 and low levels of NO.	Hydrogen Peroxide	179-183	nitric oxide synthase 1, neuronal	Mus musculus	43-47
21550412-1	2011	Nitric oxide, generated by the nitric oxide synthase (NOS) enzymes, plays pivotal roles in cardiovascular homeostasis and in the pathogenesis of cardiovascular disease.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	31-52
21756303-2	2011	Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), plays a pivotal role in endothelial dysfunction.	dimethylarginine	11-27	nitric oxide synthase 1, neuronal	Mus musculus	63-84
21745643-1	2011	PSD-95, a principal scaffolding component of the postsynaptic density, is targeted to synapses by palmitoylation, where it couples NMDA receptor stimulation to production of nitric oxide (NO) by neuronal nitric oxide synthase (nNOS).	Nitric Oxide	174-186	nitric oxide synthase 1, neuronal	Mus musculus	195-225
21745643-1	2011	PSD-95, a principal scaffolding component of the postsynaptic density, is targeted to synapses by palmitoylation, where it couples NMDA receptor stimulation to production of nitric oxide (NO) by neuronal nitric oxide synthase (nNOS).	Nitric Oxide	174-186	nitric oxide synthase 1, neuronal	Mus musculus	227-231
21756303-2	2011	Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), plays a pivotal role in endothelial dysfunction.	N,N-dimethylarginine	29-33	nitric oxide synthase 1, neuronal	Mus musculus	63-84
20608991-3	2011	The aim of our study was to investigate the effects of the new selective neuronal and inducible NOS inhibitor 1- (2-trifluoromethylphenyl) imidazole (TRIM) (10-50 mg/kg) on learning and memory and compare it to the nonselective NOS inhibitor 7-NI (15-45 mg/kg) using different behavioral tests in Swiss mice, thus clarifying the role of neuronal NOS (nNOS) and endothelial NOS (eNOS) in cognitive processes.	1-(2-trifluoromethylphenyl)imidazole	110-148	nitric oxide synthase 1, neuronal	Mus musculus	337-349
21512164-1	2011	OBJECTIVE: Tetrahydrobiopterin (BH(4)) is a critical cofactor for nitric oxide (NO) synthesis by NO synthase (NOS).	sapropterin	11-30	nitric oxide synthase 1, neuronal	Mus musculus	97-108
21512164-1	2011	OBJECTIVE: Tetrahydrobiopterin (BH(4)) is a critical cofactor for nitric oxide (NO) synthesis by NO synthase (NOS).	Nitric Oxide	66-78	nitric oxide synthase 1, neuronal	Mus musculus	97-108
21499118-13	2011	Nebivolol-induced changes were blunted by a beta3-AR antagonist and by NO synthase (NOS) inhibition.	Nebivolol	0-9	nitric oxide synthase 1, neuronal	Mus musculus	71-82
20608991-3	2011	The aim of our study was to investigate the effects of the new selective neuronal and inducible NOS inhibitor 1- (2-trifluoromethylphenyl) imidazole (TRIM) (10-50 mg/kg) on learning and memory and compare it to the nonselective NOS inhibitor 7-NI (15-45 mg/kg) using different behavioral tests in Swiss mice, thus clarifying the role of neuronal NOS (nNOS) and endothelial NOS (eNOS) in cognitive processes.	1-(2-trifluoromethylphenyl)imidazole	110-148	nitric oxide synthase 1, neuronal	Mus musculus	351-355
20608991-3	2011	The aim of our study was to investigate the effects of the new selective neuronal and inducible NOS inhibitor 1- (2-trifluoromethylphenyl) imidazole (TRIM) (10-50 mg/kg) on learning and memory and compare it to the nonselective NOS inhibitor 7-NI (15-45 mg/kg) using different behavioral tests in Swiss mice, thus clarifying the role of neuronal NOS (nNOS) and endothelial NOS (eNOS) in cognitive processes.	1-(2-trifluoromethylphenyl)imidazole	150-154	nitric oxide synthase 1, neuronal	Mus musculus	337-349
20608991-3	2011	The aim of our study was to investigate the effects of the new selective neuronal and inducible NOS inhibitor 1- (2-trifluoromethylphenyl) imidazole (TRIM) (10-50 mg/kg) on learning and memory and compare it to the nonselective NOS inhibitor 7-NI (15-45 mg/kg) using different behavioral tests in Swiss mice, thus clarifying the role of neuronal NOS (nNOS) and endothelial NOS (eNOS) in cognitive processes.	1-(2-trifluoromethylphenyl)imidazole	150-154	nitric oxide synthase 1, neuronal	Mus musculus	351-355
21497192-6	2011	In this study, we investigated the inhibitory effects of andrographolide on the induction of nitric oxide synthase (NOS) and cyclooxygenase-2 (COX-2) as well as their respective downstream products, NO and PGE2, in RAW264.7 cells treated with LPS.	andrographolide	57-72	nitric oxide synthase 1, neuronal	Mus musculus	93-114
21056589-8	2011	This increased excitotoxicity in SOD1(G93A) near-pure neuronal cultures appears to be mediated by a significant increase in NMDA-dependent rises of intraneuronal Ca2+ levels as well as enhanced production of cytosolic reactive oxygen species, while the injurious process seems to be unrelated to activation of nNOS or ERK1/2 pathways.	N-Methylaspartate	124-128	nitric oxide synthase 1, neuronal	Mus musculus	310-314
21470341-0	2011	Chronic alcohol consumption induces an overproduction of NO by nNOS- and iNOS-expressing myenteric neurons in the murine small intestine.	Alcohols	8-15	nitric oxide synthase 1, neuronal	Mus musculus	63-67
21414104-10	2011	Neurogenic ion transport, which was significantly reduced after endotoxin challenge, was normalized by SA through a nitric oxide synthase (NOS)-dependent mechanism.	salvinorin A	103-105	nitric oxide synthase 1, neuronal	Mus musculus	116-137
21470341-7	2011	Chronic alcohol consumption caused an increase in the proportion of iNOS-expressing neurons (to 33+-5%; P&lt;0.01) and a decrease in nNOS-expressing neurons (to 22+-3%; P&lt;0.0001), without altering the proportion of NO-producing neurons (control 55+-13%; CAC 56+- 11%; P=0.82).	Alcohols	8-15	nitric oxide synthase 1, neuronal	Mus musculus	133-137
21470341-8	2011	CONCLUSIONS &amp; INFERENCES: Chronic alcohol consumption induces a marked increase in NO synthesis by jejunal myenteric neurons, accompanied by an up-regulation of iNOS-expressing neurons and a downregulation of nNOS neurons.	Alcohols	38-45	nitric oxide synthase 1, neuronal	Mus musculus	213-217
21333736-9	2011	Nitric oxide synthase (NOS) activity, studied ex vivo, and NOS expression were elevated in CD11b-positive cerebral microglia from wild type mice acutely exposed to d-methamphetamine.	Methamphetamine	164-181	nitric oxide synthase 1, neuronal	Mus musculus	0-21
21439953-2	2011	Agmatine is a novel endogenous ligand at alpha2-adrenoceptors, imidazoline and N-methyl-d-aspartate (NMDA) receptors, as well as a nitric oxide synthase (NOS) inhibitor.	Agmatine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	131-152
21539806-1	2011	Neuronal nitric oxide synthase (nNOS) forms nitric oxide (NO), which functions as a signaling molecule via S-nitrosylation of various proteins and regulation of soluble guanylate cyclase (cGC)/cyclic guanosine monophosphate (cGMP) pathway in the central nervous system.	Nitric Oxide	9-21	nitric oxide synthase 1, neuronal	Mus musculus	32-36
21539806-1	2011	Neuronal nitric oxide synthase (nNOS) forms nitric oxide (NO), which functions as a signaling molecule via S-nitrosylation of various proteins and regulation of soluble guanylate cyclase (cGC)/cyclic guanosine monophosphate (cGMP) pathway in the central nervous system.	Cyclic GMP	193-223	nitric oxide synthase 1, neuronal	Mus musculus	0-30
21539806-1	2011	Neuronal nitric oxide synthase (nNOS) forms nitric oxide (NO), which functions as a signaling molecule via S-nitrosylation of various proteins and regulation of soluble guanylate cyclase (cGC)/cyclic guanosine monophosphate (cGMP) pathway in the central nervous system.	Cyclic GMP	193-223	nitric oxide synthase 1, neuronal	Mus musculus	32-36
21539806-1	2011	Neuronal nitric oxide synthase (nNOS) forms nitric oxide (NO), which functions as a signaling molecule via S-nitrosylation of various proteins and regulation of soluble guanylate cyclase (cGC)/cyclic guanosine monophosphate (cGMP) pathway in the central nervous system.	Cyclic GMP	225-229	nitric oxide synthase 1, neuronal	Mus musculus	0-30
21539806-1	2011	Neuronal nitric oxide synthase (nNOS) forms nitric oxide (NO), which functions as a signaling molecule via S-nitrosylation of various proteins and regulation of soluble guanylate cyclase (cGC)/cyclic guanosine monophosphate (cGMP) pathway in the central nervous system.	Cyclic GMP	225-229	nitric oxide synthase 1, neuronal	Mus musculus	32-36
21562256-1	2011	Nitric oxide (NO) synthesized by neuronal NO synthase (nNOS) has long been implicated in brain plasticity.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	55-59
21562256-8	2011	These results establish nNOS-derived NO as a key factor in the expression of proteins involved in neuroplasticity, an effect mediated through cGMP, PKG, and ERK signaling.	Cyclic GMP	142-146	nitric oxide synthase 1, neuronal	Mus musculus	24-28
21333736-13	2011	We propose that the effects of D-METH on sleep/wake cycles are mediated in part by actions on microglia, including possibly nNOS activity and cytokine synthesis.	d-meth	31-37	nitric oxide synthase 1, neuronal	Mus musculus	124-128
21272185-10	2011	Both apocynin and the nitric oxide synthase (NOS) inhibitor l-arginine methyl ester (L-NAME) inhibited elevated O(2) (-) production in diabetes without any additive effect between the two, indicating the presence of endothelial nitric oxide synthase (eNOS) uncoupling.	arginine methyl ester	60-83	nitric oxide synthase 1, neuronal	Mus musculus	22-43
21272185-10	2011	Both apocynin and the nitric oxide synthase (NOS) inhibitor l-arginine methyl ester (L-NAME) inhibited elevated O(2) (-) production in diabetes without any additive effect between the two, indicating the presence of endothelial nitric oxide synthase (eNOS) uncoupling.	NG-Nitroarginine Methyl Ester	85-91	nitric oxide synthase 1, neuronal	Mus musculus	22-43
21272185-10	2011	Both apocynin and the nitric oxide synthase (NOS) inhibitor l-arginine methyl ester (L-NAME) inhibited elevated O(2) (-) production in diabetes without any additive effect between the two, indicating the presence of endothelial nitric oxide synthase (eNOS) uncoupling.	o(2) (	112-118	nitric oxide synthase 1, neuronal	Mus musculus	22-43
22613021-7	2011	L-NAME, but not axotomy, increased neuronal NO synthase (nNOS) and SOD1 immunoreactive neurons, with no colocalisation, in a lamina-dependent manner in the dorsal horn of the spinal cord.	NG-Nitroarginine Methyl Ester	0-6	nitric oxide synthase 1, neuronal	Mus musculus	57-61
21434910-6	2011	application of saline or 0.096 mg/kg of the specific nNOS inhibitor Nomega-propyl-L-arginine (NPLA), NGF induced a sustained reflex facilitation within 60 minutes.	Sodium Chloride	15-21	nitric oxide synthase 1, neuronal	Mus musculus	53-57
21434910-6	2011	application of saline or 0.096 mg/kg of the specific nNOS inhibitor Nomega-propyl-L-arginine (NPLA), NGF induced a sustained reflex facilitation within 60 minutes.	N(omega)-propylarginine	68-92	nitric oxide synthase 1, neuronal	Mus musculus	53-57
21434910-6	2011	application of saline or 0.096 mg/kg of the specific nNOS inhibitor Nomega-propyl-L-arginine (NPLA), NGF induced a sustained reflex facilitation within 60 minutes.	N(omega)-propylarginine	94-98	nitric oxide synthase 1, neuronal	Mus musculus	53-57
21780643-1	2011	The work studied vasopressinergic neurons of hypothalamic supraoptic and paravenricular nuclei of the wild type mice and the neuronal nitric oxide synthase (nNOS) gene knockouted mice at a decrease of the brain catecholamine (CA) level caused by administration of the blocker of activity of tyrosine hydroxylase alpha-methyl-paratyrosine (alpha-MPT) and at the CA level decrease on the background of functional activity of the vasopressinergic neurons caused by dehydration of animals.	Catecholamines	211-224	nitric oxide synthase 1, neuronal	Mus musculus	125-155
21292018-4	2011	Pre-treatment with betulinic acid (50mg/kg/day for 7days via gavage) prior MCA occlusion prevented the ischemia reperfusion-induced upregulation of NOX2, nNOS and iNOS.	betulinic acid	19-33	nitric oxide synthase 1, neuronal	Mus musculus	154-158
21508214-5	2011	Indeed, administration of 5 mum NMDA induced a robust nNOS-dependent cGMP production in GABAergic terminals, selectively in the CA1 and CA3c areas.	N-Methylaspartate	32-36	nitric oxide synthase 1, neuronal	Mus musculus	54-58
21508214-5	2011	Indeed, administration of 5 mum NMDA induced a robust nNOS-dependent cGMP production in GABAergic terminals, selectively in the CA1 and CA3c areas.	Cyclic GMP	69-73	nitric oxide synthase 1, neuronal	Mus musculus	54-58
21486477-2	2011	We investigated if nitric oxide synthesized by neuronal (NOS1) or inducible (NOS2) nitric oxide synthases could modulate the local antiallodynic effects of morphine through the peripheral nitric oxide-cGMP-protein kinase G (PKG)-ATP-sensitive K+ (KATP) channels signaling pathway activation and affect the dorsal root ganglia MOR expression during neuropathic pain.	Nitric Oxide	19-31	nitric oxide synthase 1, neuronal	Mus musculus	57-61
21486477-2	2011	We investigated if nitric oxide synthesized by neuronal (NOS1) or inducible (NOS2) nitric oxide synthases could modulate the local antiallodynic effects of morphine through the peripheral nitric oxide-cGMP-protein kinase G (PKG)-ATP-sensitive K+ (KATP) channels signaling pathway activation and affect the dorsal root ganglia MOR expression during neuropathic pain.	Morphine	156-164	nitric oxide synthase 1, neuronal	Mus musculus	57-61
21486477-5	2011	CONCLUSIONS: These results suggest that the peripheral nitric oxide-cGMP-PKG-KATP signaling pathway activation participates in the local antiallodynic effects of morphine after sciatic nerve injury and that nitric oxide, synthesized by NOS1 and NOS2, is implicated in the dorsal root ganglia down-regulation of MOR during neuropathic pain.	Nitric Oxide	55-67	nitric oxide synthase 1, neuronal	Mus musculus	236-240
21486477-5	2011	CONCLUSIONS: These results suggest that the peripheral nitric oxide-cGMP-PKG-KATP signaling pathway activation participates in the local antiallodynic effects of morphine after sciatic nerve injury and that nitric oxide, synthesized by NOS1 and NOS2, is implicated in the dorsal root ganglia down-regulation of MOR during neuropathic pain.	Cyclic GMP	68-72	nitric oxide synthase 1, neuronal	Mus musculus	236-240
21486477-5	2011	CONCLUSIONS: These results suggest that the peripheral nitric oxide-cGMP-PKG-KATP signaling pathway activation participates in the local antiallodynic effects of morphine after sciatic nerve injury and that nitric oxide, synthesized by NOS1 and NOS2, is implicated in the dorsal root ganglia down-regulation of MOR during neuropathic pain.	Morphine	162-170	nitric oxide synthase 1, neuronal	Mus musculus	236-240
21486477-5	2011	CONCLUSIONS: These results suggest that the peripheral nitric oxide-cGMP-PKG-KATP signaling pathway activation participates in the local antiallodynic effects of morphine after sciatic nerve injury and that nitric oxide, synthesized by NOS1 and NOS2, is implicated in the dorsal root ganglia down-regulation of MOR during neuropathic pain.	Nitric Oxide	207-219	nitric oxide synthase 1, neuronal	Mus musculus	236-240
20558777-1	2011	Altered arginine metabolism, the uncoupling of nitric oxide synthase (NOS) by asymmetric dimethyl-arginine (ADMA), increased oxo-nitrosative stress, and cellular injury were reported in airway epithelial cells in asthma.	dimethylarginine	89-106	nitric oxide synthase 1, neuronal	Mus musculus	47-68
21780643-1	2011	The work studied vasopressinergic neurons of hypothalamic supraoptic and paravenricular nuclei of the wild type mice and the neuronal nitric oxide synthase (nNOS) gene knockouted mice at a decrease of the brain catecholamine (CA) level caused by administration of the blocker of activity of tyrosine hydroxylase alpha-methyl-paratyrosine (alpha-MPT) and at the CA level decrease on the background of functional activity of the vasopressinergic neurons caused by dehydration of animals.	Catecholamines	211-224	nitric oxide synthase 1, neuronal	Mus musculus	157-161
20558777-8	2011	ADMA and inducible nitric oxide synthase were reduced by simvastatin, but eNOS was increased.	Simvastatin	57-68	nitric oxide synthase 1, neuronal	Mus musculus	19-40
21104071-5	2011	Blocking NO production using the NO synthase (NOS) inhibitor L: -NAME or cells from eNOS(-/-) mice blocked Pi-induced chondrocyte apoptosis, indicating that NO production is necessary.	l	61-62	nitric oxide synthase 1, neuronal	Mus musculus	33-44
21073925-1	2011	Nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) has a role in late-phase long-term potentiation (LTP) and long-term memory (LTM) formation.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	30-60
21073925-1	2011	Nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) has a role in late-phase long-term potentiation (LTP) and long-term memory (LTM) formation.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	62-66
21073925-11	2011	The selective nNOS inhibitor S-methyl-thiocitrulline (SMTC) impaired cued and contextual LTM in WT mice.	S-methylthiocitrulline	29-52	nitric oxide synthase 1, neuronal	Mus musculus	14-18
21073925-11	2011	The selective nNOS inhibitor S-methyl-thiocitrulline (SMTC) impaired cued and contextual LTM in WT mice.	S-methylthiocitrulline	54-58	nitric oxide synthase 1, neuronal	Mus musculus	14-18
21073925-14	2011	The expression of CREB phosphorylation (Ser-133) was significantly higher in naive nNOS KO mice than in WT counterparts, and pharmacological modulators of NO had significant effects on levels of CREB phosphorylation and expression.	Serine	40-43	nitric oxide synthase 1, neuronal	Mus musculus	83-87
21423636-5	2011	DS (10-300 mug/mL) produced a concentration-dependent relaxation in mouse aorta, which was significantly attenuated by the nitric oxide synthase (NOS) inhibitor L-NAME, suggesting that DS causes vasodilation via a NO-dependent mechanism.	ds	0-2	nitric oxide synthase 1, neuronal	Mus musculus	123-144
21036913-1	2011	Nitric oxide (NO) derived from neuronal nitric-oxide synthase (nNOS) and inducible nitric-oxide synthase (iNOS) plays a key role in various pain and inflammatory states.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	31-61
21036913-1	2011	Nitric oxide (NO) derived from neuronal nitric-oxide synthase (nNOS) and inducible nitric-oxide synthase (iNOS) plays a key role in various pain and inflammatory states.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	63-67
21184738-1	2011	Excessive production of nitric oxide (NO) by NO synthase (NOS) and a subsequent oxidative stress reaction are thought to be critically involved in the pathophysiology of sepsis.	Nitric Oxide	24-36	nitric oxide synthase 1, neuronal	Mus musculus	45-56
21184738-8	2011	While nNOS inhibition at 4h was associated with a trend toward improved survival and significantly reduced contents of lung nitrite/nitrate (NO(x)) and liver malondialdehyde, the blockade of nNOS at 8h had no effect on these parameters.	4h	25-27	nitric oxide synthase 1, neuronal	Mus musculus	6-10
21184738-8	2011	While nNOS inhibition at 4h was associated with a trend toward improved survival and significantly reduced contents of lung nitrite/nitrate (NO(x)) and liver malondialdehyde, the blockade of nNOS at 8h had no effect on these parameters.	Nitrites	124-131	nitric oxide synthase 1, neuronal	Mus musculus	6-10
21184738-8	2011	While nNOS inhibition at 4h was associated with a trend toward improved survival and significantly reduced contents of lung nitrite/nitrate (NO(x)) and liver malondialdehyde, the blockade of nNOS at 8h had no effect on these parameters.	Nitrates	132-139	nitric oxide synthase 1, neuronal	Mus musculus	6-10
21184738-8	2011	While nNOS inhibition at 4h was associated with a trend toward improved survival and significantly reduced contents of lung nitrite/nitrate (NO(x)) and liver malondialdehyde, the blockade of nNOS at 8h had no effect on these parameters.	Malondialdehyde	158-173	nitric oxide synthase 1, neuronal	Mus musculus	6-10
21249195-6	2011	The capsaicin-induced reduction of LTP was completely blocked by the nitric oxide synthase (NOS) inhibitor L-NAME and was absent in neuronal NOS as well as in TRPV1 deficient mice.	Capsaicin	4-13	nitric oxide synthase 1, neuronal	Mus musculus	69-90
21249195-6	2011	The capsaicin-induced reduction of LTP was completely blocked by the nitric oxide synthase (NOS) inhibitor L-NAME and was absent in neuronal NOS as well as in TRPV1 deficient mice.	NG-Nitroarginine Methyl Ester	107-113	nitric oxide synthase 1, neuronal	Mus musculus	69-90
21209222-5	2011	Genetic deletion of nitric oxide synthase 1 (nos1) and inhibition of NOS1 with nitroindazole protected LGN neurons from apoptosis, revealing NO as a mediator.	3-NITRO-1H-INDAZOLE	79-92	nitric oxide synthase 1, neuronal	Mus musculus	69-73
21198440-1	2011	Porphyrias neuropathophysiology could be related to low levels of heme as a cofactor for nitric oxide synthase (NOS).	Heme	66-70	nitric oxide synthase 1, neuronal	Mus musculus	89-110
21111750-8	2011	PREGS enhanced the NMDAr-mediated nNOS expression to increase presynaptic glutamate release via a retrograde NO signaling.	Glutamic Acid	74-83	nitric oxide synthase 1, neuronal	Mus musculus	34-38
21118684-4	2011	Pharmacological nitric oxide synthase (NOS) inhibition protracted the duration of thromboembolic responses to ADP (adenosine diphosphate) and enhanced in vivo platelet aggregation following activation of the coagulation cascade.	Adenosine Diphosphate	110-113	nitric oxide synthase 1, neuronal	Mus musculus	16-37
21118684-4	2011	Pharmacological nitric oxide synthase (NOS) inhibition protracted the duration of thromboembolic responses to ADP (adenosine diphosphate) and enhanced in vivo platelet aggregation following activation of the coagulation cascade.	Adenosine Diphosphate	115-136	nitric oxide synthase 1, neuronal	Mus musculus	16-37
21118684-5	2011	Collagen induced in vivo platelet aggregation was enhanced in female eNOS(-/-) mice and the NOS inhibitor L-NAME (Nomega-Nitro-l-arginine methyl ester hydrochloride) potentiated collagen induced thromboembolism although selective iNOS and nNOS antagonists had no effect.	NG-Nitroarginine Methyl Ester	106-112	nitric oxide synthase 1, neuronal	Mus musculus	239-243
21118684-5	2011	Collagen induced in vivo platelet aggregation was enhanced in female eNOS(-/-) mice and the NOS inhibitor L-NAME (Nomega-Nitro-l-arginine methyl ester hydrochloride) potentiated collagen induced thromboembolism although selective iNOS and nNOS antagonists had no effect.	L-NAME hydrochloride	114-164	nitric oxide synthase 1, neuronal	Mus musculus	239-243
21075091-5	2011	To that end, we injected male mice with a bolus of METH (30 mg/kg, ip) and visualized striatal neuronal nitric oxide synthase (NOS)-positive cells by immunohistochemistry and protein levels by Western blot.	Methamphetamine	51-55	nitric oxide synthase 1, neuronal	Mus musculus	95-125
21423636-5	2011	DS (10-300 mug/mL) produced a concentration-dependent relaxation in mouse aorta, which was significantly attenuated by the nitric oxide synthase (NOS) inhibitor L-NAME, suggesting that DS causes vasodilation via a NO-dependent mechanism.	NG-Nitroarginine Methyl Ester	161-167	nitric oxide synthase 1, neuronal	Mus musculus	123-144
21423636-5	2011	DS (10-300 mug/mL) produced a concentration-dependent relaxation in mouse aorta, which was significantly attenuated by the nitric oxide synthase (NOS) inhibitor L-NAME, suggesting that DS causes vasodilation via a NO-dependent mechanism.	ds	185-187	nitric oxide synthase 1, neuronal	Mus musculus	123-144
21157027-8	2011	Together, these results show the antioxidant effect of the combination of folic acid and alpha-tocopherol, as observed by the decrease in NO generation from iNOS and nNOS, preventing an increase in the activity of mitochondrial complexes, mainly I and IV, and the neuronal death induced by the Abeta1-40 peptide.	Folic Acid	74-84	nitric oxide synthase 1, neuronal	Mus musculus	166-170
22553677-2	2011	METHODS: CRNV was induced by alkali injury in mice, nitric oxide synthetase (NOS) was inhibited by NG-nitro-L-arginine (L-NAME) and inducible nitric oxide synthetase (iNOS) was inhibited by aminoguanidine hemisulfate salt (AG).	Nitroarginine	99-118	nitric oxide synthase 1, neuronal	Mus musculus	52-75
22553677-2	2011	METHODS: CRNV was induced by alkali injury in mice, nitric oxide synthetase (NOS) was inhibited by NG-nitro-L-arginine (L-NAME) and inducible nitric oxide synthetase (iNOS) was inhibited by aminoguanidine hemisulfate salt (AG).	NG-Nitroarginine Methyl Ester	120-126	nitric oxide synthase 1, neuronal	Mus musculus	52-75
22553677-2	2011	METHODS: CRNV was induced by alkali injury in mice, nitric oxide synthetase (NOS) was inhibited by NG-nitro-L-arginine (L-NAME) and inducible nitric oxide synthetase (iNOS) was inhibited by aminoguanidine hemisulfate salt (AG).	aminoguanidine hemisulfate salt	190-221	nitric oxide synthase 1, neuronal	Mus musculus	52-75
21157027-8	2011	Together, these results show the antioxidant effect of the combination of folic acid and alpha-tocopherol, as observed by the decrease in NO generation from iNOS and nNOS, preventing an increase in the activity of mitochondrial complexes, mainly I and IV, and the neuronal death induced by the Abeta1-40 peptide.	alpha-Tocopherol	89-105	nitric oxide synthase 1, neuronal	Mus musculus	166-170
20845411-1	2011	Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase (NOS) inhibitor, is accumulated in plasma during chronic kidney disease (CKD).	dimethylarginine	11-27	nitric oxide synthase 1, neuronal	Mus musculus	50-71
20845411-1	2011	Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase (NOS) inhibitor, is accumulated in plasma during chronic kidney disease (CKD).	N,N-dimethylarginine	29-33	nitric oxide synthase 1, neuronal	Mus musculus	50-71
22031841-2	2011	We investigated if the peripheral nitric oxide-cGMP-protein kinase G (PKG)-ATP-sensitive K(+) (KATP) channels signaling pathway triggered by the neuronal nitric oxide synthase (NOS1) and modulated by opioids, participates in the local antinociceptive effects produced by a CB2R agonist (JWH-015) during chronic inflammatory pain.	Nitric Oxide	34-46	nitric oxide synthase 1, neuronal	Mus musculus	145-175
22003386-7	2011	These findings show that nNOS/NO (nitric oxide)-mediated decreases in M2c macrophages lead to a reduction in the muscle fibrosis that is associated with increased mortality in mice lacking dystrophin and utrophin.	Nitric Oxide	34-46	nitric oxide synthase 1, neuronal	Mus musculus	25-29
21240387-5	2010	Stretching of cardiomyocytes isolated from wild type mice and from NOS1(-/-)- and NOS2(-/-)- knockout mice led to the appearance in MG-currents typical for the specified magnitude of stretching, while stretching of cardiomyocytes from NOS3(-/-)- knockout mice did not produce in MG-current.	Magnesium	132-134	nitric oxide synthase 1, neuronal	Mus musculus	67-71
21240387-5	2010	Stretching of cardiomyocytes isolated from wild type mice and from NOS1(-/-)- and NOS2(-/-)- knockout mice led to the appearance in MG-currents typical for the specified magnitude of stretching, while stretching of cardiomyocytes from NOS3(-/-)- knockout mice did not produce in MG-current.	Magnesium	279-281	nitric oxide synthase 1, neuronal	Mus musculus	67-71
21606640-6	2011	RESULTS: LA-LTP induced by stimulation of the external capsule was nitric oxide (NO)-dependent because the NO synthase (NOS) inhibitor L-NAME reduced LA-LTP.	Nitric Oxide	67-79	nitric oxide synthase 1, neuronal	Mus musculus	107-118
21606640-6	2011	RESULTS: LA-LTP induced by stimulation of the external capsule was nitric oxide (NO)-dependent because the NO synthase (NOS) inhibitor L-NAME reduced LA-LTP.	NG-Nitroarginine Methyl Ester	135-141	nitric oxide synthase 1, neuronal	Mus musculus	107-118
21606640-6	2011	RESULTS: LA-LTP induced by stimulation of the external capsule was nitric oxide (NO)-dependent because the NO synthase (NOS) inhibitor L-NAME reduced LA-LTP.	la-ltp	9-15	nitric oxide synthase 1, neuronal	Mus musculus	107-118
22031841-2	2011	We investigated if the peripheral nitric oxide-cGMP-protein kinase G (PKG)-ATP-sensitive K(+) (KATP) channels signaling pathway triggered by the neuronal nitric oxide synthase (NOS1) and modulated by opioids, participates in the local antinociceptive effects produced by a CB2R agonist (JWH-015) during chronic inflammatory pain.	Adenosine Triphosphate	75-78	nitric oxide synthase 1, neuronal	Mus musculus	145-175
22031841-2	2011	We investigated if the peripheral nitric oxide-cGMP-protein kinase G (PKG)-ATP-sensitive K(+) (KATP) channels signaling pathway triggered by the neuronal nitric oxide synthase (NOS1) and modulated by opioids, participates in the local antinociceptive effects produced by a CB2R agonist (JWH-015) during chronic inflammatory pain.	Adenosine Triphosphate	75-78	nitric oxide synthase 1, neuronal	Mus musculus	177-181
22031841-2	2011	We investigated if the peripheral nitric oxide-cGMP-protein kinase G (PKG)-ATP-sensitive K(+) (KATP) channels signaling pathway triggered by the neuronal nitric oxide synthase (NOS1) and modulated by opioids, participates in the local antinociceptive effects produced by a CB2R agonist (JWH-015) during chronic inflammatory pain.	JHW 015	287-294	nitric oxide synthase 1, neuronal	Mus musculus	145-175
22031841-7	2011	Moreover, the antinociceptive effects of JWH-015 were absent in NOS1-KO mice and diminished by their co-administration with ODQ, Rp-8-pCPT-cGMPs or glibenclamide.	JHW 015	41-48	nitric oxide synthase 1, neuronal	Mus musculus	64-68
22031841-8	2011	CONCLUSIONS/SIGNIFICANCE: These data indicate that the peripheral antinociceptive effects of JWH-015 during chronic inflammatory pain are mainly produced by the local activation of the nitric oxide-cGMP-PKG-KATP signaling pathway, triggered by NOS1 and mediated by endogenous opioids.	JHW 015	93-100	nitric oxide synthase 1, neuronal	Mus musculus	244-248
22031841-8	2011	CONCLUSIONS/SIGNIFICANCE: These data indicate that the peripheral antinociceptive effects of JWH-015 during chronic inflammatory pain are mainly produced by the local activation of the nitric oxide-cGMP-PKG-KATP signaling pathway, triggered by NOS1 and mediated by endogenous opioids.	Nitric Oxide	185-197	nitric oxide synthase 1, neuronal	Mus musculus	244-248
22031841-8	2011	CONCLUSIONS/SIGNIFICANCE: These data indicate that the peripheral antinociceptive effects of JWH-015 during chronic inflammatory pain are mainly produced by the local activation of the nitric oxide-cGMP-PKG-KATP signaling pathway, triggered by NOS1 and mediated by endogenous opioids.	Cyclic GMP	198-202	nitric oxide synthase 1, neuronal	Mus musculus	244-248
21043515-1	2010	The in vivo molecular imaging of nitric oxide synthase (NOS), the enzyme responsible for the catalytic oxidation of l-arginine to citrulline and nitric oxide (NO), by noninvasive modalities could provide valuable insights into NO/NOS-related diseases.	Arginine	116-126	nitric oxide synthase 1, neuronal	Mus musculus	33-54
21043515-1	2010	The in vivo molecular imaging of nitric oxide synthase (NOS), the enzyme responsible for the catalytic oxidation of l-arginine to citrulline and nitric oxide (NO), by noninvasive modalities could provide valuable insights into NO/NOS-related diseases.	Citrulline	130-140	nitric oxide synthase 1, neuronal	Mus musculus	33-54
21179208-1	2010	BACKGROUND: Nitric oxide generated by neuronal (NOS1), inducible (NOS2) or endothelial (NOS3) nitric oxide synthases contributes to pain processing, but the exact role of NOS1 and NOS2 in the maintenance of chronic peripheral neuropathic pain as well as the possible compensatory changes in their expression in the spinal cord of wild type (WT) and NOS knockout (KO) mice at 21 days after total sciatic nerve ligation remains unknown.	Nitric Oxide	12-24	nitric oxide synthase 1, neuronal	Mus musculus	48-52
21179208-1	2010	BACKGROUND: Nitric oxide generated by neuronal (NOS1), inducible (NOS2) or endothelial (NOS3) nitric oxide synthases contributes to pain processing, but the exact role of NOS1 and NOS2 in the maintenance of chronic peripheral neuropathic pain as well as the possible compensatory changes in their expression in the spinal cord of wild type (WT) and NOS knockout (KO) mice at 21 days after total sciatic nerve ligation remains unknown.	Nitric Oxide	12-24	nitric oxide synthase 1, neuronal	Mus musculus	171-175
20889675-1	2010	Nitric oxide (NO), formed by nitric oxide synthase (NOS), is an important mediator of lung inflammation in allergic asthma.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	29-50
22031841-2	2011	We investigated if the peripheral nitric oxide-cGMP-protein kinase G (PKG)-ATP-sensitive K(+) (KATP) channels signaling pathway triggered by the neuronal nitric oxide synthase (NOS1) and modulated by opioids, participates in the local antinociceptive effects produced by a CB2R agonist (JWH-015) during chronic inflammatory pain.	Nitric Oxide	34-46	nitric oxide synthase 1, neuronal	Mus musculus	177-181
21039997-4	2010	RESULTS: Glutamate treatment induced apoptosis in HT22 cells, while reactive oxygen species (ROS) inhibitor or neuronal nitric oxide synthase (nNOS) inhibitor blocked glutamate-induced HT22 cell death.	Glutamic Acid	167-176	nitric oxide synthase 1, neuronal	Mus musculus	111-141
21039997-4	2010	RESULTS: Glutamate treatment induced apoptosis in HT22 cells, while reactive oxygen species (ROS) inhibitor or neuronal nitric oxide synthase (nNOS) inhibitor blocked glutamate-induced HT22 cell death.	Glutamic Acid	167-176	nitric oxide synthase 1, neuronal	Mus musculus	143-147
20651700-0	2010	Neuronal nitric oxide synthase supports Renin release during sodium restriction through inhibition of phosphodiesterase 3.	Sodium	61-67	nitric oxide synthase 1, neuronal	Mus musculus	0-30
21039997-8	2010	Results demonstrated that cell death, ROS accumulation and nNOS expression were related to nitration of protein tyrosine in the glutamate-stimulated cells.	Tyrosine	112-120	nitric oxide synthase 1, neuronal	Mus musculus	59-63
21039997-8	2010	Results demonstrated that cell death, ROS accumulation and nNOS expression were related to nitration of protein tyrosine in the glutamate-stimulated cells.	Glutamic Acid	128-137	nitric oxide synthase 1, neuronal	Mus musculus	59-63
20931971-1	2010	Three isoforms of nitric oxide synthase (NOS), dimeric enzymes that catalyze the formation of nitric oxide (NO) from arginine, have been identified.	Arginine	117-125	nitric oxide synthase 1, neuronal	Mus musculus	18-39
20931971-4	2010	By conformationally restricting the amide of this progenitor series, we describe the identification of a novel series of benzimidazole-quinolinone dual iNOS/nNOS inhibitors with low clearance and sustained exposure in vivo.	Amides	36-41	nitric oxide synthase 1, neuronal	Mus musculus	157-161
20931971-4	2010	By conformationally restricting the amide of this progenitor series, we describe the identification of a novel series of benzimidazole-quinolinone dual iNOS/nNOS inhibitors with low clearance and sustained exposure in vivo.	benzimidazole-quinolinone	121-146	nitric oxide synthase 1, neuronal	Mus musculus	157-161
20813105-4	2010	Hypothesized involvement of nNOS isoenzyme was addressed by preceding (0.5, 1, and 2 mg/kg) and subsequent (2 mg/kg) intraperitoneal injection of the nNOS-inhibitor NPLA.	n-propyl-l-arginine	165-169	nitric oxide synthase 1, neuronal	Mus musculus	28-32
20813105-4	2010	Hypothesized involvement of nNOS isoenzyme was addressed by preceding (0.5, 1, and 2 mg/kg) and subsequent (2 mg/kg) intraperitoneal injection of the nNOS-inhibitor NPLA.	n-propyl-l-arginine	165-169	nitric oxide synthase 1, neuronal	Mus musculus	150-154
20651700-2	2010	nNOS has a distinct expression at the macula densa (MD), and in the present study, it was tested whether nNOS supports renin release by cyclic guanosine monophosphate (cGMP)-mediated inhibition of cyclic adenosine monophosphate (cAMP)-specific phosphodiesterase 3 (PDE3) in juxtaglomerular (JG) cells.	Cyclic GMP	136-166	nitric oxide synthase 1, neuronal	Mus musculus	105-109
20651700-2	2010	nNOS has a distinct expression at the macula densa (MD), and in the present study, it was tested whether nNOS supports renin release by cyclic guanosine monophosphate (cGMP)-mediated inhibition of cyclic adenosine monophosphate (cAMP)-specific phosphodiesterase 3 (PDE3) in juxtaglomerular (JG) cells.	Cyclic GMP	168-172	nitric oxide synthase 1, neuronal	Mus musculus	105-109
20651700-2	2010	nNOS has a distinct expression at the macula densa (MD), and in the present study, it was tested whether nNOS supports renin release by cyclic guanosine monophosphate (cGMP)-mediated inhibition of cyclic adenosine monophosphate (cAMP)-specific phosphodiesterase 3 (PDE3) in juxtaglomerular (JG) cells.	Cyclic AMP	197-227	nitric oxide synthase 1, neuronal	Mus musculus	105-109
20651700-7	2010	Administration of milrinone caused a more pronounced PRC increase in nNOS-(/)-, resulting in normalized renin levels, whereas PDE5 inhibition did not affect PRC in any genotype.	Milrinone	18-27	nitric oxide synthase 1, neuronal	Mus musculus	69-73
20651700-10	2010	CONCLUSIONS: The present study provides in vivo evidence supporting the view that NO, selectively derived from nNOS, mediates renin release during sodium restriction by inhibiting PDE3, which would increase renin release by elevating cAMP levels in the JG cells.	Sodium	147-153	nitric oxide synthase 1, neuronal	Mus musculus	111-115
20651700-10	2010	CONCLUSIONS: The present study provides in vivo evidence supporting the view that NO, selectively derived from nNOS, mediates renin release during sodium restriction by inhibiting PDE3, which would increase renin release by elevating cAMP levels in the JG cells.	Cyclic AMP	234-238	nitric oxide synthase 1, neuronal	Mus musculus	111-115
20943934-8	2010	These changes in KO mice were accompanied by increased 20-HETE synthesis, reduced renal production of nitric oxide (NO), increased lipid hydroperoxides and increased apocynin-inhibitable vascular NADPH oxidase activity that was prevented by administration of NO synthase (NOS) inhibitor, suggesting endothelial nitric oxide synthase (eNOS) uncoupling.	acetovanillone	166-174	nitric oxide synthase 1, neuronal	Mus musculus	259-270
20881244-7	2010	However, we found that in states of low leptin levels, as in fasting, or lack of leptin, as in ob/ob mice, the number of neurons expressing the phosphorylated form of nNOS is decreased in the Arc, DMH, and PMV.	Dimenhydrinate	197-200	nitric oxide synthase 1, neuronal	Mus musculus	167-171
20662836-5	2010	Electron-microscopic observation at 1 h after acetone treatment indicated that barrier recovery of both nNOS and eNOS mice was faster than that of wild-type mice, and lamellar body secretion was accelerated in both types of knockout mice.	Acetone	46-53	nitric oxide synthase 1, neuronal	Mus musculus	104-108
20654633-9	2010	Both non-selective NOS inhibitors, L-NAME and 7-NI, and N(omega)-propyl-L-arginine, a selective inhibitor of nNOS resulted in a dose-dependent inhibition of i.t.	N(omega)-propylarginine	56-82	nitric oxide synthase 1, neuronal	Mus musculus	109-113
20633653-8	2010	Since NO synthase (NOS) inhibitor, l-NAME, suppressed NUF251-ECP-induced NO production, inducible NO synthase (iNOS) in RAW264.7 cells may be a main source of NO.	NG-Nitroarginine Methyl Ester	35-41	nitric oxide synthase 1, neuronal	Mus musculus	6-17
20921441-3	2010	We now hypothesize that nNOS overexpression is cardioprotective after ischemia/reperfusion because of inhibition of mitochondrial function and a reduction in reactive oxygen species generation.	Reactive Oxygen Species	158-181	nitric oxide synthase 1, neuronal	Mus musculus	24-28
20921441-9	2010	nNOS overexpression also caused a significant increase in mitochondrial nitrite levels accompanied by a decrease of cytochrome c oxidase activity.	Nitrites	72-79	nitric oxide synthase 1, neuronal	Mus musculus	0-4
20921441-10	2010	Accordingly, O(2) consumption in isolated heart muscle strips was decreased in nNOS-overexpressing nNOS(+)/alphaMHC-tTA(+) mice already under resting conditions.	Oxygen	13-17	nitric oxide synthase 1, neuronal	Mus musculus	79-83
20921441-10	2010	Accordingly, O(2) consumption in isolated heart muscle strips was decreased in nNOS-overexpressing nNOS(+)/alphaMHC-tTA(+) mice already under resting conditions.	Oxygen	13-17	nitric oxide synthase 1, neuronal	Mus musculus	99-103
20624383-2	2010	However, we have recently shown that neuronal nitric oxide synthase (nNOS)-derived H(2)O(2) is also an endothelium-dependent relaxing factor in the mouse aorta.	Hydrogen Peroxide	83-91	nitric oxide synthase 1, neuronal	Mus musculus	37-67
20064011-5	2010	Murine ESCs differentiated in the presence of NO synthase (NOS) inhibitor NG-nitroarginine methyl ester (L-NAME) for up to 11 days were not significantly different from vehicle-treated cells in EC markers.	NG-Nitroarginine Methyl Ester	74-103	nitric oxide synthase 1, neuronal	Mus musculus	46-57
20064011-5	2010	Murine ESCs differentiated in the presence of NO synthase (NOS) inhibitor NG-nitroarginine methyl ester (L-NAME) for up to 11 days were not significantly different from vehicle-treated cells in EC markers.	NG-Nitroarginine Methyl Ester	105-111	nitric oxide synthase 1, neuronal	Mus musculus	46-57
20624383-2	2010	However, we have recently shown that neuronal nitric oxide synthase (nNOS)-derived H(2)O(2) is also an endothelium-dependent relaxing factor in the mouse aorta.	Hydrogen Peroxide	83-91	nitric oxide synthase 1, neuronal	Mus musculus	69-73
20624383-8	2010	Selective pharmacological inhibition of nNOS with L-Arg(NO2)-L-Dbu-NH(2) 2TFA and specific knock-down of nNOS abrogated H(2)O(2) and decreased by half acetylcholine-induced vasodilation.	Arginine	50-55	nitric oxide synthase 1, neuronal	Mus musculus	40-44
20624383-8	2010	Selective pharmacological inhibition of nNOS with L-Arg(NO2)-L-Dbu-NH(2) 2TFA and specific knock-down of nNOS abrogated H(2)O(2) and decreased by half acetylcholine-induced vasodilation.	no2)-l-dbu-nh(2) 2tfa	56-77	nitric oxide synthase 1, neuronal	Mus musculus	40-44
20624383-8	2010	Selective pharmacological inhibition of nNOS with L-Arg(NO2)-L-Dbu-NH(2) 2TFA and specific knock-down of nNOS abrogated H(2)O(2) and decreased by half acetylcholine-induced vasodilation.	Acetylcholine	151-164	nitric oxide synthase 1, neuronal	Mus musculus	40-44
20624383-8	2010	Selective pharmacological inhibition of nNOS with L-Arg(NO2)-L-Dbu-NH(2) 2TFA and specific knock-down of nNOS abrogated H(2)O(2) and decreased by half acetylcholine-induced vasodilation.	Acetylcholine	151-164	nitric oxide synthase 1, neuronal	Mus musculus	105-109
20624383-11	2010	In eNOS knocked-down mice, pharmacological nNOS inhibition dramatically reduced H(2)O(2) production and further reduced the residual acetylcholine-induced vasodilation.	Hydrogen Peroxide	80-88	nitric oxide synthase 1, neuronal	Mus musculus	43-47
20624383-11	2010	In eNOS knocked-down mice, pharmacological nNOS inhibition dramatically reduced H(2)O(2) production and further reduced the residual acetylcholine-induced vasodilation.	Acetylcholine	133-146	nitric oxide synthase 1, neuronal	Mus musculus	43-47
20561153-0	2010	Effects of perinatal administration of Bisphenol A on the neuronal nitric oxide synthase expressing system in the hypothalamus and limbic system of CD1 mice.	bisphenol A	39-50	nitric oxide synthase 1, neuronal	Mus musculus	58-88
20826673-3	2010	We tested the hypothesis that extended (35 d) CIH results in a decrease in the surface/synaptic availability of the essential NMDA NR1 subunit in nNOS-containing neurons and NMDA-induced NO production in the PVN of mice.	cih	46-49	nitric oxide synthase 1, neuronal	Mus musculus	146-150
20826673-3	2010	We tested the hypothesis that extended (35 d) CIH results in a decrease in the surface/synaptic availability of the essential NMDA NR1 subunit in nNOS-containing neurons and NMDA-induced NO production in the PVN of mice.	N-Methylaspartate	126-130	nitric oxide synthase 1, neuronal	Mus musculus	146-150
20826673-4	2010	As compared with controls, the 35 d CIH-exposed mice showed a significant increase in blood pressure and an increased density of NR1 immunogold particles located in the cytoplasm of nNOS-containing dendrites.	cih	36-39	nitric oxide synthase 1, neuronal	Mus musculus	182-186
20826673-8	2010	We conclude that CIH produces a reduction in the surface/synaptic targeting of NR1 in nNOS neurons and decreases NMDA receptor-mediated currents in the PVN before the emergence of hypertension, the development of which may be enabled by suppression of NO signaling in this brain region.	cih	17-20	nitric oxide synthase 1, neuronal	Mus musculus	86-90
20648573-2	2010	Nitric oxide (NO), synthesized by neuronal nitric oxide synthase (nNOS) plays an important role in the control of gastrointestinal motility.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	34-64
20648573-2	2010	Nitric oxide (NO), synthesized by neuronal nitric oxide synthase (nNOS) plays an important role in the control of gastrointestinal motility.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	66-70
20655878-1	2010	Excessive production of nitric oxide (NO) by NO synthase (NOS) with subsequent formation of peroxynitrite and poly(adenosine diphosphate ribose) is critically implemented in the pathophysiology of acute lung injury and sepsis.	Nitric Oxide	24-36	nitric oxide synthase 1, neuronal	Mus musculus	45-56
20655878-1	2010	Excessive production of nitric oxide (NO) by NO synthase (NOS) with subsequent formation of peroxynitrite and poly(adenosine diphosphate ribose) is critically implemented in the pathophysiology of acute lung injury and sepsis.	Peroxynitrous Acid	92-105	nitric oxide synthase 1, neuronal	Mus musculus	45-56
20655878-1	2010	Excessive production of nitric oxide (NO) by NO synthase (NOS) with subsequent formation of peroxynitrite and poly(adenosine diphosphate ribose) is critically implemented in the pathophysiology of acute lung injury and sepsis.	Poly Adenosine Diphosphate Ribose	110-144	nitric oxide synthase 1, neuronal	Mus musculus	45-56
20498253-2	2010	We investigated whether nitric oxide synthesized by neuronal (NOS1) or inducible (NOS2) nitric-oxide synthases could modulate DOPr and/or CB2R antiallodynic and antihyperalgesic effects through the peripheral nitric oxide-cGMP-protein kinase G (PKG) pathway activation and affect their expression during neuropathic pain.	Nitric Oxide	24-36	nitric oxide synthase 1, neuronal	Mus musculus	62-66
20498253-7	2010	Results suggest that inactivation of the nitric oxide-cGMP-PKG peripheral pathway triggered by NOS1 and NOS2 enhanced the peripheral actions of DOPr and CB2R agonists and that nitric oxide synthesized by NOS1 is implicated in the peripheral regulation of DOPr and CB2R gene transcription during neuropathic pain.	Nitric Oxide	41-53	nitric oxide synthase 1, neuronal	Mus musculus	95-99
20498253-7	2010	Results suggest that inactivation of the nitric oxide-cGMP-PKG peripheral pathway triggered by NOS1 and NOS2 enhanced the peripheral actions of DOPr and CB2R agonists and that nitric oxide synthesized by NOS1 is implicated in the peripheral regulation of DOPr and CB2R gene transcription during neuropathic pain.	Nitric Oxide	41-53	nitric oxide synthase 1, neuronal	Mus musculus	204-208
20498253-7	2010	Results suggest that inactivation of the nitric oxide-cGMP-PKG peripheral pathway triggered by NOS1 and NOS2 enhanced the peripheral actions of DOPr and CB2R agonists and that nitric oxide synthesized by NOS1 is implicated in the peripheral regulation of DOPr and CB2R gene transcription during neuropathic pain.	Cyclic GMP	54-58	nitric oxide synthase 1, neuronal	Mus musculus	95-99
20498253-7	2010	Results suggest that inactivation of the nitric oxide-cGMP-PKG peripheral pathway triggered by NOS1 and NOS2 enhanced the peripheral actions of DOPr and CB2R agonists and that nitric oxide synthesized by NOS1 is implicated in the peripheral regulation of DOPr and CB2R gene transcription during neuropathic pain.	Cyclic GMP	54-58	nitric oxide synthase 1, neuronal	Mus musculus	204-208
20498253-7	2010	Results suggest that inactivation of the nitric oxide-cGMP-PKG peripheral pathway triggered by NOS1 and NOS2 enhanced the peripheral actions of DOPr and CB2R agonists and that nitric oxide synthesized by NOS1 is implicated in the peripheral regulation of DOPr and CB2R gene transcription during neuropathic pain.	Nitric Oxide	176-188	nitric oxide synthase 1, neuronal	Mus musculus	204-208
20561153-7	2010	These results indicate that BPA has a powerful effect on specific portions of the nNOS-immunoreactive system belonging to the accessory olfactory system that are particularly important for the control of sexual behaviour.	bisphenol A	28-31	nitric oxide synthase 1, neuronal	Mus musculus	82-86
20443189-6	2010	This suppression is reversed by treatment with the Nitric Oxide Synthase (NOS) inhibitor, N(6)-methyl-L-arginine acetate (L-NMMA).	n(6)-methyl-l-arginine acetate	90-120	nitric oxide synthase 1, neuronal	Mus musculus	51-72
20707900-8	2010	Additional studies revealed that the cardioprotection afforded by exogenous NO and by inhibition of nNOS were unaffected by the mitoKATP channel blocker 5-HD, although it was abrogated by p38MAPK blocker SB203580.	SB 203580	204-212	nitric oxide synthase 1, neuronal	Mus musculus	100-104
20435320-5	2010	In the Tg mice, nNOS was largely extracted with 100 mM NaCl and barely detected in the pellet fraction, suggesting fragile anchoring of nNOS to the sarcolemma.	Sodium Chloride	55-59	nitric oxide synthase 1, neuronal	Mus musculus	16-20
20223914-1	2010	Tetrahydrobiopterin (BH(4)) is an essential cofactor for nitric oxide synthases (NOS).	sapropterin	0-19	nitric oxide synthase 1, neuronal	Mus musculus	57-79
20578685-8	2010	The general nitric oxide synthase (NOS) inhibitor L-NMMA and the neuronal NOS (NOS1) inhibitor, 7-nitroindazole, added in the reincubation media decreased toxicity and protein nitration; however, neither the inducible NOS (NOS2) inhibitors L-NIL (N6-(1-iminoethyl)-L-lysine) nor SAIT (S-(2-aminoethyl)isothiourea) decreased protein nitration or toxicity.	7-nitroindazole	96-111	nitric oxide synthase 1, neuronal	Mus musculus	79-83
20506472-10	2010	Changes in cell position and protein expression subsequent to disruption of GABA signaling may be due, in part, to changes in nNOS and BDNF signaling.	gamma-Aminobutyric Acid	76-80	nitric oxide synthase 1, neuronal	Mus musculus	126-130
20443189-6	2010	This suppression is reversed by treatment with the Nitric Oxide Synthase (NOS) inhibitor, N(6)-methyl-L-arginine acetate (L-NMMA).	omega-N-Methylarginine	122-128	nitric oxide synthase 1, neuronal	Mus musculus	51-72
20503422-1	2010	Nitric oxide (NO), produced by NO synthase (NOS), modulates the function of all retinal neurons and ocular blood vessels and participates in the pathogenesis of ocular diseases.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	31-42
20576117-1	2010	BACKGROUND: Arginine is an amino acid that serves as a substrate for the enzymes nitric oxide synthase (NOS) and arginase, leading to synthesis of NO and ornithine, respectively.	Arginine	12-20	nitric oxide synthase 1, neuronal	Mus musculus	81-102
20576117-1	2010	BACKGROUND: Arginine is an amino acid that serves as a substrate for the enzymes nitric oxide synthase (NOS) and arginase, leading to synthesis of NO and ornithine, respectively.	Ornithine	154-163	nitric oxide synthase 1, neuronal	Mus musculus	81-102
20380820-8	2010	Furthermore, icariin-treated SAMP8 mice had significantly decreased malondialdehyde (MDA), nitric oxide (NO) contents, lowered nitric oxide synthase (NOS) activity and higher glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities in the brain homogenates and serum.	icariin	13-20	nitric oxide synthase 1, neuronal	Mus musculus	127-148
20519536-8	2010	Morphine withdrawal-induced MMP-9 activity is also reduced by an nNOS inhibitor.	Morphine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	65-69
20147620-0	2010	Morphine peripheral analgesia depends on activation of the PI3Kgamma/AKT/nNOS/NO/KATP signaling pathway.	Morphine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	73-77
20224887-1	2010	RATIONALE: Nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) is a retrograde neuronal messenger that participates in synaptic plasticity, including late-phase long-term potentiation (LTP) and long-term memory (LTM) formation.	Nitric Oxide	11-23	nitric oxide synthase 1, neuronal	Mus musculus	41-71
20224887-1	2010	RATIONALE: Nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) is a retrograde neuronal messenger that participates in synaptic plasticity, including late-phase long-term potentiation (LTP) and long-term memory (LTM) formation.	Nitric Oxide	11-23	nitric oxide synthase 1, neuronal	Mus musculus	73-77
20224887-7	2010	Pretraining molsidomine administration to nNOS KO mice improved their deficit in short- and long-term memories of contextual fear conditioning (46% increase).	Molsidomine	12-23	nitric oxide synthase 1, neuronal	Mus musculus	42-46
19962451-8	2010	Further, we found that the increase in ADMA levels cause an early decrease in nitric oxide (NO(x)) and a significant increase in both NO synthase (NOS)-derived superoxide and total nitrated lung proteins.	Superoxides	160-170	nitric oxide synthase 1, neuronal	Mus musculus	134-145
19962451-8	2010	Further, we found that the increase in ADMA levels cause an early decrease in nitric oxide (NO(x)) and a significant increase in both NO synthase (NOS)-derived superoxide and total nitrated lung proteins.	N,N-dimethylarginine	39-43	nitric oxide synthase 1, neuronal	Mus musculus	134-145
20019649-2	2010	Vascular integrity of the graft is critically dependent on nitric oxide (NO), synthesized by NO synthases (NOS), of which three isoforms have been located in the arterial wall: endothelial NOS (eNOS), inducible NOS, and neuronal NOS (nNOS).	Nitric Oxide	59-71	nitric oxide synthase 1, neuronal	Mus musculus	93-105
20019649-2	2010	Vascular integrity of the graft is critically dependent on nitric oxide (NO), synthesized by NO synthases (NOS), of which three isoforms have been located in the arterial wall: endothelial NOS (eNOS), inducible NOS, and neuronal NOS (nNOS).	Nitric Oxide	59-71	nitric oxide synthase 1, neuronal	Mus musculus	220-232
20019649-2	2010	Vascular integrity of the graft is critically dependent on nitric oxide (NO), synthesized by NO synthases (NOS), of which three isoforms have been located in the arterial wall: endothelial NOS (eNOS), inducible NOS, and neuronal NOS (nNOS).	Nitric Oxide	59-71	nitric oxide synthase 1, neuronal	Mus musculus	234-238
19673702-0	2010	Induction of inducible nitric oxide synthase increases the production of reactive oxygen species in RAW264.7 macrophages.	Reactive Oxygen Species	73-96	nitric oxide synthase 1, neuronal	Mus musculus	23-44
20097209-0	2010	Inducible nitric oxide synthase-mediated decrease of intestinal P-glycoprotein expression under streptozotocin-induced diabetic conditions.	Streptozocin	96-110	nitric oxide synthase 1, neuronal	Mus musculus	10-31
21190006-0	2010	Immunohistochemical study on the expression of calcium binding proteins (calbindin-D28k, calretinin, and parvalbumin) in the cerebellum of the nNOS knock-out(-/-) mice.	Calcium	47-54	nitric oxide synthase 1, neuronal	Mus musculus	143-147
19823767-2	2010	In this work, we investigate the action of the muscarinic agonist carbachol (CARB) on the expression and function of nitric oxide synthase (NOS) and cyclooxygenase (COX) in fibroblasts under normal or inflammatory conditions.	Carbachol	66-75	nitric oxide synthase 1, neuronal	Mus musculus	117-138
19823767-2	2010	In this work, we investigate the action of the muscarinic agonist carbachol (CARB) on the expression and function of nitric oxide synthase (NOS) and cyclooxygenase (COX) in fibroblasts under normal or inflammatory conditions.	Carbachol	77-81	nitric oxide synthase 1, neuronal	Mus musculus	117-138
19823767-9	2010	CARB also upregulated NOS1 protein expression via NF-kappaB activation.	Carbachol	0-4	nitric oxide synthase 1, neuronal	Mus musculus	22-26
19775503-0	2010	Discrimination between cocaine-associated context and cue in a modified conditioned place preference paradigm: role of the nNOS gene in cue conditioning.	Cocaine	23-30	nitric oxide synthase 1, neuronal	Mus musculus	123-127
20153031-1	2010	BACKGROUND: Disturbance in the delicate balance between L-arginine-metabolizing enzymes such as nitric oxide synthase (NOS) and arginase may lead to decreased L-arginine availability to constitutive forms of NOS (endothelial NOS), thereby increasing the nitro-oxidative stress and airway hyperresponsiveness (AHR).	Arginine	56-66	nitric oxide synthase 1, neuronal	Mus musculus	96-117
20153031-1	2010	BACKGROUND: Disturbance in the delicate balance between L-arginine-metabolizing enzymes such as nitric oxide synthase (NOS) and arginase may lead to decreased L-arginine availability to constitutive forms of NOS (endothelial NOS), thereby increasing the nitro-oxidative stress and airway hyperresponsiveness (AHR).	Arginine	159-169	nitric oxide synthase 1, neuronal	Mus musculus	96-117
20071630-1	2010	Nitric oxide (NO) has been recognized as an atypical neuronal messenger affecting synaptic transmission, but its cellular source has remained unresolved as the neuronal NO synthase isoform (nNOS) in brain areas such as the neocortex is expressed only by a small subset of inhibitory neurons.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	160-188
20071630-1	2010	Nitric oxide (NO) has been recognized as an atypical neuronal messenger affecting synaptic transmission, but its cellular source has remained unresolved as the neuronal NO synthase isoform (nNOS) in brain areas such as the neocortex is expressed only by a small subset of inhibitory neurons.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	190-194
18838497-5	2010	injections of saline or L-nitro-arginine (L-NOARG, 40 mg/kg), a non-selective inhibitor of neuronal nitric oxide synthase (nNOS).	l-nitro-arginine	24-40	nitric oxide synthase 1, neuronal	Mus musculus	123-127
18838497-13	2010	Animals that received repeated L-NOARG injections also showed an increase in the number of nNOS-positive neurons in the striatum.	l-noarg	31-38	nitric oxide synthase 1, neuronal	Mus musculus	91-95
20056676-3	2010	Age-dependent hypersensitivity to acetylcholine is abolished by inhibition of nitric oxide synthase (NOS) activity, indicating that Col4a1 mutations affect vasorelaxation mediated by endothelium-derived nitric oxide (NO).	Acetylcholine	34-47	nitric oxide synthase 1, neuronal	Mus musculus	78-99
19775503-8	2010	nNOS KO mice acquired approach behaviour for the cocaine-associated context but not cue.	Cocaine	49-56	nitric oxide synthase 1, neuronal	Mus musculus	0-4
20158465-0	2010	Nitric oxide production during cerebral ischemia and reperfusion in eNOS- and nNOS-knockout mice.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	78-82
20016022-4	2010	In WT mice, alcohol administration transiently increased mitochondrial ROS formation, decreased mitochondrial glutathione, depleted and damaged mtDNA, and decreased complex I and V activities; alcohol durably increased inducible nitric-oxide synthase (NOS) expression, plasma nitrites/nitrates, and the nitration of tyrosine residues in complex V proteins.	Alcohols	12-19	nitric oxide synthase 1, neuronal	Mus musculus	229-250
20016022-4	2010	In WT mice, alcohol administration transiently increased mitochondrial ROS formation, decreased mitochondrial glutathione, depleted and damaged mtDNA, and decreased complex I and V activities; alcohol durably increased inducible nitric-oxide synthase (NOS) expression, plasma nitrites/nitrates, and the nitration of tyrosine residues in complex V proteins.	Alcohols	193-200	nitric oxide synthase 1, neuronal	Mus musculus	229-250
20083682-3	2010	Hypertension can lead to a reduction in vascular NO, in part because NO synthase (NOS) becomes uncoupled when oxidative depletion of its cofactor tetrahydrobiopterin (BH(4)) occurs.	sapropterin	146-165	nitric oxide synthase 1, neuronal	Mus musculus	69-80
19959818-5	2010	Spontaneous CMMCs occurred in both wild-type (frequency: 0.3 cycles/min) and nNOS(-/-) mice (frequency: 0.4 cycles/min).	cmmcs	12-17	nitric oxide synthase 1, neuronal	Mus musculus	77-81
20164327-3	2010	Here, we show that 5-HT(1A)R-selective agonist 8-OH-DPAT and selective serotonin reuptake inhibitor (SSRI) fluoxetine downregulated hippocampal neuronal nitric oxide synthase (nNOS) expression, whereas 5-HT(1A)R-selective antagonist NAN-190 upregulated hippocampal nNOS expression.	8-Hydroxy-2-(di-n-propylamino)tetralin	47-56	nitric oxide synthase 1, neuronal	Mus musculus	144-174
20164327-3	2010	Here, we show that 5-HT(1A)R-selective agonist 8-OH-DPAT and selective serotonin reuptake inhibitor (SSRI) fluoxetine downregulated hippocampal neuronal nitric oxide synthase (nNOS) expression, whereas 5-HT(1A)R-selective antagonist NAN-190 upregulated hippocampal nNOS expression.	8-Hydroxy-2-(di-n-propylamino)tetralin	47-56	nitric oxide synthase 1, neuronal	Mus musculus	176-180
20164327-3	2010	Here, we show that 5-HT(1A)R-selective agonist 8-OH-DPAT and selective serotonin reuptake inhibitor (SSRI) fluoxetine downregulated hippocampal neuronal nitric oxide synthase (nNOS) expression, whereas 5-HT(1A)R-selective antagonist NAN-190 upregulated hippocampal nNOS expression.	8-Hydroxy-2-(di-n-propylamino)tetralin	47-56	nitric oxide synthase 1, neuronal	Mus musculus	265-269
20164327-3	2010	Here, we show that 5-HT(1A)R-selective agonist 8-OH-DPAT and selective serotonin reuptake inhibitor (SSRI) fluoxetine downregulated hippocampal neuronal nitric oxide synthase (nNOS) expression, whereas 5-HT(1A)R-selective antagonist NAN-190 upregulated hippocampal nNOS expression.	Fluoxetine	107-117	nitric oxide synthase 1, neuronal	Mus musculus	144-174
20164327-3	2010	Here, we show that 5-HT(1A)R-selective agonist 8-OH-DPAT and selective serotonin reuptake inhibitor (SSRI) fluoxetine downregulated hippocampal neuronal nitric oxide synthase (nNOS) expression, whereas 5-HT(1A)R-selective antagonist NAN-190 upregulated hippocampal nNOS expression.	Fluoxetine	107-117	nitric oxide synthase 1, neuronal	Mus musculus	176-180
20164327-3	2010	Here, we show that 5-HT(1A)R-selective agonist 8-OH-DPAT and selective serotonin reuptake inhibitor (SSRI) fluoxetine downregulated hippocampal neuronal nitric oxide synthase (nNOS) expression, whereas 5-HT(1A)R-selective antagonist NAN-190 upregulated hippocampal nNOS expression.	Fluoxetine	107-117	nitric oxide synthase 1, neuronal	Mus musculus	265-269
20164327-3	2010	Here, we show that 5-HT(1A)R-selective agonist 8-OH-DPAT and selective serotonin reuptake inhibitor (SSRI) fluoxetine downregulated hippocampal neuronal nitric oxide synthase (nNOS) expression, whereas 5-HT(1A)R-selective antagonist NAN-190 upregulated hippocampal nNOS expression.	1-(2-methoxyphenyl)-4-(4-(2-phthalimido)butyl)piperazine	233-240	nitric oxide synthase 1, neuronal	Mus musculus	144-174
20164327-4	2010	By assessing anxiety-related behaviors using the novelty suppressed feeding, open-field, and elevated plus maze tests, we show that mice lacking nNOS gene [knock-out (KO)] or treated with nNOS-selective inhibitor 7-nitroindazole (7-NI; i.p., 30 mg/kg/d for 28 d; or intrahippocampal microinjection, 16.31 microg/1.0 microl) displayed an anxiolytic-like phenotype, implicating nNOS in anxiety.	7-nitroindazole	213-228	nitric oxide synthase 1, neuronal	Mus musculus	188-192
20164327-4	2010	By assessing anxiety-related behaviors using the novelty suppressed feeding, open-field, and elevated plus maze tests, we show that mice lacking nNOS gene [knock-out (KO)] or treated with nNOS-selective inhibitor 7-nitroindazole (7-NI; i.p., 30 mg/kg/d for 28 d; or intrahippocampal microinjection, 16.31 microg/1.0 microl) displayed an anxiolytic-like phenotype, implicating nNOS in anxiety.	7-nitroindazole	213-228	nitric oxide synthase 1, neuronal	Mus musculus	188-192
20158465-1	2010	The purpose of this study was to clarify the kinetics of nitric oxide (NO) induced by either endothelial NO synthase (eNOS) or neuronal NO synthase (nNOS) after transient global forebrain ischemia.	Nitric Oxide	57-69	nitric oxide synthase 1, neuronal	Mus musculus	149-153
19765598-4	2010	Although inhibition of PDE10A causes accumulation of both cAMP and cGMP, the increase in striatal cfos expression appears to depend on changes in cAMP, since the increase is present in mice deficient in nNOS which fail to increase cGMP in response to PDE10A inhibition.	Cyclic AMP	58-62	nitric oxide synthase 1, neuronal	Mus musculus	203-207
19765598-4	2010	Although inhibition of PDE10A causes accumulation of both cAMP and cGMP, the increase in striatal cfos expression appears to depend on changes in cAMP, since the increase is present in mice deficient in nNOS which fail to increase cGMP in response to PDE10A inhibition.	Cyclic GMP	67-71	nitric oxide synthase 1, neuronal	Mus musculus	203-207
19765598-4	2010	Although inhibition of PDE10A causes accumulation of both cAMP and cGMP, the increase in striatal cfos expression appears to depend on changes in cAMP, since the increase is present in mice deficient in nNOS which fail to increase cGMP in response to PDE10A inhibition.	Cyclic AMP	146-150	nitric oxide synthase 1, neuronal	Mus musculus	203-207
19818753-0	2010	Antagonism of the antinociceptive effect of nitrous oxide by inhibition of enzyme activity or expression of neuronal nitric oxide synthase in the mouse brain and spinal cord.	Nitrous Oxide	44-57	nitric oxide synthase 1, neuronal	Mus musculus	108-138
19818753-5	2010	pretreatment with the NOS-inhibitor l-N(G)-nitro arginine methyl ester (L-NAME) or an antisense oligodeoxynucleotide (AS-ODN) directed against neuronal NOS (nNOS).	Oligodeoxyribonucleotides	96-116	nitric oxide synthase 1, neuronal	Mus musculus	143-155
19818753-5	2010	pretreatment with the NOS-inhibitor l-N(G)-nitro arginine methyl ester (L-NAME) or an antisense oligodeoxynucleotide (AS-ODN) directed against neuronal NOS (nNOS).	as-odn	118-124	nitric oxide synthase 1, neuronal	Mus musculus	143-155
19818753-13	2010	Compared to wild-type mice, nNOS knockout mice showed a 60% reduction in N(2)O-induced antinociception.	Nitrous Oxide	73-78	nitric oxide synthase 1, neuronal	Mus musculus	28-32
19812940-1	2010	Tetrahydrobiopterin (BH4) is an essential cofactor for nitric oxide synthase (NOS) and is presently used clinically to treat forms of phenylketonuria.	sapropterin	0-19	nitric oxide synthase 1, neuronal	Mus musculus	55-76
19648472-1	2010	Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), causes uncoupling of NOS leading to generation of reactive nitrogen species, such as peroxynitrite.	dimethylarginine	11-27	nitric oxide synthase 1, neuronal	Mus musculus	63-84
19648472-1	2010	Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), causes uncoupling of NOS leading to generation of reactive nitrogen species, such as peroxynitrite.	N,N-dimethylarginine	29-33	nitric oxide synthase 1, neuronal	Mus musculus	63-84
19648472-1	2010	Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), causes uncoupling of NOS leading to generation of reactive nitrogen species, such as peroxynitrite.	Reactive Nitrogen Species	142-167	nitric oxide synthase 1, neuronal	Mus musculus	63-84
19648472-1	2010	Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), causes uncoupling of NOS leading to generation of reactive nitrogen species, such as peroxynitrite.	Peroxynitrous Acid	177-190	nitric oxide synthase 1, neuronal	Mus musculus	63-84
21196947-5	2010	The interaction of celecoxib-induced effects with NO pathway was examined using a NO synthase (NOS) inhibitor, N(G)-omega-nitro-L-arginine methyl ester (L-NAME, 20 and 50 mg per kg, i.p.)	Celecoxib	19-28	nitric oxide synthase 1, neuronal	Mus musculus	82-93
21525761-3	2010	Acute alcohol administration increased mitochondrial ROS formation, decreased mitochondrial glutathione, depleted and damaged mtDNA, durably increased inducible nitric oxide synthase (NOS) expression, plasma nitrites/nitrates and the nitration of tyrosine residues in complex V proteins and decreased complex V activity in WT mice.	Alcohols	6-13	nitric oxide synthase 1, neuronal	Mus musculus	161-182
19812940-1	2010	Tetrahydrobiopterin (BH4) is an essential cofactor for nitric oxide synthase (NOS) and is presently used clinically to treat forms of phenylketonuria.	sapropterin	21-24	nitric oxide synthase 1, neuronal	Mus musculus	55-76
19853642-7	2010	Moreover, mevastatin and serum withdrawal rapidly increased the expression of the neuronal NOS isoform nNOS.	mevastatin	10-20	nitric oxide synthase 1, neuronal	Mus musculus	103-107
19706695-2	2010	Increased nitric oxide (NO) release by NO synthase (NOS) isoforms has been implicated in acute peritonitis, but the role played by the NOS isoforms expressed in the peritoneum is unknown.	Nitric Oxide	10-22	nitric oxide synthase 1, neuronal	Mus musculus	39-50
19665495-3	2009	Given that nitric oxide (NO) modulates dopamine effect our aim is to analyze the nitric oxide synthase (NOS) and soluble guanylate cyclase (sGC) inhibitors effect on PPI disruption induced by methylphenidate.	Nitric Oxide	11-23	nitric oxide synthase 1, neuronal	Mus musculus	81-102
19665495-3	2009	Given that nitric oxide (NO) modulates dopamine effect our aim is to analyze the nitric oxide synthase (NOS) and soluble guanylate cyclase (sGC) inhibitors effect on PPI disruption induced by methylphenidate.	Methylphenidate	192-207	nitric oxide synthase 1, neuronal	Mus musculus	81-102
19934018-2	2009	Reduction of nitrite to NO may occur enzymatically at low pH and oxygen tension by deoxyhemoglobin, deoxymyoglobin, xanthine oxidase, mitochondrial complexes, or NO synthase (NOS).	Nitrites	13-20	nitric oxide synthase 1, neuronal	Mus musculus	162-173
19734362-5	2009	Central administration of N(5)-(1-imino-3-butenyl)-l-ornithine (l-VNIO), a selective nNOS inhibitor, also significantly potentiated the increase in BP induced by ANG II in females (Delta17.5 + or - 3.2 vs. Delta9.2 + or - 1.5 mmHg).	N(5)-(1-imino-3-butenyl)ornithine	64-70	nitric oxide synthase 1, neuronal	Mus musculus	85-89
19856917-2	2009	In this study, we investigated the inhibitory effects of rosmanol on the induction of NO synthase (NOS) and COX-2 in RAW 264.7 cells induced by lipopolysaccharide (LPS).	rosmanol	57-65	nitric oxide synthase 1, neuronal	Mus musculus	86-97
19531381-1	2009	The gaseous neurotransmitter nitric oxide (NO), synthesized by the enzyme neuronal nitric oxide synthase (nNOS), is thought to play a major role in the modulation of memory.	Nitric Oxide	29-41	nitric oxide synthase 1, neuronal	Mus musculus	74-104
19734362-5	2009	Central administration of N(5)-(1-imino-3-butenyl)-l-ornithine (l-VNIO), a selective nNOS inhibitor, also significantly potentiated the increase in BP induced by ANG II in females (Delta17.5 + or - 3.2 vs. Delta9.2 + or - 1.5 mmHg).	n(5)-(1-imino-3-butenyl)-l-ornithine	26-62	nitric oxide synthase 1, neuronal	Mus musculus	85-89
19802465-0	2009	Purine nucleotides reduce superoxide production by nitric oxide synthase in a murine sepsis model.	Purine Nucleotides	0-18	nitric oxide synthase 1, neuronal	Mus musculus	51-72
19802465-0	2009	Purine nucleotides reduce superoxide production by nitric oxide synthase in a murine sepsis model.	Superoxides	26-36	nitric oxide synthase 1, neuronal	Mus musculus	51-72
19802465-8	2009	Nitric oxide synthase (NOS) inhibition by L-NAME blocked vascular relaxation and reduced superoxide production in LPS-treated animals.	NG-Nitroarginine Methyl Ester	42-48	nitric oxide synthase 1, neuronal	Mus musculus	0-21
19802465-8	2009	Nitric oxide synthase (NOS) inhibition by L-NAME blocked vascular relaxation and reduced superoxide production in LPS-treated animals.	Superoxides	89-99	nitric oxide synthase 1, neuronal	Mus musculus	0-21
19693000-6	2009	V1aR was found to specifically co-express at the macula densa cells with cyclooxygenase (COX)-2 and with neuronal nitric oxide synthase, which produces potent stimulators of renin, PGE(2), and NO.	Prostaglandins E	181-184	nitric oxide synthase 1, neuronal	Mus musculus	105-135
19693000-7	2009	The expression levels of renin, COX-2, and nNOS were significantly decreased in V1aR(-/-) mice, which led to the suppression of RAS activity and consequent decreases in aldosterone and blood volume.	Aldosterone	169-180	nitric oxide synthase 1, neuronal	Mus musculus	43-47
19531381-1	2009	The gaseous neurotransmitter nitric oxide (NO), synthesized by the enzyme neuronal nitric oxide synthase (nNOS), is thought to play a major role in the modulation of memory.	Nitric Oxide	29-41	nitric oxide synthase 1, neuronal	Mus musculus	106-110
19542095-4	2009	Our findings show that the expression of a muscle-specific, nNOS transgene increases the endurance of mdx mice and enhances glycogen metabolism during treadmill-running, but did not affect vascular perfusion of muscles.	Glycogen	124-132	nitric oxide synthase 1, neuronal	Mus musculus	60-64
19770398-8	2009	Treatment with the L-type Ca2+ channel blocker verapamil reduced the incidence of arrhythmia and ventricular fibrillation in nNOS(-/-) mice after MI.	Verapamil	47-56	nitric oxide synthase 1, neuronal	Mus musculus	125-129
19589334-12	2009	The selective nNOS inhibitor N(omega)-propyl-l-arginine, the selective iNOS inhibitor W1400, the soluble guanylate cyclase inhibitor ODQ and the PKG inhibitor KT-5823 inhibited dose-dependently the nociceptive response to i.t.	N(omega)-propylarginine	29-55	nitric oxide synthase 1, neuronal	Mus musculus	14-18
19559786-4	2009	Estradiol could induce nNOS expression in several brain regions in rodents.	Estradiol	0-9	nitric oxide synthase 1, neuronal	Mus musculus	23-27
19545548-0	2009	Opposing actions of neuronal nitric oxide synthase isoforms in formalin-induced pain in mice.	Formaldehyde	63-71	nitric oxide synthase 1, neuronal	Mus musculus	20-50
19545548-3	2009	An oligodeoxynucleotide targeting four nNOS isoforms given supraspinally also reduced the formalin response of both phases.	Oligodeoxyribonucleotides	3-23	nitric oxide synthase 1, neuronal	Mus musculus	39-43
19545548-3	2009	An oligodeoxynucleotide targeting four nNOS isoforms given supraspinally also reduced the formalin response of both phases.	Formaldehyde	90-98	nitric oxide synthase 1, neuronal	Mus musculus	39-43
19545548-4	2009	Supraspinal antisense mapping suggested that this effect results from the nNOS-1 splice variant, implying that nNOS-1 is important in mediating formalin pain.	Formaldehyde	144-152	nitric oxide synthase 1, neuronal	Mus musculus	74-78
19545548-4	2009	Supraspinal antisense mapping suggested that this effect results from the nNOS-1 splice variant, implying that nNOS-1 is important in mediating formalin pain.	Formaldehyde	144-152	nitric oxide synthase 1, neuronal	Mus musculus	111-115
19545548-5	2009	At the spinal level, antisense mapping suggested a role of both the nNOS-1 and the nNOS-beta variants in producing formalin pain.	Formaldehyde	115-123	nitric oxide synthase 1, neuronal	Mus musculus	68-72
19545548-5	2009	At the spinal level, antisense mapping suggested a role of both the nNOS-1 and the nNOS-beta variants in producing formalin pain.	Formaldehyde	115-123	nitric oxide synthase 1, neuronal	Mus musculus	83-87
19545548-10	2009	Local antisense mapping again showed that nNOS-1 is involved in producing phase II of the formalin response while nNOS-2 had an opposite effect similar to that seen spinally.	Formaldehyde	90-98	nitric oxide synthase 1, neuronal	Mus musculus	42-46
19545548-11	2009	Finally, downregulation of nNOS-1 by antisense prevented tolerance to morphine in both the tail-flick and the formalin test.	Morphine	70-78	nitric oxide synthase 1, neuronal	Mus musculus	27-31
19545548-11	2009	Finally, downregulation of nNOS-1 by antisense prevented tolerance to morphine in both the tail-flick and the formalin test.	Formaldehyde	110-118	nitric oxide synthase 1, neuronal	Mus musculus	27-31
19542095-8	2009	This approach yielded a polypeptide that included the flavin adenine dinucleotide (FAD)-binding domain of nNOS as the region of the molecule that promotes PFK activity.	Flavin-Adenine Dinucleotide	54-81	nitric oxide synthase 1, neuronal	Mus musculus	106-110
19542095-8	2009	This approach yielded a polypeptide that included the flavin adenine dinucleotide (FAD)-binding domain of nNOS as the region of the molecule that promotes PFK activity.	Flavin-Adenine Dinucleotide	83-86	nitric oxide synthase 1, neuronal	Mus musculus	106-110
19542095-9	2009	Smaller peptides in this domain were then synthesized and used in activity assays that showed a 36-amino acid peptide in the FAD-binding domain in which most of the positive allosteric activity of nNOS for PFK resides.	Flavin-Adenine Dinucleotide	125-128	nitric oxide synthase 1, neuronal	Mus musculus	197-201
20641345-0	2004	[(18)F]6-(2-Fluoropropyl)-4-methyl-pyridin-2-amine Nitric oxide (NO) is produced as an important mediator in physiological and pathophysiological conditions by three isoforms of NO synthase (NOS): endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS) (1, 2).	6-(2-fluoropropyl)-4-methylpyridin-2-amine	7-50	nitric oxide synthase 1, neuronal	Mus musculus	178-189
19717511-3	2009	Tyrosine nitration of CPB1 was significantly reduced in the presence of NO synthase (NOS) inhibitors and the xanthine oxidase (XO) inhibitor allopurinol and in NOS-3 knockout (KO) mice.	Tyrosine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	72-83
19570880-3	2009	We hypothesized that ATP enhances NO synthase (NOS) activity by stimulating PI3 kinase and Akt.	Adenosine Triphosphate	21-24	nitric oxide synthase 1, neuronal	Mus musculus	34-45
19570880-6	2009	In the presence of the NOS1- and NOS2-selective inhibitors 7-NI and 1400W, ATP stimulated NO by 30 +/- 2 and 33 +/- 3 AU, respectively (not significant vs. control).	7-nitroindazole	59-63	nitric oxide synthase 1, neuronal	Mus musculus	23-27
20641345-0	2004	[(18)F]6-(2-Fluoropropyl)-4-methyl-pyridin-2-amine Nitric oxide (NO) is produced as an important mediator in physiological and pathophysiological conditions by three isoforms of NO synthase (NOS): endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS) (1, 2).	6-(2-fluoropropyl)-4-methylpyridin-2-amine	7-50	nitric oxide synthase 1, neuronal	Mus musculus	221-233
20641345-0	2004	[(18)F]6-(2-Fluoropropyl)-4-methyl-pyridin-2-amine Nitric oxide (NO) is produced as an important mediator in physiological and pathophysiological conditions by three isoforms of NO synthase (NOS): endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS) (1, 2).	6-(2-fluoropropyl)-4-methylpyridin-2-amine	7-50	nitric oxide synthase 1, neuronal	Mus musculus	235-239
20641345-0	2004	[(18)F]6-(2-Fluoropropyl)-4-methyl-pyridin-2-amine Nitric oxide (NO) is produced as an important mediator in physiological and pathophysiological conditions by three isoforms of NO synthase (NOS): endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS) (1, 2).	Nitric Oxide	51-63	nitric oxide synthase 1, neuronal	Mus musculus	178-189
20641345-0	2004	[(18)F]6-(2-Fluoropropyl)-4-methyl-pyridin-2-amine Nitric oxide (NO) is produced as an important mediator in physiological and pathophysiological conditions by three isoforms of NO synthase (NOS): endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS) (1, 2).	Nitric Oxide	51-63	nitric oxide synthase 1, neuronal	Mus musculus	221-233
20641345-0	2004	[(18)F]6-(2-Fluoropropyl)-4-methyl-pyridin-2-amine Nitric oxide (NO) is produced as an important mediator in physiological and pathophysiological conditions by three isoforms of NO synthase (NOS): endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS) (1, 2).	Nitric Oxide	51-63	nitric oxide synthase 1, neuronal	Mus musculus	235-239
19365734-0	2009	Cannabinoid regulation of nitric oxide synthase I (nNOS) in neuronal cells.	Cannabinoids	0-11	nitric oxide synthase 1, neuronal	Mus musculus	51-55
19365734-2	2009	The purpose of these studies was to elucidate the signal transduction of cannabinoid-mediated neuronal nitric oxide synthase (nNOS) activation in neuronal cells.	Cannabinoids	73-84	nitric oxide synthase 1, neuronal	Mus musculus	94-124
19365734-2	2009	The purpose of these studies was to elucidate the signal transduction of cannabinoid-mediated neuronal nitric oxide synthase (nNOS) activation in neuronal cells.	Cannabinoids	73-84	nitric oxide synthase 1, neuronal	Mus musculus	126-130
19365734-7	2009	Cannabinoid-mediated NO production was attributed to nNOS activation since endothelial NOS and inducible NOS protein and mRNA were not detected in N18TG2 cells.	Cannabinoids	0-11	nitric oxide synthase 1, neuronal	Mus musculus	53-57
19365734-9	2009	Chronic treatment of N18TG2 cells with cannabinoid agonists downregulated nNOS protein and mRNA as detected using Western blot analysis and real-time polymerase chain reaction, respectively.	Cannabinoids	39-50	nitric oxide synthase 1, neuronal	Mus musculus	74-78
19365734-10	2009	Cannabinoid agonists stimulated NO production via signaling through CB(1) receptors, leading to activation of Gi/o protein and enhanced nNOS activity.	Cannabinoids	0-11	nitric oxide synthase 1, neuronal	Mus musculus	136-140
30625884-3	2009	This study was conducted to investigate the relationship between nNOS and NADPH-d expression in the DRG in a spinal nerve injury model of neuropathic pain, and to elucidate role that NO plays in neuropathic pain.	NADP	74-79	nitric oxide synthase 1, neuronal	Mus musculus	65-69
19570880-6	2009	In the presence of the NOS1- and NOS2-selective inhibitors 7-NI and 1400W, ATP stimulated NO by 30 +/- 2 and 33 +/- 3 AU, respectively (not significant vs. control).	N-((3-(aminomethyl)phenyl)methyl)ethanimidamide	68-73	nitric oxide synthase 1, neuronal	Mus musculus	23-27
19570880-6	2009	In the presence of the NOS1- and NOS2-selective inhibitors 7-NI and 1400W, ATP stimulated NO by 30 +/- 2 and 33 +/- 3 AU, respectively (not significant vs. control).	Adenosine Triphosphate	75-78	nitric oxide synthase 1, neuronal	Mus musculus	23-27
19726326-4	2009	The mice were sacrificed 14 and 28 days later, and using in situ hybridization with Digoxin-labeled nNOS cDNA oligonucleotide probe, neuronal nitric oxide synthase (nNOS) mRNA was detected in the striatum and substantia nigra in the brain of mice.	Digoxin	84-91	nitric oxide synthase 1, neuronal	Mus musculus	100-104
19726326-4	2009	The mice were sacrificed 14 and 28 days later, and using in situ hybridization with Digoxin-labeled nNOS cDNA oligonucleotide probe, neuronal nitric oxide synthase (nNOS) mRNA was detected in the striatum and substantia nigra in the brain of mice.	Digoxin	84-91	nitric oxide synthase 1, neuronal	Mus musculus	133-163
19726326-4	2009	The mice were sacrificed 14 and 28 days later, and using in situ hybridization with Digoxin-labeled nNOS cDNA oligonucleotide probe, neuronal nitric oxide synthase (nNOS) mRNA was detected in the striatum and substantia nigra in the brain of mice.	Digoxin	84-91	nitric oxide synthase 1, neuronal	Mus musculus	165-169
19726326-4	2009	The mice were sacrificed 14 and 28 days later, and using in situ hybridization with Digoxin-labeled nNOS cDNA oligonucleotide probe, neuronal nitric oxide synthase (nNOS) mRNA was detected in the striatum and substantia nigra in the brain of mice.	Oligonucleotides	110-125	nitric oxide synthase 1, neuronal	Mus musculus	133-163
19571147-8	2009	Suppression of SLE initiation in acute slices from mice was achieved by both the broad-spectrum NOS inhibitor N-methyl-L-arginine acetate and the nNOS-selective inhibitor 7-nitroindazole, whereas inhibition of inducible NOS by aminoguanidine was ineffective, suggesting that nNOS activity was crucial for SLE initiation.	7-nitroindazole	171-186	nitric oxide synthase 1, neuronal	Mus musculus	146-150
19429176-0	2009	The neuronal nitric oxide synthase (nNOS) gene contributes to the regulation of tyrosine hydroxylase (TH) by cocaine.	Cocaine	109-116	nitric oxide synthase 1, neuronal	Mus musculus	4-34
19429176-0	2009	The neuronal nitric oxide synthase (nNOS) gene contributes to the regulation of tyrosine hydroxylase (TH) by cocaine.	Cocaine	109-116	nitric oxide synthase 1, neuronal	Mus musculus	36-40
19429176-3	2009	Anderson, Y. Itzhak, Differential role of the nNOS gene in the development of behavioral sensitization to cocaine in adolescent and adult B6;129S mice, Psychopharmacology (Berl) 200 (2008) 509-519].	Cocaine	106-113	nitric oxide synthase 1, neuronal	Mus musculus	46-50
19429176-7	2009	We report that (a) nNOS KO mice express lower levels of TH-ir neurons in the VTA compared to WT counterparts, (b) cocaine administration to WT mice significantly increased striatal TH expression, and (c) the same cocaine administration to nNOS KO mice significantly decreased striatal TH expression.	Cocaine	114-121	nitric oxide synthase 1, neuronal	Mus musculus	19-23
19429176-7	2009	We report that (a) nNOS KO mice express lower levels of TH-ir neurons in the VTA compared to WT counterparts, (b) cocaine administration to WT mice significantly increased striatal TH expression, and (c) the same cocaine administration to nNOS KO mice significantly decreased striatal TH expression.	Cocaine	114-121	nitric oxide synthase 1, neuronal	Mus musculus	239-243
19364813-8	2009	Mechanistic analysis suggests that KLYP956 binds the oxygenase domain in the vicinity of the active site heme and inhibits iNOS and neuronal NOS (nNOS) by preventing the formation of enzymatically active dimers.	N-(3-chlorophenyl)-N-((8-fluoro-2-oxo-1,2-dihydroquinolin-4-yl)methyl)-4-methylthiazole-5-carboxamide	35-42	nitric oxide synthase 1, neuronal	Mus musculus	132-144
19457107-7	2009	Our results indicate that the neuronal NOS/cGMP/PKG pathway stimulates cPLA(2) phosphorylation at Ser505 by activating PKC and ERK1/2, and suggest that up-regulation of this pathway in experimental models of Parkinson"s disease may mediate dopaminergic neuron degeneration and death through activation of cPLA(2).	Cyclic GMP	43-47	nitric oxide synthase 1, neuronal	Mus musculus	30-42
19328848-5	2009	OH-Cbl and CN(2)-Cbi prevented binding of the oxygen analog carbon monoxide (CO) to the reduced NOS1 and NOS2 heme active site.	cn(2)-cbi	11-20	nitric oxide synthase 1, neuronal	Mus musculus	96-100
19328848-5	2009	OH-Cbl and CN(2)-Cbi prevented binding of the oxygen analog carbon monoxide (CO) to the reduced NOS1 and NOS2 heme active site.	Oxygen	46-52	nitric oxide synthase 1, neuronal	Mus musculus	96-100
19328848-5	2009	OH-Cbl and CN(2)-Cbi prevented binding of the oxygen analog carbon monoxide (CO) to the reduced NOS1 and NOS2 heme active site.	Carbon Monoxide	60-75	nitric oxide synthase 1, neuronal	Mus musculus	96-100
19328848-5	2009	OH-Cbl and CN(2)-Cbi prevented binding of the oxygen analog carbon monoxide (CO) to the reduced NOS1 and NOS2 heme active site.	Carbon Monoxide	77-80	nitric oxide synthase 1, neuronal	Mus musculus	96-100
19340535-5	2009	A potent nNOS inhibitor, L-VNIO, and a superoxide dismutase mimetic and peroxynitrite scavenger, MnTBAP, significantly reduced IR-induced increases of oxidative/nitrative stress and cardiac injury.	N(5)-(1-imino-3-butenyl)ornithine	25-31	nitric oxide synthase 1, neuronal	Mus musculus	9-13
19482906-5	2009	Furthermore, DHEA promoted a pro-oxidant status since it increased nitric oxide synthase (NOS) activity and decreased superoxide dismutase and catalase activities and the antioxidant metabolite glutathione levels.	Dehydroepiandrosterone	13-17	nitric oxide synthase 1, neuronal	Mus musculus	67-88
19308358-1	2009	The roles of individual nitric oxide synthases (NOS) in anthracycline-related cardiotoxicity are not completely understood.	Anthracyclines	56-69	nitric oxide synthase 1, neuronal	Mus musculus	24-46
19308358-4	2009	DOX-induced FS decrease in wild-type mice was attenuated only in eNOS knockouts, which were found to overexpress nNOS.	Doxorubicin	0-3	nitric oxide synthase 1, neuronal	Mus musculus	113-117
19308358-6	2009	Although the surviving DOX-treated nNOS knockouts exhibited no further impairment in contractility, most (70%) animals died within 7 weeks after treatment onset.	Doxorubicin	23-26	nitric oxide synthase 1, neuronal	Mus musculus	35-39
19308358-10	2009	Protection against DOX effects conferred by eNOS deletion may be mediated by a compensatory overexpression of nNOS.	Doxorubicin	19-22	nitric oxide synthase 1, neuronal	Mus musculus	110-114
19241059-4	2009	OBJECTIVES: We investigated the effects of intra-dPAG infusions of NMDA on defensive behaviors in mice pretreated with a neuronal nitric oxide synthase (nNOS) inhibitor [Nomega-propyl-L: -arginine (NPLA)], in the same midbrain site, during a confrontation with a predator in the rat exposure test (RET).	N(omega)-propylarginine	170-196	nitric oxide synthase 1, neuronal	Mus musculus	121-151
19241059-4	2009	OBJECTIVES: We investigated the effects of intra-dPAG infusions of NMDA on defensive behaviors in mice pretreated with a neuronal nitric oxide synthase (nNOS) inhibitor [Nomega-propyl-L: -arginine (NPLA)], in the same midbrain site, during a confrontation with a predator in the rat exposure test (RET).	N(omega)-propylarginine	170-196	nitric oxide synthase 1, neuronal	Mus musculus	153-157
19538708-8	2009	Consistent with the biochemical results, intraperitoneal injection of a low dose of SKF81297 significantly decreased prepulse inhibition in nNOS KO mice, but not in wild-type mice.	SK and F 81297	84-92	nitric oxide synthase 1, neuronal	Mus musculus	140-144
19364813-8	2009	Mechanistic analysis suggests that KLYP956 binds the oxygenase domain in the vicinity of the active site heme and inhibits iNOS and neuronal NOS (nNOS) by preventing the formation of enzymatically active dimers.	N-(3-chlorophenyl)-N-((8-fluoro-2-oxo-1,2-dihydroquinolin-4-yl)methyl)-4-methylthiazole-5-carboxamide	35-42	nitric oxide synthase 1, neuronal	Mus musculus	146-150
19364813-10	2009	KLYP956 thus represents the first nonimidazole-based inhibitor of iNOS and nNOS dimerization and provides a novel pharmaceutical alternative to previously described substrate competitive inhibitors.	N-(3-chlorophenyl)-N-((8-fluoro-2-oxo-1,2-dihydroquinolin-4-yl)methyl)-4-methylthiazole-5-carboxamide	0-7	nitric oxide synthase 1, neuronal	Mus musculus	75-79
19364813-10	2009	KLYP956 thus represents the first nonimidazole-based inhibitor of iNOS and nNOS dimerization and provides a novel pharmaceutical alternative to previously described substrate competitive inhibitors.	nonimidazole	34-46	nitric oxide synthase 1, neuronal	Mus musculus	75-79
19111753-6	2009	Together, the present results demonstrate that NO, produced presumably via nNOS and iNOS in the spinal cord, mediates the maintenance of neuropathic pain following peripheral nerve injury through both the NO-cGMP-PKG and the NO-peroxynitrite pathways.	Cyclic GMP	208-212	nitric oxide synthase 1, neuronal	Mus musculus	75-79
19362797-9	2009	Results show that both WT and nNOS KO mice developed significant CPA.	cpa	65-68	nitric oxide synthase 1, neuronal	Mus musculus	30-34
19362797-10	2009	The findings that the absence of the nNOS gene impaired ethanol-induced CPP but not LiCl-induced CPA suggest that NO signaling has a specific role in processing the motivational effect of ethanol.	Ethanol	56-63	nitric oxide synthase 1, neuronal	Mus musculus	37-41
19362797-10	2009	The findings that the absence of the nNOS gene impaired ethanol-induced CPP but not LiCl-induced CPA suggest that NO signaling has a specific role in processing the motivational effect of ethanol.	Ethanol	188-195	nitric oxide synthase 1, neuronal	Mus musculus	37-41
19362797-11	2009	Hence, inhibition of nNOS may attenuate the development of maladaptive behaviors associated with alcohol exposure.	Alcohols	97-104	nitric oxide synthase 1, neuronal	Mus musculus	21-25
19470729-0	2009	Nitric oxide synthase inhibition enhances the tumor vascular-damaging effects of combretastatin a-4 3-o-phosphate at clinically relevant doses.	combretastatin a-4 3-o-phosphate	81-113	nitric oxide synthase 1, neuronal	Mus musculus	0-21
19307451-5	2009	Cotreatment with the phosphatidylinositol 3 (PI3)-kinase inhibitor, LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride], or treatment of cardiomyocytes infected with a dominant negative adenovirus targeted to Akt1 (ADV-dnAkt1) blocked the effects of EPO on nNOS expression, suggesting that EPO regulates nNOS expression via PI3-kinase and Akt.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	68-76	nitric oxide synthase 1, neuronal	Mus musculus	280-284
19307451-5	2009	Cotreatment with the phosphatidylinositol 3 (PI3)-kinase inhibitor, LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride], or treatment of cardiomyocytes infected with a dominant negative adenovirus targeted to Akt1 (ADV-dnAkt1) blocked the effects of EPO on nNOS expression, suggesting that EPO regulates nNOS expression via PI3-kinase and Akt.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	68-76	nitric oxide synthase 1, neuronal	Mus musculus	327-331
19307451-5	2009	Cotreatment with the phosphatidylinositol 3 (PI3)-kinase inhibitor, LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride], or treatment of cardiomyocytes infected with a dominant negative adenovirus targeted to Akt1 (ADV-dnAkt1) blocked the effects of EPO on nNOS expression, suggesting that EPO regulates nNOS expression via PI3-kinase and Akt.	2-(4-morpholinyl	78-94	nitric oxide synthase 1, neuronal	Mus musculus	280-284
19307451-5	2009	Cotreatment with the phosphatidylinositol 3 (PI3)-kinase inhibitor, LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride], or treatment of cardiomyocytes infected with a dominant negative adenovirus targeted to Akt1 (ADV-dnAkt1) blocked the effects of EPO on nNOS expression, suggesting that EPO regulates nNOS expression via PI3-kinase and Akt.	2-(4-morpholinyl	78-94	nitric oxide synthase 1, neuronal	Mus musculus	327-331
19470653-2	2009	In the brain, nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) functions as a retrograde neuronal messenger that facilitates synaptic plasticity, including the late phase of long-term potentiation (LTP) and formation of long-term memory (LTM).	Nitric Oxide	14-26	nitric oxide synthase 1, neuronal	Mus musculus	44-74
19470653-2	2009	In the brain, nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) functions as a retrograde neuronal messenger that facilitates synaptic plasticity, including the late phase of long-term potentiation (LTP) and formation of long-term memory (LTM).	Nitric Oxide	14-26	nitric oxide synthase 1, neuronal	Mus musculus	76-80
19374401-1	2009	There are three isoforms of dimeric nitric oxide synthases (NOS) that convert arginine to citrulline and nitric oxide.	Arginine	78-86	nitric oxide synthase 1, neuronal	Mus musculus	36-58
19374401-1	2009	There are three isoforms of dimeric nitric oxide synthases (NOS) that convert arginine to citrulline and nitric oxide.	Citrulline	90-100	nitric oxide synthase 1, neuronal	Mus musculus	36-58
19401171-12	2009	Our findings suggest that age- and sex-differences in DA concentration and iNOS expression as well as sex-differences of nNOS expression after intoxication may depend on the increased susceptibility of males as well as older animals to toxic effect of MPTP and aggravated process of recovery in old brains.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	252-256	nitric oxide synthase 1, neuronal	Mus musculus	121-125
19362797-0	2009	Role of the nNOS gene in ethanol-induced conditioned place preference in mice.	Ethanol	25-32	nitric oxide synthase 1, neuronal	Mus musculus	12-16
19362797-1	2009	Nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) has a role in synaptic plasticity, and evidence suggests its role in a range of effects produced by alcohol in the central nervous system.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	30-60
19362797-1	2009	Nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) has a role in synaptic plasticity, and evidence suggests its role in a range of effects produced by alcohol in the central nervous system.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	62-66
19362797-1	2009	Nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) has a role in synaptic plasticity, and evidence suggests its role in a range of effects produced by alcohol in the central nervous system.	Alcohols	168-175	nitric oxide synthase 1, neuronal	Mus musculus	62-66
19362797-2	2009	The aim of the current study was to investigate the role of the nNOS gene in the development of ethanol-induced conditioned place preference (CPP) in mice.	Ethanol	96-103	nitric oxide synthase 1, neuronal	Mus musculus	64-68
19307451-9	2009	Furthermore, EPO treatment after ischemia significantly reduced the threshold dose of cesium chloride (CsCl) to induce VT. We conclude that EPO via nNOS protects the heart from spontaneous and CsCl-induced ventricular arrhythmia during myocardial I/R.	cesium chloride	86-101	nitric oxide synthase 1, neuronal	Mus musculus	148-152
19307451-9	2009	Furthermore, EPO treatment after ischemia significantly reduced the threshold dose of cesium chloride (CsCl) to induce VT. We conclude that EPO via nNOS protects the heart from spontaneous and CsCl-induced ventricular arrhythmia during myocardial I/R.	cesium chloride	103-107	nitric oxide synthase 1, neuronal	Mus musculus	148-152
19307451-9	2009	Furthermore, EPO treatment after ischemia significantly reduced the threshold dose of cesium chloride (CsCl) to induce VT. We conclude that EPO via nNOS protects the heart from spontaneous and CsCl-induced ventricular arrhythmia during myocardial I/R.	cesium chloride	193-197	nitric oxide synthase 1, neuronal	Mus musculus	148-152
19283362-0	2009	Prevention of neural tube defects by loss of function of inducible nitric oxide synthase in fetuses of a mouse model of streptozotocin-induced diabetes.	Streptozocin	120-134	nitric oxide synthase 1, neuronal	Mus musculus	67-88
19360314-8	2009	In contrast to diabetic wild-type mice, diabetic nNOS-/- mice had near normal nitrotyrosine and poly(ADP-ribose) immunofluorescence in dorsal root ganglia.	3-nitrotyrosine	78-91	nitric oxide synthase 1, neuronal	Mus musculus	49-53
19278978-11	2009	In conclusion, these results showed that the nNOS-PMCA4b complex regulates contractility via cAMP and phosphorylation of both PLB and cTnI.	Cyclic AMP	93-97	nitric oxide synthase 1, neuronal	Mus musculus	45-49
19526582-4	2009	Long-term exposure of the compound significantly reversed the levels of diacylgylcerol (DAG) and nitric oxide synthase (NOS) induced by DENA, thus suggesting that the compound may hinder the process of chemical carcinogenesis potentially by downregulating the signal transduction mechanism involving DAG and NOS.	Diethylnitrosamine	136-140	nitric oxide synthase 1, neuronal	Mus musculus	97-118
19340543-0	2009	Low [NaCl]-induced neuronal nitric oxide synthase (nNOS) expression and NO generation are regulated by intracellular pH in a mouse macula densa cell line (NE-MD).	Sodium Chloride	5-9	nitric oxide synthase 1, neuronal	Mus musculus	19-49
19340543-0	2009	Low [NaCl]-induced neuronal nitric oxide synthase (nNOS) expression and NO generation are regulated by intracellular pH in a mouse macula densa cell line (NE-MD).	Sodium Chloride	5-9	nitric oxide synthase 1, neuronal	Mus musculus	51-55
19340543-2	2009	This study was performed in a newly established mouse macula densa cell line (NE-MD) to investigate the effects of lowering [NaCl] on the neuronal NO synthase (nNOS) protein expression and L-arginine (Arg)-induced NO release.	Sodium Chloride	125-129	nitric oxide synthase 1, neuronal	Mus musculus	160-164
19340543-7	2009	Furosemide- and low Cl(-)-induced NO generation was completely inhibited by 50 microM 7-nitroindasole (7-NI), a nNOS inhibitor.	Furosemide	0-10	nitric oxide synthase 1, neuronal	Mus musculus	112-116
19340543-7	2009	Furosemide- and low Cl(-)-induced NO generation was completely inhibited by 50 microM 7-nitroindasole (7-NI), a nNOS inhibitor.	7-nitroindasole	86-101	nitric oxide synthase 1, neuronal	Mus musculus	112-116
19340543-7	2009	Furosemide- and low Cl(-)-induced NO generation was completely inhibited by 50 microM 7-nitroindasole (7-NI), a nNOS inhibitor.	7-nitroindazole	103-107	nitric oxide synthase 1, neuronal	Mus musculus	112-116
19442832-5	2009	Neuronal nitric oxide synthase (nNOS) can protect developing mouse neurons against alcohol toxicity by synthesizing neuroprotective nitric oxide.	Alcohols	83-90	nitric oxide synthase 1, neuronal	Mus musculus	0-30
19442832-5	2009	Neuronal nitric oxide synthase (nNOS) can protect developing mouse neurons against alcohol toxicity by synthesizing neuroprotective nitric oxide.	Alcohols	83-90	nitric oxide synthase 1, neuronal	Mus musculus	32-36
19442832-5	2009	Neuronal nitric oxide synthase (nNOS) can protect developing mouse neurons against alcohol toxicity by synthesizing neuroprotective nitric oxide.	Nitric Oxide	9-21	nitric oxide synthase 1, neuronal	Mus musculus	32-36
19442832-6	2009	This study examined whether a single exposure to alcohol, which causes no evident injury in wild type mice, can damage the brains of mice genetically deficient for nNOS (nNOS-/- mice).	Alcohols	49-56	nitric oxide synthase 1, neuronal	Mus musculus	164-168
19442832-6	2009	This study examined whether a single exposure to alcohol, which causes no evident injury in wild type mice, can damage the brains of mice genetically deficient for nNOS (nNOS-/- mice).	Alcohols	49-56	nitric oxide synthase 1, neuronal	Mus musculus	170-182
19442832-9	2009	Alcohol exposure on PD4-9 restricted brain growth and caused neuronal death in both strains of mice, but the severity of microencephaly and neuronal loss were more severe in the nNOS-/- mice than in wild type.	Alcohols	0-7	nitric oxide synthase 1, neuronal	Mus musculus	178-182
19442832-10	2009	The 4.4 mg/g alcohol dose administered on PD4 alone caused significant neuronal loss and microencephaly in the nNOS-/- mice, while this same dose caused no evident injury in the wild type mice.	Alcohols	13-20	nitric oxide synthase 1, neuronal	Mus musculus	111-123
19478875-3	2009	The increased sensitivity of nNOS-/- mice was independent of macrophage sensitivity to toxin, or cytokine responses, and could be replicated in nNOS-sufficient wild-type (WT) mice through pharmacological inhibition of the enzyme with 7-nitroindazole.	7-nitroindazole	234-249	nitric oxide synthase 1, neuronal	Mus musculus	29-33
19478875-10	2009	Surprisingly, the potent nitric oxide scavenger, carboxy-PTIO, showed some protective effect against LT. Echocardiography on LT-treated mice indicated an average reduction in ejection fraction following LT treatment in both nNOS-/- and WT mice, indicative of decreased contractile function in the heart.	Nitric Oxide	25-37	nitric oxide synthase 1, neuronal	Mus musculus	224-228
19261533-18	2009	It has been reported that oxidative stress after paraquat administration involved nitration of proteins by the activation of nitric oxide synthase (NOS).	Paraquat	49-57	nitric oxide synthase 1, neuronal	Mus musculus	125-146
19162139-0	2009	Paradoxical facilitation of pentylenetetrazole-induced convulsion susceptibility in mice lacking neuronal nitric oxide synthase.	Pentylenetetrazole	28-46	nitric oxide synthase 1, neuronal	Mus musculus	97-127
19162139-3	2009	nNOS(-/-) mice exhibited severe convulsions following injection with a subconvulsive dose of PTZ (40 mg/kg i.p.)	Pentylenetetrazole	93-96	nitric oxide synthase 1, neuronal	Mus musculus	0-4
19162139-7	2009	The higher doses of the nNOS inhibitors 1-[2-(trifluoromethyl)phenyl] imidazole (TRIM) and 3-bromo-7-nitroindazole (3Br7NI) inhibited clonic-tonic convulsions induced by a convulsive dose of PTZ (60 mg/kg) in nNOS(+/+) mice.	1-(2-trifluoromethylphenyl)imidazole	40-79	nitric oxide synthase 1, neuronal	Mus musculus	24-28
19162139-7	2009	The higher doses of the nNOS inhibitors 1-[2-(trifluoromethyl)phenyl] imidazole (TRIM) and 3-bromo-7-nitroindazole (3Br7NI) inhibited clonic-tonic convulsions induced by a convulsive dose of PTZ (60 mg/kg) in nNOS(+/+) mice.	1-(2-trifluoromethylphenyl)imidazole	40-79	nitric oxide synthase 1, neuronal	Mus musculus	209-213
19162139-7	2009	The higher doses of the nNOS inhibitors 1-[2-(trifluoromethyl)phenyl] imidazole (TRIM) and 3-bromo-7-nitroindazole (3Br7NI) inhibited clonic-tonic convulsions induced by a convulsive dose of PTZ (60 mg/kg) in nNOS(+/+) mice.	3-bromo-7-nitroindazole	91-114	nitric oxide synthase 1, neuronal	Mus musculus	24-28
19162139-7	2009	The higher doses of the nNOS inhibitors 1-[2-(trifluoromethyl)phenyl] imidazole (TRIM) and 3-bromo-7-nitroindazole (3Br7NI) inhibited clonic-tonic convulsions induced by a convulsive dose of PTZ (60 mg/kg) in nNOS(+/+) mice.	3-bromo-7-nitroindazole	91-114	nitric oxide synthase 1, neuronal	Mus musculus	209-213
19162139-7	2009	The higher doses of the nNOS inhibitors 1-[2-(trifluoromethyl)phenyl] imidazole (TRIM) and 3-bromo-7-nitroindazole (3Br7NI) inhibited clonic-tonic convulsions induced by a convulsive dose of PTZ (60 mg/kg) in nNOS(+/+) mice.	3-bromo-7-nitroindazole	116-122	nitric oxide synthase 1, neuronal	Mus musculus	209-213
19162139-7	2009	The higher doses of the nNOS inhibitors 1-[2-(trifluoromethyl)phenyl] imidazole (TRIM) and 3-bromo-7-nitroindazole (3Br7NI) inhibited clonic-tonic convulsions induced by a convulsive dose of PTZ (60 mg/kg) in nNOS(+/+) mice.	Pentylenetetrazole	191-194	nitric oxide synthase 1, neuronal	Mus musculus	24-28
19162139-8	2009	In contrast, either TRIM or 3Br7NI at lower doses enhanced convulsions following injection with a subconvulsive dose of PTZ (40 mg/kg) in nNOS(+/+) mice similar to nNOS(-/-) mice treated with PTZ.	Pentylenetetrazole	120-123	nitric oxide synthase 1, neuronal	Mus musculus	138-142
19168723-5	2009	The protective effect of NaHS-PC on LR was largely abolished by coincident pharmacological inhibition of NO synthase (NOS) in WT animals and was absent in endothelial NOS-deficient (eNOS(-/-)) mice.	nahs-pc	25-32	nitric oxide synthase 1, neuronal	Mus musculus	105-116
19220287-1	2009	BACKGROUND AND PURPOSE: We investigated the effect of nitric oxide synthase (NOS) inhibition on polymorphonuclear cell (PMN) influx in zymosan or lipopolysaccharide (LPS)-induced arthritis and peritonitis.	Zymosan	135-142	nitric oxide synthase 1, neuronal	Mus musculus	54-75
19111753-6	2009	Together, the present results demonstrate that NO, produced presumably via nNOS and iNOS in the spinal cord, mediates the maintenance of neuropathic pain following peripheral nerve injury through both the NO-cGMP-PKG and the NO-peroxynitrite pathways.	Peroxynitrous Acid	228-241	nitric oxide synthase 1, neuronal	Mus musculus	75-79
19244529-5	2009	We found that the CBF and ROS increases elicited by topical application of NMDA to the mouse neocortex were both dependent on neuronal NO synthase (nNOS), cGMP, and the cGMP effector kinase protein kinase G (PKG).	Reactive Oxygen Species	26-29	nitric oxide synthase 1, neuronal	Mus musculus	148-152
19244529-5	2009	We found that the CBF and ROS increases elicited by topical application of NMDA to the mouse neocortex were both dependent on neuronal NO synthase (nNOS), cGMP, and the cGMP effector kinase protein kinase G (PKG).	N-Methylaspartate	75-79	nitric oxide synthase 1, neuronal	Mus musculus	148-152
18703795-1	2009	Increasing evidence suggests that lung mechanics and structure are maintained in part by an intimate balance between the L-arginine-metabolizing enzymes nitric oxide synthase (NOS) and arginase.	Arginine	121-131	nitric oxide synthase 1, neuronal	Mus musculus	153-174
18987049-2	2009	METHODS AND RESULTS: Incubation with a potent nNOS inhibitor (L-VNIO) significantly increased superoxide (O2(-)) levels, with increased MAPK phosphorylation, in isolated aorta and vascular smooth muscle cells (VSMCs) from wild-type mice.	N(5)-(1-imino-3-butenyl)ornithine	62-68	nitric oxide synthase 1, neuronal	Mus musculus	46-50
19114050-1	2009	Our recent studies have shown that the neuronal nitric oxide synthase (nNOS) gene is required for the development and persistence of psychomotor sensitization to cocaine in adult but not adolescent male mice (Balda, M.A., Anderson, K.L., Itzhak, Y., 2008.	Cocaine	162-169	nitric oxide synthase 1, neuronal	Mus musculus	39-69
19114050-1	2009	Our recent studies have shown that the neuronal nitric oxide synthase (nNOS) gene is required for the development and persistence of psychomotor sensitization to cocaine in adult but not adolescent male mice (Balda, M.A., Anderson, K.L., Itzhak, Y., 2008.	Cocaine	162-169	nitric oxide synthase 1, neuronal	Mus musculus	71-75
19114050-2	2009	Differential role of the nNOS gene in the development of behavioral sensitization to cocaine in adolescent and adult B6;129S mice.	Cocaine	85-92	nitric oxide synthase 1, neuronal	Mus musculus	25-29
19114050-4	2009	The aim of the present study was to investigate the contribution of the nNOS gene to cocaine-induced behavioral sensitization in adolescent and adult female mice.	Cocaine	85-92	nitric oxide synthase 1, neuronal	Mus musculus	72-76
19114050-10	2009	The present study suggests that long-term expression of cocaine-induced behavioral sensitization in females (adolescent and adult) is nNOS-independent, unlike our previous findings in adult males.	Cocaine	56-63	nitric oxide synthase 1, neuronal	Mus musculus	134-138
18987049-4	2009	The levels of O2(-) and MAPK phosphorylation were higher in aorta from nNOS(-/-) mice than from wild-type mice.	Superoxides	14-16	nitric oxide synthase 1, neuronal	Mus musculus	71-75
18987049-11	2009	CONCLUSION: Under basal conditions, nNOS-derived NO acting as antioxidant reduces O2(-) accumulation and suppresses vascular MAPK phosphorylation.	Superoxides	82-87	nitric oxide synthase 1, neuronal	Mus musculus	36-40
18987049-2	2009	METHODS AND RESULTS: Incubation with a potent nNOS inhibitor (L-VNIO) significantly increased superoxide (O2(-)) levels, with increased MAPK phosphorylation, in isolated aorta and vascular smooth muscle cells (VSMCs) from wild-type mice.	Superoxides	94-104	nitric oxide synthase 1, neuronal	Mus musculus	46-50
18987049-2	2009	METHODS AND RESULTS: Incubation with a potent nNOS inhibitor (L-VNIO) significantly increased superoxide (O2(-)) levels, with increased MAPK phosphorylation, in isolated aorta and vascular smooth muscle cells (VSMCs) from wild-type mice.	Superoxides	106-111	nitric oxide synthase 1, neuronal	Mus musculus	46-50
19047200-3	2009	Six proteins were significantly (P &lt; or = 0.05) more highly expressed in EDL of nNOS-knockout mice than in that of C57 control mice, all of which are involved in the metabolism of reactive oxygen species (ROS).	Reactive Oxygen Species	208-211	nitric oxide synthase 1, neuronal	Mus musculus	83-87
19166483-2	2009	We found that a number of calcium handling/dependent molecules are associated with caveolae, including L-type Ca(2+) channels, Na(+)-Ca(2+) exchanger type 1 (NCX1), plasma membrane Ca(2+) pumps and neural nitric oxide synthase (nNOS), and that caveolae are close to the peripheral endo-sarcoplasmic reticulum (ER-SR).	Calcium	26-33	nitric oxide synthase 1, neuronal	Mus musculus	198-226
19166483-2	2009	We found that a number of calcium handling/dependent molecules are associated with caveolae, including L-type Ca(2+) channels, Na(+)-Ca(2+) exchanger type 1 (NCX1), plasma membrane Ca(2+) pumps and neural nitric oxide synthase (nNOS), and that caveolae are close to the peripheral endo-sarcoplasmic reticulum (ER-SR).	Calcium	26-33	nitric oxide synthase 1, neuronal	Mus musculus	228-232
19047200-8	2009	The treatment of mice with the chemical NOS inhibitor L-NAME for 3 days induced a significant 3.4-fold up-regulation of peroxiredoxin-6 in the EDL of C57 control mice (P &lt; or = 0.05), but did not alter its expression in EDL of nNOS-knockout mice.	NG-Nitroarginine Methyl Ester	54-60	nitric oxide synthase 1, neuronal	Mus musculus	230-234
19047200-9	2009	ESR spectrometry demonstrated the levels of superoxide to be 2.5-times higher (P &lt; or = 0.05) in EDL of nNOS-knockout mice than in C57 control mice while an in vitro assay based on the emission of 2,7-dichlorofluorescein fluorescence disclosed the concentration of ROS to be similar in both strains of mice.	Superoxides	44-54	nitric oxide synthase 1, neuronal	Mus musculus	107-111
19047200-9	2009	ESR spectrometry demonstrated the levels of superoxide to be 2.5-times higher (P &lt; or = 0.05) in EDL of nNOS-knockout mice than in C57 control mice while an in vitro assay based on the emission of 2,7-dichlorofluorescein fluorescence disclosed the concentration of ROS to be similar in both strains of mice.	2',7'-dichlorofluorescein	200-223	nitric oxide synthase 1, neuronal	Mus musculus	107-111
19047200-9	2009	ESR spectrometry demonstrated the levels of superoxide to be 2.5-times higher (P &lt; or = 0.05) in EDL of nNOS-knockout mice than in C57 control mice while an in vitro assay based on the emission of 2,7-dichlorofluorescein fluorescence disclosed the concentration of ROS to be similar in both strains of mice.	Reactive Oxygen Species	268-271	nitric oxide synthase 1, neuronal	Mus musculus	107-111
19047200-10	2009	We suggest that the up-regulation of proteins that are implicated in the metabolism of ROS, particularly of peroxiredoxin-6, within skeletal muscles of nNOS-knockout mice functionally compensates for the absence of nNOS in scavenging of superoxide.	Reactive Oxygen Species	87-90	nitric oxide synthase 1, neuronal	Mus musculus	152-156
19047200-10	2009	We suggest that the up-regulation of proteins that are implicated in the metabolism of ROS, particularly of peroxiredoxin-6, within skeletal muscles of nNOS-knockout mice functionally compensates for the absence of nNOS in scavenging of superoxide.	Superoxides	237-247	nitric oxide synthase 1, neuronal	Mus musculus	152-156
19047200-10	2009	We suggest that the up-regulation of proteins that are implicated in the metabolism of ROS, particularly of peroxiredoxin-6, within skeletal muscles of nNOS-knockout mice functionally compensates for the absence of nNOS in scavenging of superoxide.	Superoxides	237-247	nitric oxide synthase 1, neuronal	Mus musculus	215-219
19027033-1	2009	Arginase has been suggested to compete with nitric oxide synthase (NOS) for their common substrate, l-arginine.	Arginine	100-110	nitric oxide synthase 1, neuronal	Mus musculus	44-65
19154577-5	2009	Under confocal scanning microscopy together with the radical probe dihydrorhodamine 123 (DHR 123), we found that there was a dose-dependent formation of ONOO- in live MEF cells exposed to either TiO2 nanoparticles or C60, and the protective effects of antioxidants were demonstrated by the nitric oxide synthase (NOS) inhibitor, NG-methyl-L-arginine (L-NMMA).	onoo	153-157	nitric oxide synthase 1, neuronal	Mus musculus	290-311
19154577-5	2009	Under confocal scanning microscopy together with the radical probe dihydrorhodamine 123 (DHR 123), we found that there was a dose-dependent formation of ONOO- in live MEF cells exposed to either TiO2 nanoparticles or C60, and the protective effects of antioxidants were demonstrated by the nitric oxide synthase (NOS) inhibitor, NG-methyl-L-arginine (L-NMMA).	titanium dioxide	195-199	nitric oxide synthase 1, neuronal	Mus musculus	290-311
19134173-4	2009	Treatment of tumor-bearing mice with either the phosphodiesterase-5 inhibitor sildenafil or the nitric-oxide synthase (NOS) inhibitor L-NAME significantly restrained tumor growth and expanded the tumor-specific immune response.	NG-Nitroarginine Methyl Ester	134-140	nitric oxide synthase 1, neuronal	Mus musculus	96-117
19041302-1	2009	The aim of this study is to investigate the involvement of nitric oxide synthesized by the inducible (NOS2) or neuronal (NOS1) nitric oxide synthases in the local antinociceptive effects produced by micro- and delta-opioid receptor agonists during chronic inflammatory pain.	Nitric Oxide	59-71	nitric oxide synthase 1, neuronal	Mus musculus	121-125
19041302-8	2009	These results indicate the different roles played by nitric oxide synthesized by NOS2 or NOS1 in the maintenance of mechanical allodynia and thermal hyperalgesia induced by chronic inflammatory pain as well as, in the antinociceptive effects produced by micro- and delta-opioid receptor agonists during peripheral inflammatory pain.	Nitric Oxide	53-65	nitric oxide synthase 1, neuronal	Mus musculus	89-93
18824032-0	2008	The protective effect of neuronal nitric oxide synthase (nNOS) against alcohol toxicity depends upon the NO-cGMP-PKG pathway and NF-kappaB.	Alcohols	71-78	nitric oxide synthase 1, neuronal	Mus musculus	25-55
19047200-0	2009	Up-regulation of the peroxiredoxin-6 related metabolism of reactive oxygen species in skeletal muscle of mice lacking neuronal nitric oxide synthase.	Reactive Oxygen Species	59-82	nitric oxide synthase 1, neuronal	Mus musculus	118-148
19047200-3	2009	Six proteins were significantly (P &lt; or = 0.05) more highly expressed in EDL of nNOS-knockout mice than in that of C57 control mice, all of which are involved in the metabolism of reactive oxygen species (ROS).	Reactive Oxygen Species	183-206	nitric oxide synthase 1, neuronal	Mus musculus	83-87
18812700-7	2009	Treatment with candesartan normalized blood pressure in Cx40-/- mice, and decreased the levels of both COX-2 and nNOS.	candesartan	15-26	nitric oxide synthase 1, neuronal	Mus musculus	113-117
18952716-0	2008	Neuronal nitric oxide synthase-derived hydrogen peroxide is a major endothelium-dependent relaxing factor.	Hydrogen Peroxide	39-56	nitric oxide synthase 1, neuronal	Mus musculus	0-30
18952716-5	2008	In mice aorta rings, ACh-induced relaxation was inhibited by L-NAME and Nomega-nitro-L-arginine (L-NNA), two nonselective inhibitors of NOS, and attenuated by selective inhibition of nNOS with L-ArgNO2-L-Dbu-NH2 2TFA (L-ArgNO2-L-Dbu) and 1-(2-trifluoromethylphehyl)imidazole (TRIM).	Acetylcholine	21-24	nitric oxide synthase 1, neuronal	Mus musculus	183-187
18952716-5	2008	In mice aorta rings, ACh-induced relaxation was inhibited by L-NAME and Nomega-nitro-L-arginine (L-NNA), two nonselective inhibitors of NOS, and attenuated by selective inhibition of nNOS with L-ArgNO2-L-Dbu-NH2 2TFA (L-ArgNO2-L-Dbu) and 1-(2-trifluoromethylphehyl)imidazole (TRIM).	H-Arg(NO2)-OH	97-102	nitric oxide synthase 1, neuronal	Mus musculus	183-187
18952716-11	2008	Antisense knockdown of nNOS decreased both ACh-dependent relaxation and ACh-induced H2O2 production.	Acetylcholine	43-46	nitric oxide synthase 1, neuronal	Mus musculus	23-27
18952716-11	2008	Antisense knockdown of nNOS decreased both ACh-dependent relaxation and ACh-induced H2O2 production.	Acetylcholine	72-75	nitric oxide synthase 1, neuronal	Mus musculus	23-27
18952716-11	2008	Antisense knockdown of nNOS decreased both ACh-dependent relaxation and ACh-induced H2O2 production.	Hydrogen Peroxide	84-88	nitric oxide synthase 1, neuronal	Mus musculus	23-27
18952716-13	2008	Residual relaxation in eNOS knockdown mouse aorta was further inhibited by the selective inhibition of nNOS with L-ArgNO2-L-Dbu.	l-argno2-l-dbu	113-127	nitric oxide synthase 1, neuronal	Mus musculus	103-107
18952716-14	2008	In conclusion, these results show that nNOS is constitutively expressed in the endothelium of mouse aorta and that nNOS-derived H2O2 is a major endothelium-dependent relaxing factor.	Hydrogen Peroxide	128-132	nitric oxide synthase 1, neuronal	Mus musculus	39-43
18952716-14	2008	In conclusion, these results show that nNOS is constitutively expressed in the endothelium of mouse aorta and that nNOS-derived H2O2 is a major endothelium-dependent relaxing factor.	Hydrogen Peroxide	128-132	nitric oxide synthase 1, neuronal	Mus musculus	115-119
19192069-6	2008	NO synthase (NOS) activity was inhibited following a 20% BSA full-thickness burn by injection of non-specific NOS inhibitor, nitro-L-arginine methyl ester or inducible NOS (iNOS) inhibitors, L-N6-(1-iminoethyl) lysine, and aminoguanidine.	nitro-l-arginine methyl ester	125-154	nitric oxide synthase 1, neuronal	Mus musculus	0-11
19192069-6	2008	NO synthase (NOS) activity was inhibited following a 20% BSA full-thickness burn by injection of non-specific NOS inhibitor, nitro-L-arginine methyl ester or inducible NOS (iNOS) inhibitors, L-N6-(1-iminoethyl) lysine, and aminoguanidine.	N(6)-(1-iminoethyl)lysine	191-217	nitric oxide synthase 1, neuronal	Mus musculus	0-11
19192069-6	2008	NO synthase (NOS) activity was inhibited following a 20% BSA full-thickness burn by injection of non-specific NOS inhibitor, nitro-L-arginine methyl ester or inducible NOS (iNOS) inhibitors, L-N6-(1-iminoethyl) lysine, and aminoguanidine.	pimagedine	223-237	nitric oxide synthase 1, neuronal	Mus musculus	0-11
18953332-7	2008	In mouse models of nNOS mislocalization from the sarcolemma, prolonged inactivity was only relieved by pharmacologically enhancing the cGMP signal that results from muscle nNOS activation during the nitric oxide signalling response to mild exercise.	Cyclic GMP	135-139	nitric oxide synthase 1, neuronal	Mus musculus	19-23
18953332-7	2008	In mouse models of nNOS mislocalization from the sarcolemma, prolonged inactivity was only relieved by pharmacologically enhancing the cGMP signal that results from muscle nNOS activation during the nitric oxide signalling response to mild exercise.	Cyclic GMP	135-139	nitric oxide synthase 1, neuronal	Mus musculus	172-176
18953332-7	2008	In mouse models of nNOS mislocalization from the sarcolemma, prolonged inactivity was only relieved by pharmacologically enhancing the cGMP signal that results from muscle nNOS activation during the nitric oxide signalling response to mild exercise.	Nitric Oxide	199-211	nitric oxide synthase 1, neuronal	Mus musculus	172-176
19037590-10	2008	Stimulation of muscarinic receptors in the endothelial cells by acetylcholine increased superoxide generation, whereas preincubation with the nitric oxide synthase (NOS) inhibitor L-arginine methyl ester or endothelium removal reduced superoxide production.	arginine methyl ester	180-203	nitric oxide synthase 1, neuronal	Mus musculus	142-163
18849438-6	2008	The increased cGMP and K(f) caused by HV(T) were attenuated by nitric oxide synthase (NOS) inhibition and in lungs from endothelial NOS knockout mice.	Cyclic GMP	14-18	nitric oxide synthase 1, neuronal	Mus musculus	63-84
18926825-9	2008	Induction of HO-1 by hemin decreased reactive oxygen species, rapidly restored Kit and neuronal nitric oxide synthase expression, and completely normalized gastric emptying in all mice.	Hemin	21-26	nitric oxide synthase 1, neuronal	Mus musculus	87-117
18709655-1	2008	Tocopherols (vitamin E) are potent antioxidants as well as modulators of enzymes involved in signal transduction, like nitric oxide synthase (NOS).	Tocopherols	0-11	nitric oxide synthase 1, neuronal	Mus musculus	119-140
18709655-1	2008	Tocopherols (vitamin E) are potent antioxidants as well as modulators of enzymes involved in signal transduction, like nitric oxide synthase (NOS).	Vitamin E	13-22	nitric oxide synthase 1, neuronal	Mus musculus	119-140
18683823-2	2008	In this study, we investigated the inhibitory effects of 6-shogaol and a related compound, 6-gingerol, on the induction of nitric oxide synthase (NOS) and cyclooxygenase-2 (COX-2) in murine RAW 264.7 cells activated with LPS.	shogaol	57-66	nitric oxide synthase 1, neuronal	Mus musculus	123-144
18683823-2	2008	In this study, we investigated the inhibitory effects of 6-shogaol and a related compound, 6-gingerol, on the induction of nitric oxide synthase (NOS) and cyclooxygenase-2 (COX-2) in murine RAW 264.7 cells activated with LPS.	gingerol	91-101	nitric oxide synthase 1, neuronal	Mus musculus	123-144
18793618-2	2008	We have recently demonstrated that the vigorous defensive-like behaviors (e.g. jumping and running) and antinociception induced by intra-PAG injection of N-methyl-D-aspartate (NMDA) were completely blocked by prior infusion of N(omega)-propyl-L-arginine (NPLA), a specific neuronal nitric oxide synthesis (nNOS) enzyme inhibitor, into the same midbrain structure.	N-Methylaspartate	154-174	nitric oxide synthase 1, neuronal	Mus musculus	273-304
18793618-2	2008	We have recently demonstrated that the vigorous defensive-like behaviors (e.g. jumping and running) and antinociception induced by intra-PAG injection of N-methyl-D-aspartate (NMDA) were completely blocked by prior infusion of N(omega)-propyl-L-arginine (NPLA), a specific neuronal nitric oxide synthesis (nNOS) enzyme inhibitor, into the same midbrain structure.	N-Methylaspartate	154-174	nitric oxide synthase 1, neuronal	Mus musculus	306-310
18793618-2	2008	We have recently demonstrated that the vigorous defensive-like behaviors (e.g. jumping and running) and antinociception induced by intra-PAG injection of N-methyl-D-aspartate (NMDA) were completely blocked by prior infusion of N(omega)-propyl-L-arginine (NPLA), a specific neuronal nitric oxide synthesis (nNOS) enzyme inhibitor, into the same midbrain structure.	N-Methylaspartate	176-180	nitric oxide synthase 1, neuronal	Mus musculus	273-304
18793618-2	2008	We have recently demonstrated that the vigorous defensive-like behaviors (e.g. jumping and running) and antinociception induced by intra-PAG injection of N-methyl-D-aspartate (NMDA) were completely blocked by prior infusion of N(omega)-propyl-L-arginine (NPLA), a specific neuronal nitric oxide synthesis (nNOS) enzyme inhibitor, into the same midbrain structure.	N-Methylaspartate	176-180	nitric oxide synthase 1, neuronal	Mus musculus	306-310
18793618-2	2008	We have recently demonstrated that the vigorous defensive-like behaviors (e.g. jumping and running) and antinociception induced by intra-PAG injection of N-methyl-D-aspartate (NMDA) were completely blocked by prior infusion of N(omega)-propyl-L-arginine (NPLA), a specific neuronal nitric oxide synthesis (nNOS) enzyme inhibitor, into the same midbrain structure.	N(omega)-propylarginine	227-253	nitric oxide synthase 1, neuronal	Mus musculus	273-304
18793618-2	2008	We have recently demonstrated that the vigorous defensive-like behaviors (e.g. jumping and running) and antinociception induced by intra-PAG injection of N-methyl-D-aspartate (NMDA) were completely blocked by prior infusion of N(omega)-propyl-L-arginine (NPLA), a specific neuronal nitric oxide synthesis (nNOS) enzyme inhibitor, into the same midbrain structure.	N(omega)-propylarginine	227-253	nitric oxide synthase 1, neuronal	Mus musculus	306-310
18824032-0	2008	The protective effect of neuronal nitric oxide synthase (nNOS) against alcohol toxicity depends upon the NO-cGMP-PKG pathway and NF-kappaB.	Alcohols	71-78	nitric oxide synthase 1, neuronal	Mus musculus	57-61
18824032-0	2008	The protective effect of neuronal nitric oxide synthase (nNOS) against alcohol toxicity depends upon the NO-cGMP-PKG pathway and NF-kappaB.	Cyclic GMP	108-112	nitric oxide synthase 1, neuronal	Mus musculus	25-55
18824032-0	2008	The protective effect of neuronal nitric oxide synthase (nNOS) against alcohol toxicity depends upon the NO-cGMP-PKG pathway and NF-kappaB.	Cyclic GMP	108-112	nitric oxide synthase 1, neuronal	Mus musculus	57-61
18824032-4	2008	Animal studies have demonstrated that one particular gene, neuronal nitric oxide synthase (nNOS), protects developing neurons in vivo against alcohol-induced death.	Alcohols	142-149	nitric oxide synthase 1, neuronal	Mus musculus	59-89
18824032-4	2008	Animal studies have demonstrated that one particular gene, neuronal nitric oxide synthase (nNOS), protects developing neurons in vivo against alcohol-induced death.	Alcohols	142-149	nitric oxide synthase 1, neuronal	Mus musculus	91-95
18824032-5	2008	We utilized pharmacologic techniques to demonstrate that nNOS protects neurons against alcohol toxicity by activating the NO-cGMP-PKG signaling pathway.	Alcohols	87-94	nitric oxide synthase 1, neuronal	Mus musculus	57-61
18824032-5	2008	We utilized pharmacologic techniques to demonstrate that nNOS protects neurons against alcohol toxicity by activating the NO-cGMP-PKG signaling pathway.	Cyclic GMP	125-129	nitric oxide synthase 1, neuronal	Mus musculus	57-61
18824032-6	2008	Cerebellar granule cell cultures derived from mice carrying a null mutation for nNOS (nNOS-/- mice) were substantially more vulnerable than cultures from wild-type mice to alcohol-induced cell death.	Alcohols	172-179	nitric oxide synthase 1, neuronal	Mus musculus	80-84
18824032-6	2008	Cerebellar granule cell cultures derived from mice carrying a null mutation for nNOS (nNOS-/- mice) were substantially more vulnerable than cultures from wild-type mice to alcohol-induced cell death.	Alcohols	172-179	nitric oxide synthase 1, neuronal	Mus musculus	86-98
18824032-7	2008	However, activation of the pathway at sites downstream of nNOS protected the cultures against alcohol toxicity.	Alcohols	94-101	nitric oxide synthase 1, neuronal	Mus musculus	58-62
18824032-10	2008	Tumor necrosis factor-alpha (TNF-alpha), which activates NF-kappaB, ameliorated alcohol-induced cell death in nNOS-/- and wild-type cultures, while an NF-kappaB inhibitor (NFi) blocked the protective effects of TNF-alpha and worsened alcohol-induced cell death.	Alcohols	80-87	nitric oxide synthase 1, neuronal	Mus musculus	110-114
18592222-0	2008	Differential role of the nNOS gene in the development of behavioral sensitization to cocaine in adolescent and adult B6;129S mice.	Cocaine	85-92	nitric oxide synthase 1, neuronal	Mus musculus	25-29
18824032-14	2008	Thus, nNOS protects developing neurons against alcohol toxicity by activating the NO-cGMP-PKG-NF-kappaB pathway and is crucial for the acquisition of maturation-dependent alcohol resistance.	Alcohols	47-54	nitric oxide synthase 1, neuronal	Mus musculus	6-10
18824032-14	2008	Thus, nNOS protects developing neurons against alcohol toxicity by activating the NO-cGMP-PKG-NF-kappaB pathway and is crucial for the acquisition of maturation-dependent alcohol resistance.	Cyclic GMP	85-89	nitric oxide synthase 1, neuronal	Mus musculus	6-10
18824032-14	2008	Thus, nNOS protects developing neurons against alcohol toxicity by activating the NO-cGMP-PKG-NF-kappaB pathway and is crucial for the acquisition of maturation-dependent alcohol resistance.	Alcohols	171-178	nitric oxide synthase 1, neuronal	Mus musculus	6-10
18592222-7	2008	RESULTS: Repeated administration of cocaine to either WT or nNOS KO mice during adolescence resulted in locomotor sensitization, which persisted into adulthood.	Cocaine	36-43	nitric oxide synthase 1, neuronal	Mus musculus	60-64
18592222-9	2008	Repeated cocaine administration resulted in a 96% increase in the expression of nNOS-ir neurons in the dorsal striatum of adult but not adolescent WT mice.	Cocaine	9-16	nitric oxide synthase 1, neuronal	Mus musculus	80-84
18592222-10	2008	CONCLUSIONS: The nNOS gene is essential for the induction of behavioral sensitization to cocaine in adulthood but not in adolescence.	Cocaine	89-96	nitric oxide synthase 1, neuronal	Mus musculus	17-21
18652592-0	2008	Ethanol-induced behavioral sensitization in adolescent and adult mice: role of the nNOS gene.	Ethanol	0-7	nitric oxide synthase 1, neuronal	Mus musculus	83-87
18652592-1	2008	BACKGROUND: In the brain, nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) has a role in synaptic plasticity.	Nitric Oxide	26-38	nitric oxide synthase 1, neuronal	Mus musculus	56-86
18652592-1	2008	BACKGROUND: In the brain, nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) has a role in synaptic plasticity.	Nitric Oxide	26-38	nitric oxide synthase 1, neuronal	Mus musculus	88-92
18652592-3	2008	The current study investigated the role of the nNOS gene in the development of behavioral sensitization to ethanol in adolescent and adult mice.	Ethanol	107-114	nitric oxide synthase 1, neuronal	Mus musculus	47-51
18652592-10	2008	CONCLUSIONS: (1) The nNOS gene is required for the development of behavioral sensitization to ethanol in adolescent male and female mice.	Ethanol	94-101	nitric oxide synthase 1, neuronal	Mus musculus	21-25
18652592-13	2008	(4) Ethanol-induced behavioral sensitization in adulthood is nNOS-dependent in males but not in females.	Ethanol	4-11	nitric oxide synthase 1, neuronal	Mus musculus	61-65
18723768-7	2008	FIP plasma-induced oxidant stress, occludin rearrangement, and MCVEC permeability were effectively attenuated by antioxidant, 1-pyrrolidinecarbodithioic acid (PDTC; 0.5 mM), or interfering with nitric oxide synthase (NOS) activity [0.1 mM nitro-L-arginine methyl ester (L-NAME) or endothelial NOS (eNOS)-deficient MCVEC].	pyrrolidine dithiocarbamic acid	159-163	nitric oxide synthase 1, neuronal	Mus musculus	194-215
18991881-6	2008	In the present study the effects of the NMDA receptor antagonist, MK-801, and the nNOS inhibitor 7-nitroindazole (7-NI) on memory reconsolidation of cocaine-induced CPP in mice were investigated.	7-nitroindazole	97-112	nitric oxide synthase 1, neuronal	Mus musculus	82-86
18991881-9	2008	Male nNOS knockout (KO) mice acquired short-lived cocaine CPP compared to wild-type (WT) mice.	Cocaine	50-57	nitric oxide synthase 1, neuronal	Mus musculus	5-9
18991881-10	2008	A single acute administration of the NO-donor molsidomine to nNOS KO mice immediately after retrieval of CPP prolonged the expression of place preference compared to controls that received saline, suggesting partial strengthening of memory reconsolidation.	Molsidomine	46-57	nitric oxide synthase 1, neuronal	Mus musculus	61-65
18596627-12	2008	Ascorbate rapidly (10 mins) rescued impaired flow in WT, nNOS-/-, iNOS-/- but not eNOS-/- mice.	Ascorbic Acid	0-9	nitric oxide synthase 1, neuronal	Mus musculus	57-61
18501719-5	2008	We sought to determine how exogenous nitrite affects steady-state concentrations of NO metabolites thought to originate from nitric oxide synthase (NOS)-derived NO as well as blood pressure and myocardial ischemia-reperfusion (I/R) injury.	Nitrites	37-44	nitric oxide synthase 1, neuronal	Mus musculus	125-146
18634866-6	2008	Treatment of rd1 mice with a mixture of nitric oxide synthase (NOS) inhibitors markedly reduced S-nitrosocysteine and nitrotyrosine staining and significantly increased cone survival, indicating that NO-derived peroxynitrite contributes to cone cell death.	S-nitrosocysteine	96-113	nitric oxide synthase 1, neuronal	Mus musculus	40-61
18634866-6	2008	Treatment of rd1 mice with a mixture of nitric oxide synthase (NOS) inhibitors markedly reduced S-nitrosocysteine and nitrotyrosine staining and significantly increased cone survival, indicating that NO-derived peroxynitrite contributes to cone cell death.	3-nitrotyrosine	118-131	nitric oxide synthase 1, neuronal	Mus musculus	40-61
18634866-6	2008	Treatment of rd1 mice with a mixture of nitric oxide synthase (NOS) inhibitors markedly reduced S-nitrosocysteine and nitrotyrosine staining and significantly increased cone survival, indicating that NO-derived peroxynitrite contributes to cone cell death.	Peroxynitrous Acid	211-224	nitric oxide synthase 1, neuronal	Mus musculus	40-61
18635601-3	2008	The LC8 immunoprecipitate (IP) showed three nNOS bands, suggesting that LC8 was bound with all three forms of nNOS but dissociated from them during SDS-PAGE.	lc8	4-7	nitric oxide synthase 1, neuronal	Mus musculus	44-48
18635601-5	2008	Probing these fractions with anti-serine847-P-nNOS showed that 320-kDa serine847-phosphorylated-nNOS consisted of LC8-bound and LC8-lacking components.	serine847	34-43	nitric oxide synthase 1, neuronal	Mus musculus	46-50
18635601-5	2008	Probing these fractions with anti-serine847-P-nNOS showed that 320-kDa serine847-phosphorylated-nNOS consisted of LC8-bound and LC8-lacking components.	serine847	34-43	nitric oxide synthase 1, neuronal	Mus musculus	96-100
18635601-5	2008	Probing these fractions with anti-serine847-P-nNOS showed that 320-kDa serine847-phosphorylated-nNOS consisted of LC8-bound and LC8-lacking components.	lc8	114-117	nitric oxide synthase 1, neuronal	Mus musculus	46-50
18635601-5	2008	Probing these fractions with anti-serine847-P-nNOS showed that 320-kDa serine847-phosphorylated-nNOS consisted of LC8-bound and LC8-lacking components.	lc8	114-117	nitric oxide synthase 1, neuronal	Mus musculus	96-100
18635601-5	2008	Probing these fractions with anti-serine847-P-nNOS showed that 320-kDa serine847-phosphorylated-nNOS consisted of LC8-bound and LC8-lacking components.	lc8	128-131	nitric oxide synthase 1, neuronal	Mus musculus	96-100
18635601-6	2008	Subsequent studies with varicosity membrane and cytosolic fractions separately showed that membrane contained CaM-bound and CaM-lacking, serine847-phosphorylated 320-kDa nNOS; both these fractions lacked LC8.	serine847	137-146	nitric oxide synthase 1, neuronal	Mus musculus	170-174
18635601-8	2008	These studies, along with in vitro nitric oxide assays, show that in gut nitrergic nerve varicosities 1) all cytosolic serine847-phosphorylated nNOS was catalytically inactive and bound with LC8, and 2) membrane-associated nNOS consisted of catalytically active, CaM-bound and catalytically inactive, CaM-lacking, serine847-phosphorylated nNOSalpha dimers, both of which lacked LC8.	serine847	119-128	nitric oxide synthase 1, neuronal	Mus musculus	144-148
18586241-4	2008	SCH58261 chronically administered increased the number of nNOS-immunoreactive neurons (nNOS-IR) in the striatum of R6/2 mice.	5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	58-62
18586241-4	2008	SCH58261 chronically administered increased the number of nNOS-immunoreactive neurons (nNOS-IR) in the striatum of R6/2 mice.	5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	87-91
18586241-7	2008	These findings demonstrate for the first time a role of adenosine A(2A) receptors in regulating nNOS expression in the striatum.	Adenosine	56-65	nitric oxide synthase 1, neuronal	Mus musculus	96-100
18648914-8	2008	The present study demonstrates that the overexpression of nNOS may play a major role in the neurotoxic processes of MPTP, as compared with the production of ROS, the overexpression of iNOS, the modulation of eNOS and the involvement of inflammatory response.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	116-120	nitric oxide synthase 1, neuronal	Mus musculus	58-62
18648914-8	2008	The present study demonstrates that the overexpression of nNOS may play a major role in the neurotoxic processes of MPTP, as compared with the production of ROS, the overexpression of iNOS, the modulation of eNOS and the involvement of inflammatory response.	Reactive Oxygen Species	157-160	nitric oxide synthase 1, neuronal	Mus musculus	58-62
18656926-2	2008	Here, we investigated the inhibitory effects of pterostilbene on the induction of NO synthase (NOS) and cyclooxygenase-2 (COX-2) in murine RAW 264.7 cells activated with lipopolysaccharide (LPS).	pterostilbene	48-61	nitric oxide synthase 1, neuronal	Mus musculus	82-93
18580182-0	2008	Cholinesterase inhibitor donepezil dilates cerebral parenchymal arterioles via the activation of neuronal nitric oxide synthase.	Donepezil	25-34	nitric oxide synthase 1, neuronal	Mus musculus	97-127
18400048-1	2008	Neuronal nitric oxide synthase (nNOS) in myenteric neurons is activated during peristalsis to produce nitric oxide which relaxes intestinal smooth muscle.	Nitric Oxide	9-21	nitric oxide synthase 1, neuronal	Mus musculus	32-36
18400048-7	2008	Disruption of caveolae with 40 mM methyl-beta cyclodextrin in tissues from control mice led to the loss of Cav-1 and nNOS immunoreactivity from smooth muscle as shown by immunohistochemistry and a reduction in the response of these tissues to N-omega-nitro-L-arginine (LNNA).	methyl-beta-cyclodextrin	34-58	nitric oxide synthase 1, neuronal	Mus musculus	117-121
18400048-11	2008	We conclude that the activation of nNOS, localized in smooth muscle caveolae, by calcium entering through L-type calcium channels triggers nitric oxide production which modulates muscle contraction by a cGMP-dependent mechanism.	Calcium	81-88	nitric oxide synthase 1, neuronal	Mus musculus	35-39
18400048-11	2008	We conclude that the activation of nNOS, localized in smooth muscle caveolae, by calcium entering through L-type calcium channels triggers nitric oxide production which modulates muscle contraction by a cGMP-dependent mechanism.	Nitric Oxide	139-151	nitric oxide synthase 1, neuronal	Mus musculus	35-39
18456872-0	2008	Sustained soluble guanylate cyclase stimulation offsets nitric-oxide synthase inhibition to restore acute cardiac modulation by sildenafil.	Sildenafil Citrate	128-138	nitric oxide synthase 1, neuronal	Mus musculus	56-77
18456004-2	2008	Nitric oxide (NO), shown to have protective effects in I/R, is produced by nitric oxide synthase (NOS) from the substrate arginine.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	75-96
18456004-2	2008	Nitric oxide (NO), shown to have protective effects in I/R, is produced by nitric oxide synthase (NOS) from the substrate arginine.	Arginine	122-130	nitric oxide synthase 1, neuronal	Mus musculus	75-96
18580182-13	2008	CONCLUSIONS: Donepezil produces acute vasodilation induced by a selective activation of neuronal nitric oxide synthase in the cerebral parenchymal arterioles.	Donepezil	13-22	nitric oxide synthase 1, neuronal	Mus musculus	88-118
18400048-11	2008	We conclude that the activation of nNOS, localized in smooth muscle caveolae, by calcium entering through L-type calcium channels triggers nitric oxide production which modulates muscle contraction by a cGMP-dependent mechanism.	Cyclic GMP	203-207	nitric oxide synthase 1, neuronal	Mus musculus	35-39
18440890-7	2008	Mechanical strain still increased NO production in the absence of eNOS, and was abolished by SMTC, a specific nNOS inhibitor.	smtc	93-97	nitric oxide synthase 1, neuronal	Mus musculus	110-114
19108575-6	2008	These results indicate that nNOS is the main supplier of nitric oxide in shear stress-induced vasodilation in skeletal muscle, but that the sarcolemmal localization of nNOS is not indispensable for the function.	Nitric Oxide	57-69	nitric oxide synthase 1, neuronal	Mus musculus	28-32
18556069-5	2008	Nitric oxide synthase (NOS) activity was quantified by evaluating citrulline level and pyramidal neuron dendrites and spines were evaluated using rapid Golgi stains and a Neurolucida system.	Citrulline	66-76	nitric oxide synthase 1, neuronal	Mus musculus	0-21
18476963-2	2008	Nitric oxide synthases (NOS) may contribute to the increase of inflammation in tissues by the generation of nitrotyrosine residues (NTR).	3-nitrotyrosine	108-121	nitric oxide synthase 1, neuronal	Mus musculus	0-22
18476963-9	2008	TK inhibitor genistein inhibited both nNOS and iNOS expression on the membrane of basal keratinocytes, and nuclear translocation of NF-kappaB.	Genistein	13-22	nitric oxide synthase 1, neuronal	Mus musculus	38-42
18457833-12	2008	[a specific neuronal nitric oxide synthase (nNOS) inhibitor] potentiated the anti-convulsant action of sub-effective dose of adenosine (50 mg/kg i.p.).	Adenosine	125-134	nitric oxide synthase 1, neuronal	Mus musculus	12-42
18541744-0	2008	Cardiomyocyte overexpression of neuronal nitric oxide synthase delays transition toward heart failure in response to pressure overload by preserving calcium cycling.	Calcium	149-156	nitric oxide synthase 1, neuronal	Mus musculus	32-62
18541744-9	2008	CONCLUSIONS: Cardiomyocyte NOS1 may be a useful target against cardiac deterioration during chronic pressure-overload-induced HF through modulation of calcium cycling.	Calcium	151-158	nitric oxide synthase 1, neuronal	Mus musculus	27-31
18457833-12	2008	[a specific neuronal nitric oxide synthase (nNOS) inhibitor] potentiated the anti-convulsant action of sub-effective dose of adenosine (50 mg/kg i.p.).	Adenosine	125-134	nitric oxide synthase 1, neuronal	Mus musculus	44-48
18413672-3	2008	As we have demonstrated before, these effects are mediated in part through inhibition of neuronal nitric oxide synthase (nNOS), resulting in increased availability of arginine.	Arginine	167-175	nitric oxide synthase 1, neuronal	Mus musculus	89-119
18400986-7	2008	We observed similar effects in myocytes with NOS1 knockout or specific NOS1 inhibition with S-methyl-l-thiocitrulline (SMLT) in WT myocytes (i.e., decreased Ca2+ transient and cell shortening amplitudes and prolonged decline of [Ca2+]i).	S-methylthiocitrulline	92-117	nitric oxide synthase 1, neuronal	Mus musculus	71-75
18417648-8	2008	Chronic ingestion of the neuronal nitric oxide synthase inhibitor S-methylthiocitrulline for 2-3 wk after Nx had no effect on SNGFR or the TGF response.	S-methylthiocitrulline	66-88	nitric oxide synthase 1, neuronal	Mus musculus	25-55
18413672-3	2008	As we have demonstrated before, these effects are mediated in part through inhibition of neuronal nitric oxide synthase (nNOS), resulting in increased availability of arginine.	Arginine	167-175	nitric oxide synthase 1, neuronal	Mus musculus	121-125
18458097-2	2008	Recently, the use of L-arginine, the substrate of nitric oxide synthase (nNOS), has been proposed as a pharmacological treatment to attenuate the dystrophic pattern of DMD.	Arginine	21-31	nitric oxide synthase 1, neuronal	Mus musculus	73-77
18458097-9	2008	We show that the inhibitory effect of L-arginine on the NF-kappaB/MMP cascade reduces beta-dystroglycan cleavage and translocates utrophin and nNOS throughout the sarcolemma.	Arginine	38-48	nitric oxide synthase 1, neuronal	Mus musculus	143-147
18622509-1	2008	Nitric oxide (NO) is an endogenous vasoactive compound that contributes to pulmonary vascular homeostasis and is produced by three nitric oxide synthase (NOS) isoforms-neuronal NOS (nNOS); inducible NOS (iNOS); and endothelial NOS (eNOS)-all three of which are present in the lung.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	131-152
18400986-9	2008	Acute inhibition of NOS1 with SMLT in WT myocytes also decreased basal PLB serine16 phosphorylation.	serine16	75-83	nitric oxide synthase 1, neuronal	Mus musculus	20-24
18622509-1	2008	Nitric oxide (NO) is an endogenous vasoactive compound that contributes to pulmonary vascular homeostasis and is produced by three nitric oxide synthase (NOS) isoforms-neuronal NOS (nNOS); inducible NOS (iNOS); and endothelial NOS (eNOS)-all three of which are present in the lung.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	168-180
18622509-1	2008	Nitric oxide (NO) is an endogenous vasoactive compound that contributes to pulmonary vascular homeostasis and is produced by three nitric oxide synthase (NOS) isoforms-neuronal NOS (nNOS); inducible NOS (iNOS); and endothelial NOS (eNOS)-all three of which are present in the lung.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	182-186
18421425-10	2008	Moreover, our findings suggest that nitric oxide synthesized by the nNOS may play some role for neuronal growth during postnatal development.	Nitric Oxide	36-48	nitric oxide synthase 1, neuronal	Mus musculus	68-72
18400986-11	2008	Perfusion with FeTPPS (peroxynitrite decomposition catalyst) mimicked the effects of NOS1 knockout or inhibition.	Peroxynitrous Acid	23-36	nitric oxide synthase 1, neuronal	Mus musculus	85-89
18400986-14	2008	Thus NOS1 signaling modulates PLB serine16 phosphorylation, in part, via peroxynitrite.	serine16	34-42	nitric oxide synthase 1, neuronal	Mus musculus	5-9
18400986-14	2008	Thus NOS1 signaling modulates PLB serine16 phosphorylation, in part, via peroxynitrite.	Peroxynitrous Acid	73-86	nitric oxide synthase 1, neuronal	Mus musculus	5-9
18235988-15	2008	These findings demonstrate that the overexpression of nNOS may play a major role in the neurotoxic processes of MPTP, as compared to the production of ROS, the overexpression of iNOS and the modulation of eNOS.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	112-116	nitric oxide synthase 1, neuronal	Mus musculus	54-58
18235988-15	2008	These findings demonstrate that the overexpression of nNOS may play a major role in the neurotoxic processes of MPTP, as compared to the production of ROS, the overexpression of iNOS and the modulation of eNOS.	Reactive Oxygen Species	151-154	nitric oxide synthase 1, neuronal	Mus musculus	54-58
18570588-4	2008	CB(1) activation of NB41A3 cells by the synthetic cannabinoid, WIN55,212-2, is associated with an inhibition of Ca(2+) mobilization, leading to diminished nitric oxide synthase (NOS)-1 activity and the production of NO, in vitro.	Cannabinoids	50-61	nitric oxide synthase 1, neuronal	Mus musculus	155-184
18270316-1	2008	7-Nitroindazole (NI) is a widely used inhibitor of neuronal nitricoxide synthase (nNOS) used to study the role of the neuronal NO pathway in the nervous system.	7-nitroindazole	0-15	nitric oxide synthase 1, neuronal	Mus musculus	51-80
18505586-5	2008	S-methionyl-L-thiocitrulline (SMTC), and tin protoporphyrin (SnPP) were used to inhibit neuronal/constitutive NOS-1 and heme-oxygenase, respectively, and alter NO and CO production, respectively, as assessed by paired t-tests.	s-methionyl-l-thiocitrulline	0-28	nitric oxide synthase 1, neuronal	Mus musculus	110-115
18505586-5	2008	S-methionyl-L-thiocitrulline (SMTC), and tin protoporphyrin (SnPP) were used to inhibit neuronal/constitutive NOS-1 and heme-oxygenase, respectively, and alter NO and CO production, respectively, as assessed by paired t-tests.	smtc	30-34	nitric oxide synthase 1, neuronal	Mus musculus	110-115
18505586-5	2008	S-methionyl-L-thiocitrulline (SMTC), and tin protoporphyrin (SnPP) were used to inhibit neuronal/constitutive NOS-1 and heme-oxygenase, respectively, and alter NO and CO production, respectively, as assessed by paired t-tests.	tin protoporphyrin IX	41-59	nitric oxide synthase 1, neuronal	Mus musculus	110-115
18505586-5	2008	S-methionyl-L-thiocitrulline (SMTC), and tin protoporphyrin (SnPP) were used to inhibit neuronal/constitutive NOS-1 and heme-oxygenase, respectively, and alter NO and CO production, respectively, as assessed by paired t-tests.	S-Nitroso-N-propionyl-D,L-penicillamine	61-65	nitric oxide synthase 1, neuronal	Mus musculus	110-115
18326824-8	2008	In addition, we demonstrated that nitric oxide derived from nNOS is involved in a neurogenic mechanism of HBO2-induced lung injury that is linked to central nervous system oxygen toxicity through adrenergic/cholinergic pathways.	Nitric Oxide	34-46	nitric oxide synthase 1, neuronal	Mus musculus	60-64
18326824-8	2008	In addition, we demonstrated that nitric oxide derived from nNOS is involved in a neurogenic mechanism of HBO2-induced lung injury that is linked to central nervous system oxygen toxicity through adrenergic/cholinergic pathways.	Oxygen	172-178	nitric oxide synthase 1, neuronal	Mus musculus	60-64
18270316-1	2008	7-Nitroindazole (NI) is a widely used inhibitor of neuronal nitricoxide synthase (nNOS) used to study the role of the neuronal NO pathway in the nervous system.	7-nitroindazole	0-15	nitric oxide synthase 1, neuronal	Mus musculus	82-86
18270316-3	2008	Herein, we examined nNOS involvement in glufosinate-induced convulsions and the specificity of 7-NI for nNOS.	7-nitroindazole	95-99	nitric oxide synthase 1, neuronal	Mus musculus	104-108
18270316-4	2008	Another nNOS inhibitor, 1-[2-(trifluoromethyl)phenyl]imidazole (TRIM), inhibited NOS activity in vivo, and it prevented glufosinate-induced convulsions.	1-(2-trifluoromethylphenyl)imidazole	24-62	nitric oxide synthase 1, neuronal	Mus musculus	8-12
18270316-4	2008	Another nNOS inhibitor, 1-[2-(trifluoromethyl)phenyl]imidazole (TRIM), inhibited NOS activity in vivo, and it prevented glufosinate-induced convulsions.	1-(2-trifluoromethylphenyl)imidazole	64-68	nitric oxide synthase 1, neuronal	Mus musculus	8-12
18270316-4	2008	Another nNOS inhibitor, 1-[2-(trifluoromethyl)phenyl]imidazole (TRIM), inhibited NOS activity in vivo, and it prevented glufosinate-induced convulsions.	phosphinothricin	120-131	nitric oxide synthase 1, neuronal	Mus musculus	8-12
18270316-6	2008	These results suggest the involvement of nNOS in glufosinate-induced convulsions.	phosphinothricin	49-60	nitric oxide synthase 1, neuronal	Mus musculus	41-45
18270316-9	2008	Moreover, glufosinate elicited convulsions in nNOS-deficient mice.	phosphinothricin	10-21	nitric oxide synthase 1, neuronal	Mus musculus	46-50
18160315-3	2008	Previous results demonstrated that the immediate post-training intraperitoneal administration of N(omega)-nitro-l-arginine methyl ester (L-NAME), a non-specific inhibitor of nitric oxide synthase (NOS), impairs retention test performance of a one-trial step-through inhibitory avoidance response in adult mice.	NG-Nitroarginine Methyl Ester	97-135	nitric oxide synthase 1, neuronal	Mus musculus	174-195
18160315-3	2008	Previous results demonstrated that the immediate post-training intraperitoneal administration of N(omega)-nitro-l-arginine methyl ester (L-NAME), a non-specific inhibitor of nitric oxide synthase (NOS), impairs retention test performance of a one-trial step-through inhibitory avoidance response in adult mice.	NG-Nitroarginine Methyl Ester	137-143	nitric oxide synthase 1, neuronal	Mus musculus	174-195
18164516-1	2008	The neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI) is neuroprotective against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism.	7-nitroindazole	70-74	nitric oxide synthase 1, neuronal	Mus musculus	36-40
18164516-0	2008	In vitro and in vivo evidences that antioxidant action contributes to the neuroprotective effects of the neuronal nitric oxide synthase and monoamine oxidase-B inhibitor, 7-nitroindazole.	7-nitroindazole	171-186	nitric oxide synthase 1, neuronal	Mus musculus	105-135
18164516-1	2008	The neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI) is neuroprotective against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism.	7-nitroindazole	53-68	nitric oxide synthase 1, neuronal	Mus musculus	4-34
18164516-1	2008	The neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI) is neuroprotective against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	103-147	nitric oxide synthase 1, neuronal	Mus musculus	4-34
18164516-1	2008	The neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI) is neuroprotective against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism.	7-nitroindazole	53-68	nitric oxide synthase 1, neuronal	Mus musculus	36-40
18164516-1	2008	The neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI) is neuroprotective against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism.	7-nitroindazole	70-74	nitric oxide synthase 1, neuronal	Mus musculus	4-34
18164516-1	2008	The neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI) is neuroprotective against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	103-147	nitric oxide synthase 1, neuronal	Mus musculus	36-40
18164516-1	2008	The neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI) is neuroprotective against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	149-153	nitric oxide synthase 1, neuronal	Mus musculus	4-34
18164516-1	2008	The neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI) is neuroprotective against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	149-153	nitric oxide synthase 1, neuronal	Mus musculus	36-40
18164516-5	2008	The nNOS inhibitor caused dose-dependent inhibition in the production of OH in (i) Fenton-like reaction employing ferrous citrate in a cell-free system in test tubes, (ii) in isolated mitochondrial preparation in presence of MPP+, and (iii) in the striatum of mice systemically treated with MPTP.	ferrous citrate	114-129	nitric oxide synthase 1, neuronal	Mus musculus	4-8
18164516-5	2008	The nNOS inhibitor caused dose-dependent inhibition in the production of OH in (i) Fenton-like reaction employing ferrous citrate in a cell-free system in test tubes, (ii) in isolated mitochondrial preparation in presence of MPP+, and (iii) in the striatum of mice systemically treated with MPTP.	mangion-purified polysaccharide (Candida albicans)	225-229	nitric oxide synthase 1, neuronal	Mus musculus	4-8
18164516-5	2008	The nNOS inhibitor caused dose-dependent inhibition in the production of OH in (i) Fenton-like reaction employing ferrous citrate in a cell-free system in test tubes, (ii) in isolated mitochondrial preparation in presence of MPP+, and (iii) in the striatum of mice systemically treated with MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	291-295	nitric oxide synthase 1, neuronal	Mus musculus	4-8
18164516-7	2008	The nNOS-mediated recovery of GSH paralleled attenuation of MPTP-induced depletion of striatal dopamine.	Glutathione	30-33	nitric oxide synthase 1, neuronal	Mus musculus	4-8
18164516-7	2008	The nNOS-mediated recovery of GSH paralleled attenuation of MPTP-induced depletion of striatal dopamine.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	60-64	nitric oxide synthase 1, neuronal	Mus musculus	4-8
18164516-7	2008	The nNOS-mediated recovery of GSH paralleled attenuation of MPTP-induced depletion of striatal dopamine.	Dopamine	95-103	nitric oxide synthase 1, neuronal	Mus musculus	4-8
18234259-2	2008	Here we report that apocynin increased the accumulation of nitrite, the stable derivative of nitric oxide (NO), in the extracellular medium of N11 cell cultures, and the NO synthase (NOS) activity in cell lysates.	acetovanillone	20-28	nitric oxide synthase 1, neuronal	Mus musculus	170-181
18294449-11	2008	Constriction in the knockout artery appeared to be potentiated by the addition of the nitric oxide synthase (NOS) inhibitor l-NAME, suggesting that elevated nitric oxide (NO) production occurs in the knockout vasculature and contributes to the weakened vasoconstriction.	NG-Nitroarginine Methyl Ester	124-130	nitric oxide synthase 1, neuronal	Mus musculus	86-107
18239148-2	2008	Asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of NO synthase (NOS).	dimethylarginine	13-29	nitric oxide synthase 1, neuronal	Mus musculus	67-78
18239148-2	2008	Asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of NO synthase (NOS).	N,N-dimethylarginine	31-35	nitric oxide synthase 1, neuronal	Mus musculus	67-78
18342297-0	2008	Repetitive hyperbaric oxygen exposures enhance sensitivity to convulsion by upregulation of eNOS and nNOS.	Oxygen	22-28	nitric oxide synthase 1, neuronal	Mus musculus	101-105
18096606-1	2008	Nitric oxide (NO) is responsible for nitrergic neurotransmission in the gut, and its release is dependent on its de novo synthesis by neuronal nitric oxide synthase (nNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	134-164
18096606-1	2008	Nitric oxide (NO) is responsible for nitrergic neurotransmission in the gut, and its release is dependent on its de novo synthesis by neuronal nitric oxide synthase (nNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	166-170
18096606-5	2008	Low-temperature SDS-PAGE of these varicosity extracts showed 320-, 250-, and 155-kDa bands when blotted with anti-nNOS(1422-1433) and 320- and 155-kDa bands when blotted with anti-nNOS(1-20) antibodies, respectively.	Sodium Dodecyl Sulfate	16-19	nitric oxide synthase 1, neuronal	Mus musculus	114-118
18096606-9	2008	The CaM-lacking nNOS fractions reacted with anti-serine 847-phospho-nNOS.	Serine	49-55	nitric oxide synthase 1, neuronal	Mus musculus	16-20
18096606-9	2008	The CaM-lacking nNOS fractions reacted with anti-serine 847-phospho-nNOS.	Serine	49-55	nitric oxide synthase 1, neuronal	Mus musculus	68-72
18199585-7	2008	Diabetes-induced O2(-) accumulation was ablated by the NO synthase (NOS) inhibitor nitro-L-arginine methyl ester (L-NAME), indicating endothelial NOS (eNOS) uncoupling, all of which except heart size were negated by IGF-I.	Oxygen	17-19	nitric oxide synthase 1, neuronal	Mus musculus	55-66
18184766-0	2008	Estradiol increases urethral tone through the local inhibition of neuronal nitric oxide synthase expression.	Estradiol	0-9	nitric oxide synthase 1, neuronal	Mus musculus	66-96
18184766-2	2008	The aim of this study was to explore the effects of endogenous and supraestrus levels of 17beta-estradiol (E2) on LUT and urethral nNOS expression and function.	Estradiol	89-105	nitric oxide synthase 1, neuronal	Mus musculus	131-135
18184766-6	2008	Acute nNOS inhibition by 7-nitroindazole decreased frequency and increased residual volumes in ovariectomized mice but had no additive effect on the micturition pattern of long-term supraestrus mice, showing that long-term supraestrus E2 levels and acute inhibition of nNOS activity had similar functional effects.	7-nitroindazole	25-40	nitric oxide synthase 1, neuronal	Mus musculus	6-10
18199585-7	2008	Diabetes-induced O2(-) accumulation was ablated by the NO synthase (NOS) inhibitor nitro-L-arginine methyl ester (L-NAME), indicating endothelial NOS (eNOS) uncoupling, all of which except heart size were negated by IGF-I.	nitro-l-arginine methyl ester	83-112	nitric oxide synthase 1, neuronal	Mus musculus	55-66
18199585-7	2008	Diabetes-induced O2(-) accumulation was ablated by the NO synthase (NOS) inhibitor nitro-L-arginine methyl ester (L-NAME), indicating endothelial NOS (eNOS) uncoupling, all of which except heart size were negated by IGF-I.	NG-Nitroarginine Methyl Ester	114-120	nitric oxide synthase 1, neuronal	Mus musculus	55-66
18023823-7	2008	Another possible mechanism of action for tirapazamine could involve its ability to inhibit nitric oxide synthase (NOS).	Tirapazamine	41-53	nitric oxide synthase 1, neuronal	Mus musculus	91-112
18030609-0	2008	Protective action of neuronal nitric oxide synthase inhibitor in the MPTP mouse model of Parkinson"s disease.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	69-73	nitric oxide synthase 1, neuronal	Mus musculus	21-51
18030609-12	2008	Thus, nNOS inhibitor 7-nitroindazole protected dopaminergic neurons against MPTP neurotoxicity in mice and ameliorated neurological deficits.	7-nitroindazole	21-36	nitric oxide synthase 1, neuronal	Mus musculus	6-10
18030609-12	2008	Thus, nNOS inhibitor 7-nitroindazole protected dopaminergic neurons against MPTP neurotoxicity in mice and ameliorated neurological deficits.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	76-80	nitric oxide synthase 1, neuronal	Mus musculus	6-10
18091753-2	2008	This study was conducted to further elucidate the role of neuronal nitric oxide synthase (nNOS) in blood pressure regulation and renin release in relation to different sodium loads.	Sodium	168-174	nitric oxide synthase 1, neuronal	Mus musculus	58-88
18179826-5	2008	In the enzyme assay using cellular extracts of BMDC, the IDO activity of BMDC stimulated with CpG was enhanced by the addition of a NO synthase (NOS) inhibitor, suggesting that IDO activity was suppressed by NO production.	bmdc	47-51	nitric oxide synthase 1, neuronal	Mus musculus	132-143
18179826-5	2008	In the enzyme assay using cellular extracts of BMDC, the IDO activity of BMDC stimulated with CpG was enhanced by the addition of a NO synthase (NOS) inhibitor, suggesting that IDO activity was suppressed by NO production.	bmdc	73-77	nitric oxide synthase 1, neuronal	Mus musculus	132-143
17959704-4	2008	N(G)-nitro-L-arginine methyl ester (L-NAME) did not change basal arteriolar diameters, but augmented angiotensin II contraction, reducing diameters to 23% and 13% in eNOS(+/+), and 7% and 10% in nNOS(+/+) at 10(-8) and 10(-6) mol/l.	NG-Nitroarginine Methyl Ester	0-34	nitric oxide synthase 1, neuronal	Mus musculus	195-199
17959704-4	2008	N(G)-nitro-L-arginine methyl ester (L-NAME) did not change basal arteriolar diameters, but augmented angiotensin II contraction, reducing diameters to 23% and 13% in eNOS(+/+), and 7% and 10% in nNOS(+/+) at 10(-8) and 10(-6) mol/l.	NG-Nitroarginine Methyl Ester	36-42	nitric oxide synthase 1, neuronal	Mus musculus	195-199
18046021-1	2008	Nitric oxide (NO) is mainly generated by endothelial NO synthase (eNOS) or neuronal NOS (nNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	75-87
18046021-1	2008	Nitric oxide (NO) is mainly generated by endothelial NO synthase (eNOS) or neuronal NOS (nNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	89-93
18046021-8	2008	The nonselective NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME; 0.3 mM) enhanced angiotensin II-induced pressor responses in nNOS(-/-) and wild-type mice but not in eNOS(-/-) mice.	NG-Nitroarginine Methyl Ester	31-69	nitric oxide synthase 1, neuronal	Mus musculus	140-144
18046021-8	2008	The nonselective NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME; 0.3 mM) enhanced angiotensin II-induced pressor responses in nNOS(-/-) and wild-type mice but not in eNOS(-/-) mice.	NG-Nitroarginine Methyl Ester	71-77	nitric oxide synthase 1, neuronal	Mus musculus	140-144
18046021-9	2008	In nNOS(+/+) mice, 7-nitroindazole monosodium salt (7-NINA; 0.3 mM), a selective nNOS inhibitor, enhanced angiotensin II-induced pressor responses slightly.	7-NiNa	19-50	nitric oxide synthase 1, neuronal	Mus musculus	3-7
18046021-9	2008	In nNOS(+/+) mice, 7-nitroindazole monosodium salt (7-NINA; 0.3 mM), a selective nNOS inhibitor, enhanced angiotensin II-induced pressor responses slightly.	7-NiNa	19-50	nitric oxide synthase 1, neuronal	Mus musculus	81-85
18046021-11	2008	L-NAME (0.3 mM) reduced angiotensin II-mediated facilitation of norepinephrine release in nNOS(-/-) and wild-type mice but not in eNOS(-/-) mice.	NG-Nitroarginine Methyl Ester	0-6	nitric oxide synthase 1, neuronal	Mus musculus	90-94
18046021-11	2008	L-NAME (0.3 mM) reduced angiotensin II-mediated facilitation of norepinephrine release in nNOS(-/-) and wild-type mice but not in eNOS(-/-) mice.	Norepinephrine	64-78	nitric oxide synthase 1, neuronal	Mus musculus	90-94
18239274-2	2008	Ionizing irradiation is known to cause genotoxic damage through the generation of reactive oxygen species (ROS) and nitrogen species (RNS) and we have found that a signaling pathway for the nuclear translocation of Translin is initiated in association and efficiently blocked by a specific inhibitor of nitric oxide synthase (NOS).	Reactive Oxygen Species	82-105	nitric oxide synthase 1, neuronal	Mus musculus	303-324
18239274-2	2008	Ionizing irradiation is known to cause genotoxic damage through the generation of reactive oxygen species (ROS) and nitrogen species (RNS) and we have found that a signaling pathway for the nuclear translocation of Translin is initiated in association and efficiently blocked by a specific inhibitor of nitric oxide synthase (NOS).	Reactive Oxygen Species	107-110	nitric oxide synthase 1, neuronal	Mus musculus	303-324
18239274-2	2008	Ionizing irradiation is known to cause genotoxic damage through the generation of reactive oxygen species (ROS) and nitrogen species (RNS) and we have found that a signaling pathway for the nuclear translocation of Translin is initiated in association and efficiently blocked by a specific inhibitor of nitric oxide synthase (NOS).	Nitrogen	116-124	nitric oxide synthase 1, neuronal	Mus musculus	303-324
18239274-2	2008	Ionizing irradiation is known to cause genotoxic damage through the generation of reactive oxygen species (ROS) and nitrogen species (RNS) and we have found that a signaling pathway for the nuclear translocation of Translin is initiated in association and efficiently blocked by a specific inhibitor of nitric oxide synthase (NOS).	Radon	134-137	nitric oxide synthase 1, neuronal	Mus musculus	303-324
18007024-8	2008	Taken together, our findings identify a novel mechanism by which myocardial nNOS promotes left ventricular relaxation by regulating the protein kinase A-mediated phosphorylation of PLN and the rate of sarcoplasmic reticulum Ca2+ reuptake via a cGMP-independent effect on protein phosphatase activity.	Cyclic GMP	244-248	nitric oxide synthase 1, neuronal	Mus musculus	76-80
17459122-0	2008	Testosterone decreased urinary-frequency in nNOS-deficient mice.	Testosterone	0-12	nitric oxide synthase 1, neuronal	Mus musculus	44-48
17459122-3	2008	While testosterone treatment did not affect the urination patterns in wild-type, it decreased the daytime frequency of urination (5.4 vs. 3.7 times, p = 0.0198) and the nighttime urination (4.4 vs. 2.9 times, p = 0.039) in nNOS(-/-) mice.	Testosterone	6-18	nitric oxide synthase 1, neuronal	Mus musculus	223-227
17459122-5	2008	Testosterone improved the functional abnormalities in the voiding of nNOS(-/-) mice.	Testosterone	0-12	nitric oxide synthase 1, neuronal	Mus musculus	69-73
18091753-2	2008	This study was conducted to further elucidate the role of neuronal nitric oxide synthase (nNOS) in blood pressure regulation and renin release in relation to different sodium loads.	Sodium	168-174	nitric oxide synthase 1, neuronal	Mus musculus	90-94
18091753-7	2008	On the low sodium diet, nNOS(-/-) mice also showed increased urine flow rate and osmolar excretion, observations not made during a high sodium diet.	Sodium	11-17	nitric oxide synthase 1, neuronal	Mus musculus	24-28
18091753-7	2008	On the low sodium diet, nNOS(-/-) mice also showed increased urine flow rate and osmolar excretion, observations not made during a high sodium diet.	Sodium	136-142	nitric oxide synthase 1, neuronal	Mus musculus	24-28
18091753-8	2008	CONCLUSIONS: Our results show that nNOS is necessary for stimulation of renin in response to sodium restriction.	Sodium	93-99	nitric oxide synthase 1, neuronal	Mus musculus	35-39
17951372-7	2008	Similarly, the positive chronotropic response to the adenylate cyclase activator forskolin (10(-7)-10(-5) mol/l) was attenuated in nNOS(-/-) atria (P &lt; 0.05).	Colforsin	81-90	nitric oxide synthase 1, neuronal	Mus musculus	131-135
21614134-6	2008	Pre-incubation of the myotubes with nitric oxide synthase (NOS) inhibitor L-NAME or S-ethylisothiourea (SETU) blocked the stimulation of NO production by the cocktail.	NG-Nitroarginine Methyl Ester	74-80	nitric oxide synthase 1, neuronal	Mus musculus	36-57
17936885-5	2008	in the TST was prevented by pretreatment of mice with L-arginine [a substrate for nitric oxide synthase (NOS)], methylene blue [an inhibitor of NO synthase and sGC] and sildenafil [a phosphodiesterase 5 inhibitor].	Arginine	54-64	nitric oxide synthase 1, neuronal	Mus musculus	82-103
21614134-6	2008	Pre-incubation of the myotubes with nitric oxide synthase (NOS) inhibitor L-NAME or S-ethylisothiourea (SETU) blocked the stimulation of NO production by the cocktail.	etiron	104-108	nitric oxide synthase 1, neuronal	Mus musculus	36-57
18063827-1	2008	BACKGROUND AND PURPOSE: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS).	dimethylarginine	35-51	nitric oxide synthase 1, neuronal	Mus musculus	89-110
18554543-1	2008	Nitric oxide (NO) and carbon monoxide (CO) are synthesized from l-arginine and heme by the catalytic reaction of NO synthase (NOS) and heme oxygenase (HO).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	113-124
18554543-1	2008	Nitric oxide (NO) and carbon monoxide (CO) are synthesized from l-arginine and heme by the catalytic reaction of NO synthase (NOS) and heme oxygenase (HO).	Carbon Monoxide	22-37	nitric oxide synthase 1, neuronal	Mus musculus	113-124
18554543-1	2008	Nitric oxide (NO) and carbon monoxide (CO) are synthesized from l-arginine and heme by the catalytic reaction of NO synthase (NOS) and heme oxygenase (HO).	Carbon Monoxide	39-41	nitric oxide synthase 1, neuronal	Mus musculus	113-124
18554543-1	2008	Nitric oxide (NO) and carbon monoxide (CO) are synthesized from l-arginine and heme by the catalytic reaction of NO synthase (NOS) and heme oxygenase (HO).	Arginine	64-74	nitric oxide synthase 1, neuronal	Mus musculus	113-124
18554543-1	2008	Nitric oxide (NO) and carbon monoxide (CO) are synthesized from l-arginine and heme by the catalytic reaction of NO synthase (NOS) and heme oxygenase (HO).	Heme	79-83	nitric oxide synthase 1, neuronal	Mus musculus	113-124
19097389-4	2008	The aim of this work was to observe the effect of two NO synthase (NOS) inhibitors (N omega-Nitro-L-arginine, NA; 7-nitroindazole, NI) on spontaneous behaviour, spatial learning and motor functions in Lurcher (+/Lc) and wild type (+/+) mice, derived from the B6CBA strain.	7-nitroindazole	114-129	nitric oxide synthase 1, neuronal	Mus musculus	54-65
17853069-3	2008	Also, in the adrenal glands basal levels of tyrosine hydroxylase protein, the rate-limiting enzyme for catecholamine biosynthesis, and of phenylethanolamine N-methyltransferase, which converts norepinephrine to epinephrine, were significantly reduced in nNOS KO mice.	Norepinephrine	193-207	nitric oxide synthase 1, neuronal	Mus musculus	254-258
17853069-7	2008	These data suggest that the chronic absence of nNOS reduces the capacity of epinephrine synthesising enzymes in the adrenal gland to respond to acute stressor exposure with an adequate epinephrine release.	Epinephrine	76-87	nitric oxide synthase 1, neuronal	Mus musculus	47-51
17853069-7	2008	These data suggest that the chronic absence of nNOS reduces the capacity of epinephrine synthesising enzymes in the adrenal gland to respond to acute stressor exposure with an adequate epinephrine release.	Epinephrine	185-196	nitric oxide synthase 1, neuronal	Mus musculus	47-51
18063827-1	2008	BACKGROUND AND PURPOSE: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS).	N,N-dimethylarginine	53-57	nitric oxide synthase 1, neuronal	Mus musculus	89-110
18197485-3	2007	nNOS is expressed in skeletal muscle tissue where it may regulate glucose uptake.	Glucose	66-73	nitric oxide synthase 1, neuronal	Mus musculus	0-4
18197485-5	2007	Finally, nNOS dependent NO in the central nervous system may facilitate glucose disposal by decreasing sympathetic nerve activity.	Glucose	72-79	nitric oxide synthase 1, neuronal	Mus musculus	9-13
18197485-8	2007	RESULTS: as expected, the glucose infusion rate during clamping was roughly 15 percent lower in nNOS null than in control mice (89 (17) vs 101 (12) [-22 to -2]).	Glucose	26-33	nitric oxide synthase 1, neuronal	Mus musculus	96-100
18197485-10	2007	Phentolamine, which had no effect in the wild-type mice, normalised the insulin sensitivity in the mice lacking the nNOS gene.	Phentolamine	0-12	nitric oxide synthase 1, neuronal	Mus musculus	116-120
17989510-8	2007	These results suggest that nNOS and phospholipase A2, which might increase free radicals, play an important role in the expression of morphine-induced withdrawal syndrome.	Free Radicals	75-88	nitric oxide synthase 1, neuronal	Mus musculus	27-31
18056350-5	2007	Treatment reduced total lung NO synthase activity to 14.7+/-6.1% of saline-treated 10-wk-old SP-D-/- littermates.	Sodium Chloride	68-74	nitric oxide synthase 1, neuronal	Mus musculus	29-40
18056350-8	2007	Two weeks of treatment with 1400W reduced total lung NO synthase (NOS) activity to 12.7+/-6.3% of saline-treated SP-D-/- mice.	N-((3-(aminomethyl)phenyl)methyl)ethanimidamide	28-33	nitric oxide synthase 1, neuronal	Mus musculus	53-64
17989510-8	2007	These results suggest that nNOS and phospholipase A2, which might increase free radicals, play an important role in the expression of morphine-induced withdrawal syndrome.	Morphine	134-142	nitric oxide synthase 1, neuronal	Mus musculus	27-31
17854382-8	2007	These results suggest that reduced nNOS is involved in ischemia-induced hippocampal neurogenesis by up-regulating iNOS expression and cAMP response element-binding protein phosphorylation.	Cyclic AMP	134-138	nitric oxide synthase 1, neuronal	Mus musculus	35-39
17853433-4	2007	LTM of cocaine-associated context was established in both WT and nNOS KO mice by conditioned place preference learning.	Cocaine	7-14	nitric oxide synthase 1, neuronal	Mus musculus	65-69
17684724-6	2007	MEASUREMENTS AND MAIN RESULTS: After CLP, genetic deficiency and pharmacologic inhibition of NOS1 significantly increased risk of mortality [8.69 (3.27, 23.1), p&lt;0.0001 and 1.71 (1.00, 2.92) p=0.05, hazard ratio of death (95% confidence interval) for NOS1-/- and 7-NI-treated NOS1+/+ respectively] compared with NOS1+/+ animals.	7-nitroindazole	266-270	nitric oxide synthase 1, neuronal	Mus musculus	93-97
17766468-2	2007	Hallmark reactions of peroxynitrite include the accumulation of 3-nitrotyrosine (3-NT) in proteins and oxidation of the NO synthase (NOS) cofactor, tetrahydrobiopterin (BH(4)).	Peroxynitrous Acid	22-35	nitric oxide synthase 1, neuronal	Mus musculus	120-131
17766468-2	2007	Hallmark reactions of peroxynitrite include the accumulation of 3-nitrotyrosine (3-NT) in proteins and oxidation of the NO synthase (NOS) cofactor, tetrahydrobiopterin (BH(4)).	sapropterin	148-167	nitric oxide synthase 1, neuronal	Mus musculus	120-131
17602202-3	2007	METHODS AND RESULTS: Cine MRI showed higher LV mass to end-diastolic volume ratio (2.3 +/- 0.2 mg/microL nNOS(-/-) vs. 1.7 +/- 0.1 mg/microL WT; P=0.032) and LV ejection fraction (64.9 +/- 2.1% nNOS(-/-) vs. 55.8 +/- 1.1% WT; P = 0.003) in nNOS(-/-).	nicotinuric acid	21-25	nitric oxide synthase 1, neuronal	Mus musculus	105-109
17602202-3	2007	METHODS AND RESULTS: Cine MRI showed higher LV mass to end-diastolic volume ratio (2.3 +/- 0.2 mg/microL nNOS(-/-) vs. 1.7 +/- 0.1 mg/microL WT; P=0.032) and LV ejection fraction (64.9 +/- 2.1% nNOS(-/-) vs. 55.8 +/- 1.1% WT; P = 0.003) in nNOS(-/-).	nicotinuric acid	21-25	nitric oxide synthase 1, neuronal	Mus musculus	194-198
17602202-3	2007	METHODS AND RESULTS: Cine MRI showed higher LV mass to end-diastolic volume ratio (2.3 +/- 0.2 mg/microL nNOS(-/-) vs. 1.7 +/- 0.1 mg/microL WT; P=0.032) and LV ejection fraction (64.9 +/- 2.1% nNOS(-/-) vs. 55.8 +/- 1.1% WT; P = 0.003) in nNOS(-/-).	nicotinuric acid	21-25	nitric oxide synthase 1, neuronal	Mus musculus	194-198
17684724-7	2007	In 7-NI-treated NOS1+/+ animals, there were increases (6 h) and then decreases (24 h), whereas in NOS-/- animals persistent increases in blood bacteria counts (p=0.04 for differing effects of 7-NI and NOS1-/-) were seen compared with NOS1(+/+) animals.	7-nitroindazole	3-7	nitric oxide synthase 1, neuronal	Mus musculus	16-20
17684724-7	2007	In 7-NI-treated NOS1+/+ animals, there were increases (6 h) and then decreases (24 h), whereas in NOS-/- animals persistent increases in blood bacteria counts (p=0.04 for differing effects of 7-NI and NOS1-/-) were seen compared with NOS1(+/+) animals.	7-nitroindazole	3-7	nitric oxide synthase 1, neuronal	Mus musculus	201-205
17684724-7	2007	In 7-NI-treated NOS1+/+ animals, there were increases (6 h) and then decreases (24 h), whereas in NOS-/- animals persistent increases in blood bacteria counts (p=0.04 for differing effects of 7-NI and NOS1-/-) were seen compared with NOS1(+/+) animals.	7-nitroindazole	3-7	nitric oxide synthase 1, neuronal	Mus musculus	201-205
17904738-5	2007	Treatment with alpha-mpt, a pharmacologic inhibitor of catecholamine synthesis, resulted in increased vasopressin mRNA levels in wild-type mice and in reduced vasopressin immunoreactivity in both wild-type and nNOS knockout mice.	alpha-Methyltyrosine	15-24	nitric oxide synthase 1, neuronal	Mus musculus	210-214
17904738-6	2007	From these results, we conclude: (1) neuronal nitric oxide suppresses vasopressin expression under basal conditions and during activation of the vasopressinergic system by dehydration; (2) catecholamines limit vasopressin expression; (3) nNOS is required for the effects of catecholamines on vasopressin expression.	Nitric Oxide	46-58	nitric oxide synthase 1, neuronal	Mus musculus	238-242
17904738-6	2007	From these results, we conclude: (1) neuronal nitric oxide suppresses vasopressin expression under basal conditions and during activation of the vasopressinergic system by dehydration; (2) catecholamines limit vasopressin expression; (3) nNOS is required for the effects of catecholamines on vasopressin expression.	Catecholamines	189-203	nitric oxide synthase 1, neuronal	Mus musculus	238-242
17922909-1	2007	Neuronal nitric oxide synthase (nNOS) is a key enzyme for nitric oxide production in neuronal tissues and contributes to the spinal central sensitization in inflammatory pain.	Nitric Oxide	9-21	nitric oxide synthase 1, neuronal	Mus musculus	32-36
17922909-6	2007	Intrathecal injection of 7-nitroindazole (8.15 microg/5 microl), a selective nNOS inhibitor, also dramatically attenuated nerve injury-induced mechanical hypersensitivity.	7-nitroindazole	25-40	nitric oxide synthase 1, neuronal	Mus musculus	77-81
17868368-4	2007	LTD(DHPG) required nitric oxide (NO) synthesis as it was blocked by the broad-spectrum NO synthase (NOS) inhibitor Nomega-nitro-l-arginine (NL-Arg) and impaired under blockade of neuronal NOS and in endothelial NOS-deficient mice.	3,4-dihydroxyphenylglycol	4-8	nitric oxide synthase 1, neuronal	Mus musculus	87-98
17868368-4	2007	LTD(DHPG) required nitric oxide (NO) synthesis as it was blocked by the broad-spectrum NO synthase (NOS) inhibitor Nomega-nitro-l-arginine (NL-Arg) and impaired under blockade of neuronal NOS and in endothelial NOS-deficient mice.	Nitric Oxide	19-31	nitric oxide synthase 1, neuronal	Mus musculus	87-98
17868368-4	2007	LTD(DHPG) required nitric oxide (NO) synthesis as it was blocked by the broad-spectrum NO synthase (NOS) inhibitor Nomega-nitro-l-arginine (NL-Arg) and impaired under blockade of neuronal NOS and in endothelial NOS-deficient mice.	Nitroarginine	115-138	nitric oxide synthase 1, neuronal	Mus musculus	87-98
17868368-4	2007	LTD(DHPG) required nitric oxide (NO) synthesis as it was blocked by the broad-spectrum NO synthase (NOS) inhibitor Nomega-nitro-l-arginine (NL-Arg) and impaired under blockade of neuronal NOS and in endothelial NOS-deficient mice.	Nitroarginine	140-146	nitric oxide synthase 1, neuronal	Mus musculus	87-98
17628500-9	2007	Addition of 1 mM EGTA during the incubation with NA reduced the AVP increase by half, indicating that both nNOS and iNOS activities are involved in the regulation.	Egtazic Acid	17-21	nitric oxide synthase 1, neuronal	Mus musculus	107-111
17596536-9	2007	N(omega)-Nitro-L-arginine methyl ester inhibited BAY 41-2272-evoked responses in CC from WT and nNOS(-/-), but not eNOS(-/-).1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one reduced and sildenafil potentiated the relaxations induced by BAY 41-2272 in all groups.	NG-Nitroarginine Methyl Ester	0-38	nitric oxide synthase 1, neuronal	Mus musculus	96-100
17962481-1	2007	PURPOSE: Nitric oxide (NO) is involved in leukostasis and blood-retinal barrier (BRB) breakdown in the early stages of diabetic retinopathy (DR), but it is unclear which NO synthase (NOS) isoforms are primarily involved.	Nitric Oxide	9-21	nitric oxide synthase 1, neuronal	Mus musculus	170-181
19097389-4	2008	The aim of this work was to observe the effect of two NO synthase (NOS) inhibitors (N omega-Nitro-L-arginine, NA; 7-nitroindazole, NI) on spontaneous behaviour, spatial learning and motor functions in Lurcher (+/Lc) and wild type (+/+) mice, derived from the B6CBA strain.	Nitroarginine	84-108	nitric oxide synthase 1, neuronal	Mus musculus	54-65
17588309-10	2007	In the presence of a nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), the expression levels of MMP-2 were decreased, but the expression of MMP-9 was not decreased by agmatine administration.	NG-Nitroarginine Methyl Ester	60-98	nitric oxide synthase 1, neuronal	Mus musculus	21-42
17588309-10	2007	In the presence of a nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), the expression levels of MMP-2 were decreased, but the expression of MMP-9 was not decreased by agmatine administration.	NG-Nitroarginine Methyl Ester	100-106	nitric oxide synthase 1, neuronal	Mus musculus	21-42
17588309-10	2007	In the presence of a nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), the expression levels of MMP-2 were decreased, but the expression of MMP-9 was not decreased by agmatine administration.	Agmatine	205-213	nitric oxide synthase 1, neuronal	Mus musculus	21-42
17786240-7	2007	Furthermore, an nNOS-specific inhibitor, 7-nitroindazole, significantly prevented suspension-induced muscle atrophy.	7-nitroindazole	41-56	nitric oxide synthase 1, neuronal	Mus musculus	16-20
17885995-2	2007	The authors hypothesized that ascorbate inhibits the conduction deficit by reducing nNOS-derived NO production.	Ascorbic Acid	30-39	nitric oxide synthase 1, neuronal	Mus musculus	84-88
17885995-8	2007	Ascorbate at 0 and 23 h prevented/reversed the conduction deficit and the increases in nNOS activity and nitrite/nitrate level.	Ascorbic Acid	0-9	nitric oxide synthase 1, neuronal	Mus musculus	87-91
17885995-11	2007	CONCLUSION: These data indicate that early and delayed intravenous boluses of ascorbate prevent/reverse sepsis-induced deficit in arteriolar conducted vasoconstriction in the cremaster muscle by inhibiting nNOS-derived NO production.	Ascorbic Acid	78-87	nitric oxide synthase 1, neuronal	Mus musculus	206-210
17596536-9	2007	N(omega)-Nitro-L-arginine methyl ester inhibited BAY 41-2272-evoked responses in CC from WT and nNOS(-/-), but not eNOS(-/-).1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one reduced and sildenafil potentiated the relaxations induced by BAY 41-2272 in all groups.	3-(4-Amino-5-cyclopropylpyrimidine-2-yl)-1-(2-fluorobenzyl)-1H-pyrazolo(3,4-b)pyridine	49-60	nitric oxide synthase 1, neuronal	Mus musculus	96-100
17640569-5	2007	Cells overexpressing endothelial NO synthase (NOS) exhibited a similar protection, which was abolished by the NOS inhibitor N(omega)-nitro-l-arginine methyl ester.	NG-Nitroarginine Methyl Ester	124-162	nitric oxide synthase 1, neuronal	Mus musculus	33-44
17827917-1	2007	The nitric oxide (NO) synthases (NOSs) system consists of three different isoforms, including neuronal (nNOS), inducible (iNOS), and endothelial NOSs (eNOS).	Nitric Oxide	4-16	nitric oxide synthase 1, neuronal	Mus musculus	104-108
17574882-2	2007	Nevertheless, how nitric oxide production by NOS1 contributes to airway responsiveness remains unclear.	Nitric Oxide	18-30	nitric oxide synthase 1, neuronal	Mus musculus	45-49
17585901-26	2007	[a specific neuronal nitric oxide synthase (nNOS) inhibitor] produced potentiation of the action of subeffective dose of berberine (2 mg/kg, i.p.).	Berberine	121-130	nitric oxide synthase 1, neuronal	Mus musculus	12-42
17585901-26	2007	[a specific neuronal nitric oxide synthase (nNOS) inhibitor] produced potentiation of the action of subeffective dose of berberine (2 mg/kg, i.p.).	Berberine	121-130	nitric oxide synthase 1, neuronal	Mus musculus	44-48
17585901-28	2007	[direct inhibitor of both nitric oxide synthase (NOS) and soluble guanylate cyclase (sGC)] potentiated the effect of berberine (2 mg/kg, i.p.)	Berberine	117-126	nitric oxide synthase 1, neuronal	Mus musculus	26-47
21162268-0	2007	[The effect of sinomenine on nNOS activity of brain tissues in morphine dependent and withdrawal mice].	sinomenine	15-25	nitric oxide synthase 1, neuronal	Mus musculus	29-33
17503478-10	2007	Moreover, nNOS often co-localized with GABA, neuropeptide-Y, and somatostatin in the cat neocortex.	gamma-Aminobutyric Acid	39-43	nitric oxide synthase 1, neuronal	Mus musculus	10-14
17466955-1	2007	OBJECTIVE: Neuronal nitric oxide synthase (nNOS) has been shown to regulate intracellular calcium in cardiomyocytes.	Calcium	90-97	nitric oxide synthase 1, neuronal	Mus musculus	11-41
17466955-1	2007	OBJECTIVE: Neuronal nitric oxide synthase (nNOS) has been shown to regulate intracellular calcium in cardiomyocytes.	Calcium	90-97	nitric oxide synthase 1, neuronal	Mus musculus	43-47
17466955-7	2007	Treatment with an antisense oligonucleotide against nNOS also significantly enhanced TNF-alpha expression during LPS stimulation.	Oligonucleotides	28-43	nitric oxide synthase 1, neuronal	Mus musculus	52-56
17548218-1	2007	We have recently demonstrated that nitric oxide (NO) produced by neuronal NO synthase (nNOS) in the spinal cord is involved in the maintenance of neuropathic pain.	Nitric Oxide	35-47	nitric oxide synthase 1, neuronal	Mus musculus	87-91
17548218-2	2007	To clarify whether NO itself affected nNOS activity in the spinal cord as a retrograde messenger, we examined the involvement of the NO/cGMP signaling pathway in the regulation of nNOS activity by NADPH-diaphorase histochemistry.	Cyclic GMP	136-140	nitric oxide synthase 1, neuronal	Mus musculus	180-184
17548218-7	2007	Additionally, the NOR3-enhanced nNOS activity was completely inhibited by NMDA antagonists MK-801 and d-AP5, partially by the GluRepsilon2-selective antagonist CP-101,606, and was attenuated in GluRepsilon1(-/-) and GluRepsilon1(-/-)/epsilon4(-/-) mice.	N-Methylaspartate	74-78	nitric oxide synthase 1, neuronal	Mus musculus	32-36
17548218-7	2007	Additionally, the NOR3-enhanced nNOS activity was completely inhibited by NMDA antagonists MK-801 and d-AP5, partially by the GluRepsilon2-selective antagonist CP-101,606, and was attenuated in GluRepsilon1(-/-) and GluRepsilon1(-/-)/epsilon4(-/-) mice.	Dizocilpine Maleate	91-97	nitric oxide synthase 1, neuronal	Mus musculus	32-36
17548218-7	2007	Additionally, the NOR3-enhanced nNOS activity was completely inhibited by NMDA antagonists MK-801 and d-AP5, partially by the GluRepsilon2-selective antagonist CP-101,606, and was attenuated in GluRepsilon1(-/-) and GluRepsilon1(-/-)/epsilon4(-/-) mice.	2-amino-4-oxo-5-phosphonopentanoic acid	102-107	nitric oxide synthase 1, neuronal	Mus musculus	32-36
17509558-19	2007	[a specific neuronal nitric oxide synthase (nNOS) inhibitor] produced potentiation of the action of subeffective dose of bupropion (10 mg/kg i.p.).	Bupropion	121-130	nitric oxide synthase 1, neuronal	Mus musculus	12-42
17509558-19	2007	[a specific neuronal nitric oxide synthase (nNOS) inhibitor] produced potentiation of the action of subeffective dose of bupropion (10 mg/kg i.p.).	Bupropion	121-130	nitric oxide synthase 1, neuronal	Mus musculus	44-48
17509558-21	2007	[direct inhibitor of both nitric oxide synthase (NOS) and soluble guanylate cyclase (sGC)] potentiated the effect of bupropion (10 mg/kg., i.p.)	Bupropion	117-126	nitric oxide synthase 1, neuronal	Mus musculus	26-47
17446183-8	2007	Inhibition of nitric oxide type I (NOSI) by 7-nitroindazole also reversed GnRH-mediated inhibition by 60%.	Nitric Oxide	14-26	nitric oxide synthase 1, neuronal	Mus musculus	35-39
17559823-3	2007	We have recently shown that NO biosynthesis can be disturbed by the endogenous NO synthase (NOS) inhibitor ADMA and that these changes are mediated by an impairment of its metabolism by dimethylarginine dimethylaminohydrolase (DDAH).	N,N-dimethylarginine	107-111	nitric oxide synthase 1, neuronal	Mus musculus	79-90
17446183-8	2007	Inhibition of nitric oxide type I (NOSI) by 7-nitroindazole also reversed GnRH-mediated inhibition by 60%.	7-nitroindazole	44-59	nitric oxide synthase 1, neuronal	Mus musculus	35-39
17446183-10	2007	These data support the concept that chronic GnRH inhibits activin-induced ovine FSHB expression by sequential activation of CREB and NOSI through the cAMP and/or protein kinase C pathways.	Cyclic AMP	150-154	nitric oxide synthase 1, neuronal	Mus musculus	133-137
17419805-10	2007	Moreover, ROS formation was higher in the presence of nNOS inhibitor in both control and CMS mice.	Reactive Oxygen Species	10-13	nitric oxide synthase 1, neuronal	Mus musculus	54-58
17579782-0	2007	[Effects of sinomenine on NO/nNOS system in cerebellum and spinal cord of morphine-dependent and withdrawal mice].	sinomenine	12-22	nitric oxide synthase 1, neuronal	Mus musculus	29-33
17579782-6	2007	(2) Sinomenine also reduced the increases in nNOS mRNA expression and nNOS activity resulting from morphine-dependence, and simultaneously attenuated the high level of NO in both tissues following morphine-withdrawal.	sinomenine	4-14	nitric oxide synthase 1, neuronal	Mus musculus	45-49
17579782-6	2007	(2) Sinomenine also reduced the increases in nNOS mRNA expression and nNOS activity resulting from morphine-dependence, and simultaneously attenuated the high level of NO in both tissues following morphine-withdrawal.	sinomenine	4-14	nitric oxide synthase 1, neuronal	Mus musculus	70-74
17579782-8	2007	The results obtained indicate that sinomenine may attenuate morphine addiction and significantly alleviate morphine-withdrawal symptoms, and the mechanism may be associated with the effect of sinomenine on the NO/nNOS system in the cerebellum and spinal cord.	sinomenine	35-45	nitric oxide synthase 1, neuronal	Mus musculus	213-217
17579782-8	2007	The results obtained indicate that sinomenine may attenuate morphine addiction and significantly alleviate morphine-withdrawal symptoms, and the mechanism may be associated with the effect of sinomenine on the NO/nNOS system in the cerebellum and spinal cord.	sinomenine	192-202	nitric oxide synthase 1, neuronal	Mus musculus	213-217
17466955-9	2007	The enhanced TNF-alpha expression in nNOS(-/-) cardiomyocytes was abrogated by an L-type calcium channel blocker verapamil or ERK1 siRNA.	Verapamil	113-122	nitric oxide synthase 1, neuronal	Mus musculus	37-41
17374527-5	2007	Over 8 and 16 weeks on alternate days, mice were treated with and without exercise, and additional exercise-treated mice were orally given 25 mg/kg/day of NG-nitro-L-arginine methylester (L-NAME), an inhibitor of nitric oxide synthase (NOS).	NG-Nitroarginine Methyl Ester	188-194	nitric oxide synthase 1, neuronal	Mus musculus	213-234
17368487-1	2007	We have previously shown that the co-localization of neuronal nitric oxide synthase (nNOS) with neurofilament (NF) aggregates in motor neurons derived from transgenic mice over-expressing the human low molecular weight NF protein (hNFL+/+) is associated with a deregulation of calcium influx via the N-methyl-d-aspartate (NMDA) receptor, resulting in apoptosis.	Calcium	277-284	nitric oxide synthase 1, neuronal	Mus musculus	53-83
17368487-1	2007	We have previously shown that the co-localization of neuronal nitric oxide synthase (nNOS) with neurofilament (NF) aggregates in motor neurons derived from transgenic mice over-expressing the human low molecular weight NF protein (hNFL+/+) is associated with a deregulation of calcium influx via the N-methyl-d-aspartate (NMDA) receptor, resulting in apoptosis.	Calcium	277-284	nitric oxide synthase 1, neuronal	Mus musculus	85-89
17158357-2	2007	Low L-arginine levels can result in the uncoupling of nitric oxide synthase (NOS) leading to production of both ROS and RNS.	Arginine	4-14	nitric oxide synthase 1, neuronal	Mus musculus	54-75
17158357-2	2007	Low L-arginine levels can result in the uncoupling of nitric oxide synthase (NOS) leading to production of both ROS and RNS.	Reactive Oxygen Species	112-115	nitric oxide synthase 1, neuronal	Mus musculus	54-75
17158357-2	2007	Low L-arginine levels can result in the uncoupling of nitric oxide synthase (NOS) leading to production of both ROS and RNS.	Reactive Nitrogen Species	120-123	nitric oxide synthase 1, neuronal	Mus musculus	54-75
17426488-7	2007	The present results show that oxidative stress, which is mediated by the activation of neuronal nitric oxide synthase, is associated with methamphetamine-induced self-injurious behavior.	Methamphetamine	138-153	nitric oxide synthase 1, neuronal	Mus musculus	87-117
17379358-0	2007	The effect of subchronic, intermittent L-DOPA treatment on neuronal nitric oxide synthase and soluble guanylyl cyclase expression and activity in the striatum and midbrain of normal and MPTP-treated mice.	Levodopa	39-45	nitric oxide synthase 1, neuronal	Mus musculus	59-89
17379358-1	2007	We have investigated the effects of low (10 mg/kg) and high (100 mg/kg) doses of L-DOPA on the expression and activity of neuronal nitric oxide synthase (nNOS) and guanylyl cyclase (GC) in the striatum and midbrain of mice.	Levodopa	81-87	nitric oxide synthase 1, neuronal	Mus musculus	122-152
17379358-1	2007	We have investigated the effects of low (10 mg/kg) and high (100 mg/kg) doses of L-DOPA on the expression and activity of neuronal nitric oxide synthase (nNOS) and guanylyl cyclase (GC) in the striatum and midbrain of mice.	Levodopa	81-87	nitric oxide synthase 1, neuronal	Mus musculus	154-158
17379358-7	2007	In normal mice, L-DOPA upregulates the expression and activity of nNOS and GC to levels found in MPTP-injected mice.	Levodopa	16-22	nitric oxide synthase 1, neuronal	Mus musculus	66-70
17379358-7	2007	In normal mice, L-DOPA upregulates the expression and activity of nNOS and GC to levels found in MPTP-injected mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	97-101	nitric oxide synthase 1, neuronal	Mus musculus	66-70
17379358-8	2007	Due to upregulation of nNOS and GC, cGMP levels in the mouse striatum and midbrain are also elevated, however, significantly lower in mice administrated with low dose of L-DOPA.	Cyclic GMP	36-40	nitric oxide synthase 1, neuronal	Mus musculus	23-27
17379358-8	2007	Due to upregulation of nNOS and GC, cGMP levels in the mouse striatum and midbrain are also elevated, however, significantly lower in mice administrated with low dose of L-DOPA.	Levodopa	170-176	nitric oxide synthase 1, neuronal	Mus musculus	23-27
17379358-10	2007	The enhancement of nNOS mRNA and GCbeta1 mRNA levels were generated by both doses of L-DOPA, given in a time-dependent fashion.	Levodopa	85-91	nitric oxide synthase 1, neuronal	Mus musculus	19-23
17652825-0	2007	Different effects of nitric oxide synthase inhibitors on convulsions induced by nicotine in mice.	Nicotine	80-88	nitric oxide synthase 1, neuronal	Mus musculus	21-42
17652825-2	2007	administration of N(G)-nitro-L-arginine (NNA, 10, 20 and 40 mg/kg), a non-selective nitric oxide synthase (NOS) inhibitor, significantly and dose-dependently decreased the incidence of convulsions induced by i.p.	Nitroarginine	18-39	nitric oxide synthase 1, neuronal	Mus musculus	84-105
17652825-2	2007	administration of N(G)-nitro-L-arginine (NNA, 10, 20 and 40 mg/kg), a non-selective nitric oxide synthase (NOS) inhibitor, significantly and dose-dependently decreased the incidence of convulsions induced by i.p.	Nitroarginine	41-44	nitric oxide synthase 1, neuronal	Mus musculus	84-105
17306238-0	2007	Stimulation of the cAMP pathway protects cultured cerebellar granule neurons against alcohol-induced cell death by activating the neuronal nitric oxide synthase (nNOS) gene.	Cyclic AMP	19-23	nitric oxide synthase 1, neuronal	Mus musculus	130-160
17306238-0	2007	Stimulation of the cAMP pathway protects cultured cerebellar granule neurons against alcohol-induced cell death by activating the neuronal nitric oxide synthase (nNOS) gene.	Cyclic AMP	19-23	nitric oxide synthase 1, neuronal	Mus musculus	162-166
17306238-0	2007	Stimulation of the cAMP pathway protects cultured cerebellar granule neurons against alcohol-induced cell death by activating the neuronal nitric oxide synthase (nNOS) gene.	Alcohols	85-92	nitric oxide synthase 1, neuronal	Mus musculus	130-160
17306238-0	2007	Stimulation of the cAMP pathway protects cultured cerebellar granule neurons against alcohol-induced cell death by activating the neuronal nitric oxide synthase (nNOS) gene.	Alcohols	85-92	nitric oxide synthase 1, neuronal	Mus musculus	162-166
17306238-3	2007	We have previously reported that neuronal nitric oxide synthase (nNOS) can protect developing cerebellar granule neurons (CGN) against alcohol-induced death both in vitro and in vivo.	Alcohols	135-142	nitric oxide synthase 1, neuronal	Mus musculus	33-63
17306238-3	2007	We have previously reported that neuronal nitric oxide synthase (nNOS) can protect developing cerebellar granule neurons (CGN) against alcohol-induced death both in vitro and in vivo.	Alcohols	135-142	nitric oxide synthase 1, neuronal	Mus musculus	65-69
17306238-6	2007	Furthermore, the promoter of the nNOS gene contains two cAMP response elements (CRE).	Cyclic AMP	56-60	nitric oxide synthase 1, neuronal	Mus musculus	33-37
17306238-7	2007	Using cultures of CGN, we tested the hypothesis that cAMP mediates nNOS activation and the protective effect of nNOS against alcohol-induced cell death.	Cyclic AMP	53-57	nitric oxide synthase 1, neuronal	Mus musculus	67-71
17306238-7	2007	Using cultures of CGN, we tested the hypothesis that cAMP mediates nNOS activation and the protective effect of nNOS against alcohol-induced cell death.	Alcohols	125-132	nitric oxide synthase 1, neuronal	Mus musculus	112-116
17306238-8	2007	Forskolin, an activator of the cAMP pathway, stimulated expression of a reporter gene under the control of the nNOS promoter, and this stimulation was substantially reduced when the two CREs were mutated.	Colforsin	0-9	nitric oxide synthase 1, neuronal	Mus musculus	111-115
17306238-8	2007	Forskolin, an activator of the cAMP pathway, stimulated expression of a reporter gene under the control of the nNOS promoter, and this stimulation was substantially reduced when the two CREs were mutated.	Cyclic AMP	31-35	nitric oxide synthase 1, neuronal	Mus musculus	111-115
17306238-9	2007	Forskolin increased nNOS mRNA levels several fold, increased production of nitric oxide, and abolished alcohol"s toxic effect in wild type CGN.	Colforsin	0-9	nitric oxide synthase 1, neuronal	Mus musculus	20-24
17306238-10	2007	Furthermore, forskolin"s protective effect was substantially reduced in CGN cultures genetically deficient for nNOS (from nNOS-/- mice).	Colforsin	13-22	nitric oxide synthase 1, neuronal	Mus musculus	111-115
17306238-10	2007	Furthermore, forskolin"s protective effect was substantially reduced in CGN cultures genetically deficient for nNOS (from nNOS-/- mice).	Colforsin	13-22	nitric oxide synthase 1, neuronal	Mus musculus	122-134
17306238-11	2007	Delivery of nNOS cDNA using a replication-deficient adenoviral vector into nNOS-/- CGN abolished alcohol-induced neuronal death.	Alcohols	97-104	nitric oxide synthase 1, neuronal	Mus musculus	12-16
17306238-11	2007	Delivery of nNOS cDNA using a replication-deficient adenoviral vector into nNOS-/- CGN abolished alcohol-induced neuronal death.	Alcohols	97-104	nitric oxide synthase 1, neuronal	Mus musculus	75-79
17306238-12	2007	In addition, overexpression of nNOS in wild type CGN ameliorated alcohol-induced cell death.	Alcohols	65-72	nitric oxide synthase 1, neuronal	Mus musculus	31-35
17306238-13	2007	These results indicate that the neuroprotective effect of the cAMP pathway is mediated, in part, by the pathway"s downstream target, the nNOS gene.	Cyclic AMP	62-66	nitric oxide synthase 1, neuronal	Mus musculus	137-141
16359645-1	2007	Nitric oxide (NO) is a diffusible messenger molecule produced primarily by neuronal nitric oxide synthase (nNOS) in the central nervous system.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	75-105
17387708-1	2007	Nitric oxide (NO) is an essential messenger molecule in brain, where it is produced in neurons mostly by the activity of the neuronal isoform of nitric oxide synthase (nNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	168-172
17138723-0	2007	High salt intake reduces endothelium-dependent dilation of mouse arterioles via superoxide anion generated from nitric oxide synthase.	Salts	5-9	nitric oxide synthase 1, neuronal	Mus musculus	112-133
17138723-0	2007	High salt intake reduces endothelium-dependent dilation of mouse arterioles via superoxide anion generated from nitric oxide synthase.	Superoxides	80-96	nitric oxide synthase 1, neuronal	Mus musculus	112-133
17138723-4	2007	Inhibition of nitric oxide synthase (NOS) with N(G) monomethyl L-arginine (L-NMMA) significantly reduced resting diameters and reduced responses to ACh (by 45-63%) in NS mice but not in HS mice.	omega-N-Methylarginine	47-73	nitric oxide synthase 1, neuronal	Mus musculus	14-35
17138723-4	2007	Inhibition of nitric oxide synthase (NOS) with N(G) monomethyl L-arginine (L-NMMA) significantly reduced resting diameters and reduced responses to ACh (by 45-63%) in NS mice but not in HS mice.	omega-N-Methylarginine	75-81	nitric oxide synthase 1, neuronal	Mus musculus	14-35
17138723-4	2007	Inhibition of nitric oxide synthase (NOS) with N(G) monomethyl L-arginine (L-NMMA) significantly reduced resting diameters and reduced responses to ACh (by 45-63%) in NS mice but not in HS mice.	Acetylcholine	148-151	nitric oxide synthase 1, neuronal	Mus musculus	14-35
17469926-3	2007	Neuronal nitric oxide synthase (nNOS) produces gaseous nitric oxide, which functions as a neurotransmitter and is known to affect several types of behavior including mating and aggression.	Nitric Oxide	9-21	nitric oxide synthase 1, neuronal	Mus musculus	32-36
17469926-5	2007	Similar results were observed in mice treated with the selective nNOS inhibitor 3-bromo-7-nitroindazole (3BrN).	3-bromo-7-nitroindazole	80-103	nitric oxide synthase 1, neuronal	Mus musculus	65-69
17469926-5	2007	Similar results were observed in mice treated with the selective nNOS inhibitor 3-bromo-7-nitroindazole (3BrN).	3-bromo-7-nitroindazole	105-109	nitric oxide synthase 1, neuronal	Mus musculus	65-69
17258180-8	2007	Accordingly, pharmacological inhibition of nNOS with 7-nitroindazole reversed this impairment in WT mice.	7-nitroindazole	53-68	nitric oxide synthase 1, neuronal	Mus musculus	43-47
17258180-15	2007	Both genetic deletion and inhibition of nNOS protect against this impairment when the dilation occurs via the EDRF but not EDHF pathway.	edhf	123-127	nitric oxide synthase 1, neuronal	Mus musculus	40-44
17343612-9	2007	The best candidate for this soluble factor is nitric oxide (NO) based on the following observations: the factor in the ascites is unstable; Fas expression is induced to a lesser degree after injection into inducible NO synthase (NOS)-deficient (iNOS(-/-)) mice when compared to control mice; similarly, coculture with iNOS(-/-) splenocytes induces Fas less effectively than coculture with control splenocytes; and finally, the NO donor SNAP induces considerable Fas up-regulation in tumours in vitro.	Nitric Oxide	46-58	nitric oxide synthase 1, neuronal	Mus musculus	216-227
17343612-9	2007	The best candidate for this soluble factor is nitric oxide (NO) based on the following observations: the factor in the ascites is unstable; Fas expression is induced to a lesser degree after injection into inducible NO synthase (NOS)-deficient (iNOS(-/-)) mice when compared to control mice; similarly, coculture with iNOS(-/-) splenocytes induces Fas less effectively than coculture with control splenocytes; and finally, the NO donor SNAP induces considerable Fas up-regulation in tumours in vitro.	ammonium ferrous sulfate	140-143	nitric oxide synthase 1, neuronal	Mus musculus	216-227
17379375-10	2007	[a specific neuronal nitric oxide synthase (nNOS) inhibitor] produced potentiation of the action of subeffective dose of venlafaxine (2 mg/kg, i.p.).	Venlafaxine Hydrochloride	121-132	nitric oxide synthase 1, neuronal	Mus musculus	12-42
17379375-10	2007	[a specific neuronal nitric oxide synthase (nNOS) inhibitor] produced potentiation of the action of subeffective dose of venlafaxine (2 mg/kg, i.p.).	Venlafaxine Hydrochloride	121-132	nitric oxide synthase 1, neuronal	Mus musculus	44-48
17379375-12	2007	[direct inhibitor of both nitric oxide synthase (NOS) and soluble guanylate cyclase (sGC)] potentiated the effect of venlafaxine (2 mg/kg, i.p.)	Venlafaxine Hydrochloride	117-128	nitric oxide synthase 1, neuronal	Mus musculus	26-47
16982182-2	2007	Overproduction of nitric oxide by nitric oxide synthase (NOS) is thought to promote hyperoxic lung injury.	Nitric Oxide	18-30	nitric oxide synthase 1, neuronal	Mus musculus	34-55
16359645-1	2007	Nitric oxide (NO) is a diffusible messenger molecule produced primarily by neuronal nitric oxide synthase (nNOS) in the central nervous system.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	107-111
16359645-2	2007	Both nNOS expression and NO production are regulated by calcium ions.	Calcium	56-63	nitric oxide synthase 1, neuronal	Mus musculus	5-9
17349891-2	2007	BACKGROUND: Asymmetric dimethylarginine is an endogenous inhibitor of nitric oxide synthase (NOS).	dimethylarginine	23-39	nitric oxide synthase 1, neuronal	Mus musculus	70-91
17350656-6	2007	The N/OFQ-stimulated nNOS activity was inhibited by NMDA receptor antagonists MK-801 and D-AP5, but not by the NR2B-selective antagonist CP-101,606; and the stimulated activity was observed in NR2D(-/-) mice, but not in NR2A(-/-) or NR2A(-/-)/NR2D(-/-) mice.	Dizocilpine Maleate	78-84	nitric oxide synthase 1, neuronal	Mus musculus	21-25
17350656-6	2007	The N/OFQ-stimulated nNOS activity was inhibited by NMDA receptor antagonists MK-801 and D-AP5, but not by the NR2B-selective antagonist CP-101,606; and the stimulated activity was observed in NR2D(-/-) mice, but not in NR2A(-/-) or NR2A(-/-)/NR2D(-/-) mice.	2-amino-4-oxo-5-phosphonopentanoic acid	89-94	nitric oxide synthase 1, neuronal	Mus musculus	21-25
17353023-5	2007	morphine could influence the activation of the extracellular signal-regulated kinase (ERK), a mitogen-activated protein (MAP) kinase in neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS) activation.	Morphine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	136-166
17353023-5	2007	morphine could influence the activation of the extracellular signal-regulated kinase (ERK), a mitogen-activated protein (MAP) kinase in neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS) activation.	Morphine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	168-172
17353023-6	2007	Both 7-NI and TRIM, selective inhibitors of nNOS, resulted in a dose-dependent inhibition of high-dose i.t.	7-nitroindazole	5-9	nitric oxide synthase 1, neuronal	Mus musculus	44-48
17353023-15	2007	morphine may be triggered by the nNOS-ERK pathway in the dorsal spinal cord.	Morphine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	33-37
17272813-6	2007	Measuring of total NOS activity by conversion of [(3)H]-l-arginine to [(3)H]-l-citrulline showed a 30% increase in nNOS overexpressing mice (n=18; P&lt;0.05).	[(3)h]-l-arginine	49-66	nitric oxide synthase 1, neuronal	Mus musculus	115-119
17265179-4	2007	In the present study, we have investigated whether one source of free radicals, neuronal nitric oxide synthase (NOS1), contributes to the dopamine deficit associated with HPRT deficiency.	Free Radicals	65-78	nitric oxide synthase 1, neuronal	Mus musculus	80-110
17265179-4	2007	In the present study, we have investigated whether one source of free radicals, neuronal nitric oxide synthase (NOS1), contributes to the dopamine deficit associated with HPRT deficiency.	Free Radicals	65-78	nitric oxide synthase 1, neuronal	Mus musculus	112-116
17265179-4	2007	In the present study, we have investigated whether one source of free radicals, neuronal nitric oxide synthase (NOS1), contributes to the dopamine deficit associated with HPRT deficiency.	Dopamine	138-146	nitric oxide synthase 1, neuronal	Mus musculus	80-110
17265179-4	2007	In the present study, we have investigated whether one source of free radicals, neuronal nitric oxide synthase (NOS1), contributes to the dopamine deficit associated with HPRT deficiency.	Dopamine	138-146	nitric oxide synthase 1, neuronal	Mus musculus	112-116
17265179-7	2007	These results indicate that NOS1 produced nitric oxide does not contribute to the dopamine deficit seen in HPRT deficiency.	Nitric Oxide	42-54	nitric oxide synthase 1, neuronal	Mus musculus	28-32
17272813-6	2007	Measuring of total NOS activity by conversion of [(3)H]-l-arginine to [(3)H]-l-citrulline showed a 30% increase in nNOS overexpressing mice (n=18; P&lt;0.05).	[(3)h]-l-citrulline	70-89	nitric oxide synthase 1, neuronal	Mus musculus	115-119
16769231-1	2007	This study was undertaken to examine the importance of nitric oxide (NO) generated by the neural isoform of the nitric oxide synthase (nNOS) on the activity of the hypothalamic neurohypophyseal system in neural nitric oxide synthase knock-out (KO) and wild-type (WT) mice under basal conditions and in response to forced swimming.	Nitric Oxide	55-67	nitric oxide synthase 1, neuronal	Mus musculus	135-139
17242280-8	2007	Treatment with a specific nNOS inhibitor (N omega-propyl-L-arginine) reduced the beta-adrenergic response in wild-type and ct120 transgenic mice to levels comparable to those of PMCA4b transgenic animals.	N(omega)-propylarginine	42-67	nitric oxide synthase 1, neuronal	Mus musculus	26-30
17272813-8	2007	In vivo examinations of the nNOS overexpressing mice revealed a 17+/-3% decrease of +dp/dt(max) compared with noninduced mice (P&lt;0.05).	dp	85-87	nitric oxide synthase 1, neuronal	Mus musculus	28-32
17082483-9	2007	CONCLUSIONS: These results indicate that atorvastatin upregulates vascular nNOS through Akt/NF-kappaB pathway, demonstrating a novel nNOS-mediated vascular effect of the statin.	Atorvastatin	41-53	nitric oxide synthase 1, neuronal	Mus musculus	75-79
17082483-9	2007	CONCLUSIONS: These results indicate that atorvastatin upregulates vascular nNOS through Akt/NF-kappaB pathway, demonstrating a novel nNOS-mediated vascular effect of the statin.	Atorvastatin	41-53	nitric oxide synthase 1, neuronal	Mus musculus	133-137
17272813-8	2007	In vivo examinations of the nNOS overexpressing mice revealed a 17+/-3% decrease of +dp/dt(max) compared with noninduced mice (P&lt;0.05).	Thymidine	88-90	nitric oxide synthase 1, neuronal	Mus musculus	28-32
17052925-5	2007	The second experiment showed that more nitric oxide (NO) was produced in the culture medium in the clinostat rotation group after 72 h (P&lt;0.05), and the nitric oxide synthase (NOS) activity in this group was significantly higher than in the controls (P&lt;0.01).	Nitric Oxide	39-51	nitric oxide synthase 1, neuronal	Mus musculus	156-177
17082483-4	2007	Inhibition of Akt by dominant-negative Akt suppressed atorvastatin-induced nNOS expression as well as Akt and NF-kappaB activation.	Atorvastatin	54-66	nitric oxide synthase 1, neuronal	Mus musculus	75-79
17082483-5	2007	Inhibition of NF-kappaB by dominant-negative IkappaB also attenuated atorvastatin-induced nNOS expression and NF-kappaB activation, but not Akt activation.	Atorvastatin	69-81	nitric oxide synthase 1, neuronal	Mus musculus	90-94
17198882-1	2007	OBJECTIVE: Neuronal nitric oxide synthase (NOS1, mitochondrial NOS, neuronal NOS) homozygous deletion recombinant negative mice demonstrate ionizing irradiation resistance in vivo, attributable to the decrease in mitochondrial-localized production of peroxynitrite, a potent lipid toxic free radical species resulting from the combination of nitric oxide and superoxide.	Nitric Oxide	20-32	nitric oxide synthase 1, neuronal	Mus musculus	43-47
17198882-1	2007	OBJECTIVE: Neuronal nitric oxide synthase (NOS1, mitochondrial NOS, neuronal NOS) homozygous deletion recombinant negative mice demonstrate ionizing irradiation resistance in vivo, attributable to the decrease in mitochondrial-localized production of peroxynitrite, a potent lipid toxic free radical species resulting from the combination of nitric oxide and superoxide.	Nitric Oxide	20-32	nitric oxide synthase 1, neuronal	Mus musculus	68-80
17198882-2	2007	The present studies were designed to determine whether reduced mitochondrial generation of toxic radical oxygen species in NOS1-/- mice also increased the longevity of hematopoiesis in continuous bone marrow cultures and conferred radioresistance to cells in vitro.	toxic radical oxygen species	91-119	nitric oxide synthase 1, neuronal	Mus musculus	123-127
17127359-3	2007	Recent studies showed that translocated neuronal nitric oxide synthase (nNOS) is posttranslationally modified including phosphorylation at Ser 1412 (in mice) and myristoylation in an internal residue.	Serine	139-142	nitric oxide synthase 1, neuronal	Mus musculus	40-70
17127359-3	2007	Recent studies showed that translocated neuronal nitric oxide synthase (nNOS) is posttranslationally modified including phosphorylation at Ser 1412 (in mice) and myristoylation in an internal residue.	Serine	139-142	nitric oxide synthase 1, neuronal	Mus musculus	72-76
17098301-9	2007	We also identified TsM nNOS-immunoreactive protein by both NADPH-diaphorase histochemical staining, and immunohistochemical localization and immunoprecipitation with antibodies specific to nNOS N-terminus.	NADP	59-64	nitric oxide synthase 1, neuronal	Mus musculus	23-27
16949556-2	2006	In this study, we investigated the inhibitory effects of acacetin and a related compound, wogonin, on the induction of NO synthase (NOS) and COX-2 in RAW 264.7 cells activated with lipopolysaccharide (LPS).	acacetin	57-65	nitric oxide synthase 1, neuronal	Mus musculus	119-130
16949556-2	2006	In this study, we investigated the inhibitory effects of acacetin and a related compound, wogonin, on the induction of NO synthase (NOS) and COX-2 in RAW 264.7 cells activated with lipopolysaccharide (LPS).	wogonin	90-97	nitric oxide synthase 1, neuronal	Mus musculus	119-130
16977619-0	2006	Severe alcohol-induced neuronal deficits in the hippocampus and neocortex of neonatal mice genetically deficient for neuronal nitric oxide synthase (nNOS).	Alcohols	7-14	nitric oxide synthase 1, neuronal	Mus musculus	117-147
16977619-0	2006	Severe alcohol-induced neuronal deficits in the hippocampus and neocortex of neonatal mice genetically deficient for neuronal nitric oxide synthase (nNOS).	Alcohols	7-14	nitric oxide synthase 1, neuronal	Mus musculus	149-153
16977619-11	2006	These results demonstrate that nNOS deficiency decreases the ability of developing neurons in vivo to survive the toxic effects of alcohol and strengthen the hypothesis that NO exerts a neuroprotective effect against alcohol toxicity in the developing brain.	Alcohols	217-224	nitric oxide synthase 1, neuronal	Mus musculus	31-35
16977619-4	2006	We tested the hypothesis that neonatal mice carrying a null mutation for neuronal nitric oxide synthase (nNOS), the enzyme that synthesizes NO in neurons, have an increased vulnerability to alcohol-induced neuronal loss in the neocortex and hippocampus.	Alcohols	190-197	nitric oxide synthase 1, neuronal	Mus musculus	73-103
16977619-4	2006	We tested the hypothesis that neonatal mice carrying a null mutation for neuronal nitric oxide synthase (nNOS), the enzyme that synthesizes NO in neurons, have an increased vulnerability to alcohol-induced neuronal loss in the neocortex and hippocampus.	Alcohols	190-197	nitric oxide synthase 1, neuronal	Mus musculus	105-109
16977619-8	2006	Alcohol induced dose-dependent reductions in all four neuronal populations, and the losses were substantially more severe in the nNOS-/- mice than in wildtype.	Alcohols	0-7	nitric oxide synthase 1, neuronal	Mus musculus	129-133
16977619-9	2006	Furthermore, the threshold dose of alcohol to induce cell death was lower in the nNOS-/- mice than in the wildtype mice for all neuronal populations.	Alcohols	35-42	nitric oxide synthase 1, neuronal	Mus musculus	81-85
16977619-10	2006	While nNOS deficiency worsened alcohol-induced neuronal losses, the magnitude of this exacerbation varied among brain regions and depended on alcohol dose.	Alcohols	31-38	nitric oxide synthase 1, neuronal	Mus musculus	6-10
16977619-10	2006	While nNOS deficiency worsened alcohol-induced neuronal losses, the magnitude of this exacerbation varied among brain regions and depended on alcohol dose.	Alcohols	142-149	nitric oxide synthase 1, neuronal	Mus musculus	6-10
16977619-11	2006	These results demonstrate that nNOS deficiency decreases the ability of developing neurons in vivo to survive the toxic effects of alcohol and strengthen the hypothesis that NO exerts a neuroprotective effect against alcohol toxicity in the developing brain.	Alcohols	131-138	nitric oxide synthase 1, neuronal	Mus musculus	31-35
17093072-3	2006	NMDA increased NO production in a manner that was potently inhibited by three different neuronal NO synthase (nNOS) inhibitors.	N-Methylaspartate	0-4	nitric oxide synthase 1, neuronal	Mus musculus	110-114
16952382-1	2006	Nitric oxide (NO) supposedly derived via L-arginine-NO synthase (NOS) pathway has been implicated in inhibiting steroidogenesis by binding the heme moiety of steroidogenic enzymes.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	41-63
16952382-1	2006	Nitric oxide (NO) supposedly derived via L-arginine-NO synthase (NOS) pathway has been implicated in inhibiting steroidogenesis by binding the heme moiety of steroidogenic enzymes.	Heme	143-147	nitric oxide synthase 1, neuronal	Mus musculus	41-63
16831955-0	2006	Role for neuronal nitric-oxide synthase in cannabinoid-induced neurogenesis.	Cannabinoids	43-54	nitric oxide synthase 1, neuronal	Mus musculus	9-39
16887252-9	2006	Surprisingly, we found that METH-induced nNOS overexpression was further increased by the pretreatment with baicalein while the level of nNOS was not altered significantly by baicalein treatment alone.	baicalein	108-117	nitric oxide synthase 1, neuronal	Mus musculus	41-45
16887252-9	2006	Surprisingly, we found that METH-induced nNOS overexpression was further increased by the pretreatment with baicalein while the level of nNOS was not altered significantly by baicalein treatment alone.	Methamphetamine	28-32	nitric oxide synthase 1, neuronal	Mus musculus	41-45
16790251-1	2006	Nitric oxide has both an inhibitory and excitatory role in the regulation of pre-ganglionic sympathetic neurons, involving the iNOS and nNOS systems respectively.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	136-140
16925766-10	2006	Choline acetyltransferase- and nNOS-positive nerves also had high cGMP levels in response to 100 microm diethylamine NONOate.	Cyclic GMP	66-70	nitric oxide synthase 1, neuronal	Mus musculus	31-35
16925766-10	2006	Choline acetyltransferase- and nNOS-positive nerves also had high cGMP levels in response to 100 microm diethylamine NONOate.	1,1-diethyl-2-hydroxy-2-nitrosohydrazine	104-124	nitric oxide synthase 1, neuronal	Mus musculus	31-35
16865092-9	2006	The antinociceptive effect of atorvastatin upon LPS- or PGE(2)-induced hypernociception was prevented by non-selective inhibitors of nitric oxide synthase (NOS) but not by selective inhibition of inducible NOS or in mice lacking this enzyme.	Atorvastatin	30-42	nitric oxide synthase 1, neuronal	Mus musculus	133-154
16865092-9	2006	The antinociceptive effect of atorvastatin upon LPS- or PGE(2)-induced hypernociception was prevented by non-selective inhibitors of nitric oxide synthase (NOS) but not by selective inhibition of inducible NOS or in mice lacking this enzyme.	Dinoprostone	56-62	nitric oxide synthase 1, neuronal	Mus musculus	133-154
17345819-1	2006	INTRODUCTION: New nitric oxide synthase (NOS) inhibitors: 3-bromo-7-nitroindazole (3-Br-7-NI), 1-(2-trifluoromethylphenyl) imidazole (TRIM), S-methyl-L-thiocitrulline (S-Me-TC) and 7-nitroindazole (7-NI) reduce spontaneous locomotor activity in mice.	3-bromo-7-nitroindazole	58-81	nitric oxide synthase 1, neuronal	Mus musculus	18-39
17345819-1	2006	INTRODUCTION: New nitric oxide synthase (NOS) inhibitors: 3-bromo-7-nitroindazole (3-Br-7-NI), 1-(2-trifluoromethylphenyl) imidazole (TRIM), S-methyl-L-thiocitrulline (S-Me-TC) and 7-nitroindazole (7-NI) reduce spontaneous locomotor activity in mice.	3-bromo-7-nitroindazole	83-92	nitric oxide synthase 1, neuronal	Mus musculus	18-39
17345819-1	2006	INTRODUCTION: New nitric oxide synthase (NOS) inhibitors: 3-bromo-7-nitroindazole (3-Br-7-NI), 1-(2-trifluoromethylphenyl) imidazole (TRIM), S-methyl-L-thiocitrulline (S-Me-TC) and 7-nitroindazole (7-NI) reduce spontaneous locomotor activity in mice.	1-(2-trifluoromethylphenyl)imidazole	134-138	nitric oxide synthase 1, neuronal	Mus musculus	18-39
17345819-1	2006	INTRODUCTION: New nitric oxide synthase (NOS) inhibitors: 3-bromo-7-nitroindazole (3-Br-7-NI), 1-(2-trifluoromethylphenyl) imidazole (TRIM), S-methyl-L-thiocitrulline (S-Me-TC) and 7-nitroindazole (7-NI) reduce spontaneous locomotor activity in mice.	S-methylthiocitrulline	141-166	nitric oxide synthase 1, neuronal	Mus musculus	18-39
17345819-1	2006	INTRODUCTION: New nitric oxide synthase (NOS) inhibitors: 3-bromo-7-nitroindazole (3-Br-7-NI), 1-(2-trifluoromethylphenyl) imidazole (TRIM), S-methyl-L-thiocitrulline (S-Me-TC) and 7-nitroindazole (7-NI) reduce spontaneous locomotor activity in mice.	S-methylthiocitrulline	168-175	nitric oxide synthase 1, neuronal	Mus musculus	18-39
17345819-1	2006	INTRODUCTION: New nitric oxide synthase (NOS) inhibitors: 3-bromo-7-nitroindazole (3-Br-7-NI), 1-(2-trifluoromethylphenyl) imidazole (TRIM), S-methyl-L-thiocitrulline (S-Me-TC) and 7-nitroindazole (7-NI) reduce spontaneous locomotor activity in mice.	7-nitroindazole	66-81	nitric oxide synthase 1, neuronal	Mus musculus	18-39
17345819-1	2006	INTRODUCTION: New nitric oxide synthase (NOS) inhibitors: 3-bromo-7-nitroindazole (3-Br-7-NI), 1-(2-trifluoromethylphenyl) imidazole (TRIM), S-methyl-L-thiocitrulline (S-Me-TC) and 7-nitroindazole (7-NI) reduce spontaneous locomotor activity in mice.	7-nitroindazole	88-92	nitric oxide synthase 1, neuronal	Mus musculus	18-39
17085858-1	2006	7-Nitroindazole (7NI, a nitric oxide synthase [NOS] inhibitor) administered intraperitoneally (ip), 30 min before the test, at doses ranging between 50-200 mg/kg, raised the threshold for electroconvulsions in mice.	7-nitroindazole	0-15	nitric oxide synthase 1, neuronal	Mus musculus	24-45
17085858-1	2006	7-Nitroindazole (7NI, a nitric oxide synthase [NOS] inhibitor) administered intraperitoneally (ip), 30 min before the test, at doses ranging between 50-200 mg/kg, raised the threshold for electroconvulsions in mice.	7-nitroindazole	17-20	nitric oxide synthase 1, neuronal	Mus musculus	24-45
16735094-0	2006	Neuronal nitric oxide synthase-derived nitric oxide inhibits neurogenesis in the adult dentate gyrus by down-regulating cyclic AMP response element binding protein phosphorylation.	Cyclic AMP	120-130	nitric oxide synthase 1, neuronal	Mus musculus	0-30
16716528-8	2006	The specific neuronal nitric oxide synthase inhibitor 7-nitroindazole (10 microM) and the specific inducible nitric oxide synthase inhibitor 1400W (10 microM) inhibited the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced excess in nitric oxide synthase activity by 63-70 and 13-25%, respectively.	7-nitroindazole	54-69	nitric oxide synthase 1, neuronal	Mus musculus	13-43
16716528-8	2006	The specific neuronal nitric oxide synthase inhibitor 7-nitroindazole (10 microM) and the specific inducible nitric oxide synthase inhibitor 1400W (10 microM) inhibited the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced excess in nitric oxide synthase activity by 63-70 and 13-25%, respectively.	-phenyl-1,2,3,6-tetrahydropyridine	183-217	nitric oxide synthase 1, neuronal	Mus musculus	13-43
16809378-4	2006	Therefore, the treatment with DHEA diminished both ovarian nitric oxide synthase (NOS) activity and prostaglandin E (PGE) production.	Dehydroepiandrosterone	30-34	nitric oxide synthase 1, neuronal	Mus musculus	59-80
16735094-3	2006	Here we show that 5-bromodeoxyuridine-labeled dividing progenitor cells in the dentate gyrus were significantly increased in mice receiving 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitor, and in null mutant mice lacking neuronal nitric oxide synthase gene (nNOS-/-) 6 h and 4 weeks after 5-bromodeoxyuridine incorporation.	Bromodeoxyuridine	18-37	nitric oxide synthase 1, neuronal	Mus musculus	169-199
16735094-3	2006	Here we show that 5-bromodeoxyuridine-labeled dividing progenitor cells in the dentate gyrus were significantly increased in mice receiving 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitor, and in null mutant mice lacking neuronal nitric oxide synthase gene (nNOS-/-) 6 h and 4 weeks after 5-bromodeoxyuridine incorporation.	Bromodeoxyuridine	18-37	nitric oxide synthase 1, neuronal	Mus musculus	243-273
16735094-3	2006	Here we show that 5-bromodeoxyuridine-labeled dividing progenitor cells in the dentate gyrus were significantly increased in mice receiving 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitor, and in null mutant mice lacking neuronal nitric oxide synthase gene (nNOS-/-) 6 h and 4 weeks after 5-bromodeoxyuridine incorporation.	7-nitroindazole	140-155	nitric oxide synthase 1, neuronal	Mus musculus	169-199
16735094-3	2006	Here we show that 5-bromodeoxyuridine-labeled dividing progenitor cells in the dentate gyrus were significantly increased in mice receiving 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitor, and in null mutant mice lacking neuronal nitric oxide synthase gene (nNOS-/-) 6 h and 4 weeks after 5-bromodeoxyuridine incorporation.	7-nitroindazole	140-155	nitric oxide synthase 1, neuronal	Mus musculus	243-273
16735094-6	2006	Furthermore, neuronal nitric oxide synthase inhibition significantly enhanced the survival of newborn cells and the number of 5-bromodeoxyuridine positive/NeuN positive cells in the dentate gyrus.	Bromodeoxyuridine	126-145	nitric oxide synthase 1, neuronal	Mus musculus	13-43
16735094-7	2006	These results indicate that neuronal nitric oxide synthase-derived nitric oxide suppresses neurogenesis in the adult dentate gyrus, in which N-methyl-D-aspartate receptor functions and cyclic AMP response element binding protein phosphorylation may be involved.	Cyclic AMP	185-195	nitric oxide synthase 1, neuronal	Mus musculus	28-58
16837587-6	2006	The predominantly presynaptic LTP in the GluR1 knock-outs was blocked by postsynaptic antagonism of nitric oxide synthase (NOS), either with intracellular N-omega-nitro-L-arginine methyl ester or N-nitro-L-arginine, providing the first evidence for a retrograde transmitter role for NO at this synapse.	NG-Nitroarginine Methyl Ester	155-192	nitric oxide synthase 1, neuronal	Mus musculus	100-121
16837587-6	2006	The predominantly presynaptic LTP in the GluR1 knock-outs was blocked by postsynaptic antagonism of nitric oxide synthase (NOS), either with intracellular N-omega-nitro-L-arginine methyl ester or N-nitro-L-arginine, providing the first evidence for a retrograde transmitter role for NO at this synapse.	Nitroarginine	196-214	nitric oxide synthase 1, neuronal	Mus musculus	100-121
16713369-9	2006	In nNOS-/- group, heart rate reflex by PE injection was significantly reduced (P&lt;0.05).	Phenylephrine	39-41	nitric oxide synthase 1, neuronal	Mus musculus	3-7
16380459-10	2006	Low chloride increased COX-2 expression (2.7 +/- 0.4-fold control, n = 6, P &lt; 0.01) and pp38 expression (2.8 +/- 0.3-fold; n = 5, P &lt; 0.01), which were reversed by the specific NO synthase (NOS) inhibitor 7-nitroindazole.	Chlorides	4-12	nitric oxide synthase 1, neuronal	Mus musculus	183-194
16621629-3	2006	The treatment of mice with NO synthase (NOS) inhibitors, NG-nitro-l-arginine, aminoguanidine or with a soluble guanylate cyclase (sGC) inhibitor, ODQ enhanced LPS- or Cg-induced neutrophil migration, rolling and adhesion on venular endothelium.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	146-149	nitric oxide synthase 1, neuronal	Mus musculus	27-38
16698049-3	2006	The aims of the present study were to investigate: a) the acquisition, expression, maintenance and reinstatement of cocaine CPP from periadolescence (PD24-45) through adulthood (PD70); b) potential sexual dimorphism in adolescence and adulthood in response to cocaine-induced CPP; and c) the role of the neuronal nitric oxide synthase (nNOS) gene in long-term neural plasticity underlying responsiveness to cocaine and cocaine-associated cues.	Cocaine	116-123	nitric oxide synthase 1, neuronal	Mus musculus	304-334
16698049-3	2006	The aims of the present study were to investigate: a) the acquisition, expression, maintenance and reinstatement of cocaine CPP from periadolescence (PD24-45) through adulthood (PD70); b) potential sexual dimorphism in adolescence and adulthood in response to cocaine-induced CPP; and c) the role of the neuronal nitric oxide synthase (nNOS) gene in long-term neural plasticity underlying responsiveness to cocaine and cocaine-associated cues.	Cocaine	116-123	nitric oxide synthase 1, neuronal	Mus musculus	336-340
16698049-6	2006	In contrast, cocaine CPP acquired between PD26 and PD31 in adolescent nNOS knockout (KO) mice, was neither maintained nor reinstated by cocaine.	Cocaine	13-20	nitric oxide synthase 1, neuronal	Mus musculus	70-74
16698049-11	2006	Results suggest that the nNOS gene is essential during adolescence of both sexes for the development of long-term neural plasticity underlying responsiveness to the incentive value of cocaine reward.	Cocaine	184-191	nitric oxide synthase 1, neuronal	Mus musculus	25-29
16386798-5	2006	Nitric oxide synthase (NOS) catalyzes nitric oxide (NO) formation.	Nitric Oxide	38-50	nitric oxide synthase 1, neuronal	Mus musculus	0-21
16551646-7	2006	Immunofluorescence studies employing terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (DUTP)-biotin nick-end labeling revealed the presence of apoptotic neurons expressing neuronal nitric oxide synthase (NOS), choline acetyltransferase, and enkephalin in both the striatum and globus pallidus.	deoxyuridine triphosphate	84-109	nitric oxide synthase 1, neuronal	Mus musculus	196-226
16551646-7	2006	Immunofluorescence studies employing terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (DUTP)-biotin nick-end labeling revealed the presence of apoptotic neurons expressing neuronal nitric oxide synthase (NOS), choline acetyltransferase, and enkephalin in both the striatum and globus pallidus.	deoxyuridine triphosphate	111-115	nitric oxide synthase 1, neuronal	Mus musculus	196-226
16357097-13	2006	Thus nitric oxide inhibits the AVP secretory response induced by ET(B) receptor activation within the hypothalamo-neurohypophyseal system and is generated primarily by the nNOS isoform.	Nitric Oxide	5-17	nitric oxide synthase 1, neuronal	Mus musculus	172-176
16700725-5	2006	The inhibitory effect of prokineticin 1 on giant contractions was blocked by the nitric oxide synthase (NOS) inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME).	NG-Nitroarginine Methyl Ester	119-155	nitric oxide synthase 1, neuronal	Mus musculus	81-102
16700725-5	2006	The inhibitory effect of prokineticin 1 on giant contractions was blocked by the nitric oxide synthase (NOS) inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME).	NG-Nitroarginine Methyl Ester	157-163	nitric oxide synthase 1, neuronal	Mus musculus	81-102
16556439-6	2006	administration of NG-nitro-L-arginine methyl ester (L-NAME, 30 nmol), a nitric oxide synthase (NOS) inhibitor, in naive mice.	NG-Nitroarginine Methyl Ester	18-50	nitric oxide synthase 1, neuronal	Mus musculus	72-93
16339386-8	2006	After infusion of the neuronal nitric oxide synthase (nNOS) inhibitor S-methylthiocitrulline, SNGFR fell in both db/db and db/m mice.	S-methylthiocitrulline	70-92	nitric oxide synthase 1, neuronal	Mus musculus	22-52
16339386-8	2006	After infusion of the neuronal nitric oxide synthase (nNOS) inhibitor S-methylthiocitrulline, SNGFR fell in both db/db and db/m mice.	S-methylthiocitrulline	70-92	nitric oxide synthase 1, neuronal	Mus musculus	54-58
16380459-11	2006	Administration of a low-salt diet increased immunoreactive COX-2 and neuronal NOS (nNOS) in the macula densa and surrounding cTAL of kidneys of wild-type mice but did not significantly elevate COX-2 expression in nNOS-/- mice.	Salts	24-28	nitric oxide synthase 1, neuronal	Mus musculus	69-81
16380459-11	2006	Administration of a low-salt diet increased immunoreactive COX-2 and neuronal NOS (nNOS) in the macula densa and surrounding cTAL of kidneys of wild-type mice but did not significantly elevate COX-2 expression in nNOS-/- mice.	Salts	24-28	nitric oxide synthase 1, neuronal	Mus musculus	83-87
16510153-14	2006	The nNOS-cGMP pathway negatively modulates beta(3)-AR activation.	Cyclic GMP	9-13	nitric oxide synthase 1, neuronal	Mus musculus	4-8
16557219-1	2006	In the last decade, various groups have found evidence of nitric oxide production by mitochondrial nitric oxide synthase (mNOS) in a range of experimental models.	Nitric Oxide	58-70	nitric oxide synthase 1, neuronal	Mus musculus	122-126
16425058-1	2006	RATIONALE: Sildenafil citrate is widely prescribed for erectile dysfunction and acts by inhibiting phosphodiesterase type-5, resulting in accumulation of cyclic-guanosine monophosphate (cGMP) via activation of nitric oxide synthase (NOS).	Sildenafil Citrate	11-29	nitric oxide synthase 1, neuronal	Mus musculus	210-231
16425058-1	2006	RATIONALE: Sildenafil citrate is widely prescribed for erectile dysfunction and acts by inhibiting phosphodiesterase type-5, resulting in accumulation of cyclic-guanosine monophosphate (cGMP) via activation of nitric oxide synthase (NOS).	Cyclic GMP	154-184	nitric oxide synthase 1, neuronal	Mus musculus	210-231
16425058-1	2006	RATIONALE: Sildenafil citrate is widely prescribed for erectile dysfunction and acts by inhibiting phosphodiesterase type-5, resulting in accumulation of cyclic-guanosine monophosphate (cGMP) via activation of nitric oxide synthase (NOS).	Cyclic GMP	186-190	nitric oxide synthase 1, neuronal	Mus musculus	210-231
16536556-1	2006	Intersubunit intramolecular electron transfer (IET) from FMN to heme is essential in the delivery of electrons required for O2 activation in the heme domain and the subsequent nitric oxide (NO) synthesis by NO synthase (NOS).	1-(4-CYANO-PHENYL)-3-[2-(2,6-DICHLORO-PHENYL)-1-IMINO-ETHYL]-THIOUREA	47-50	nitric oxide synthase 1, neuronal	Mus musculus	207-218
16536556-1	2006	Intersubunit intramolecular electron transfer (IET) from FMN to heme is essential in the delivery of electrons required for O2 activation in the heme domain and the subsequent nitric oxide (NO) synthesis by NO synthase (NOS).	Flavin Mononucleotide	57-60	nitric oxide synthase 1, neuronal	Mus musculus	207-218
16536556-1	2006	Intersubunit intramolecular electron transfer (IET) from FMN to heme is essential in the delivery of electrons required for O2 activation in the heme domain and the subsequent nitric oxide (NO) synthesis by NO synthase (NOS).	Heme	64-68	nitric oxide synthase 1, neuronal	Mus musculus	207-218
16536556-1	2006	Intersubunit intramolecular electron transfer (IET) from FMN to heme is essential in the delivery of electrons required for O2 activation in the heme domain and the subsequent nitric oxide (NO) synthesis by NO synthase (NOS).	Oxygen	124-126	nitric oxide synthase 1, neuronal	Mus musculus	207-218
16536556-1	2006	Intersubunit intramolecular electron transfer (IET) from FMN to heme is essential in the delivery of electrons required for O2 activation in the heme domain and the subsequent nitric oxide (NO) synthesis by NO synthase (NOS).	Heme	145-149	nitric oxide synthase 1, neuronal	Mus musculus	207-218
16536556-1	2006	Intersubunit intramolecular electron transfer (IET) from FMN to heme is essential in the delivery of electrons required for O2 activation in the heme domain and the subsequent nitric oxide (NO) synthesis by NO synthase (NOS).	Nitric Oxide	176-188	nitric oxide synthase 1, neuronal	Mus musculus	207-218
16300892-0	2006	Differential effects of morphine- and cocaine-induced nNOS immunoreactivity in the dentate gyrus of hippocampus of mice lacking mu-opioid receptors.	Morphine	24-32	nitric oxide synthase 1, neuronal	Mus musculus	54-58
16300892-0	2006	Differential effects of morphine- and cocaine-induced nNOS immunoreactivity in the dentate gyrus of hippocampus of mice lacking mu-opioid receptors.	Cocaine	38-45	nitric oxide synthase 1, neuronal	Mus musculus	54-58
16300892-1	2006	This study investigated the expression of nNOS after repeated morphine or cocaine administration in order to determine if nNOS (neuronal nitric oxide synthase) is involved in the morphine- or cocaine-induced behavioral sensitization in mu-opioid receptor knockout (MOR(-/-)) mice.	Morphine	62-70	nitric oxide synthase 1, neuronal	Mus musculus	42-46
16300892-1	2006	This study investigated the expression of nNOS after repeated morphine or cocaine administration in order to determine if nNOS (neuronal nitric oxide synthase) is involved in the morphine- or cocaine-induced behavioral sensitization in mu-opioid receptor knockout (MOR(-/-)) mice.	Cocaine	74-81	nitric oxide synthase 1, neuronal	Mus musculus	42-46
16300892-1	2006	This study investigated the expression of nNOS after repeated morphine or cocaine administration in order to determine if nNOS (neuronal nitric oxide synthase) is involved in the morphine- or cocaine-induced behavioral sensitization in mu-opioid receptor knockout (MOR(-/-)) mice.	Morphine	179-187	nitric oxide synthase 1, neuronal	Mus musculus	122-126
16300892-1	2006	This study investigated the expression of nNOS after repeated morphine or cocaine administration in order to determine if nNOS (neuronal nitric oxide synthase) is involved in the morphine- or cocaine-induced behavioral sensitization in mu-opioid receptor knockout (MOR(-/-)) mice.	Morphine	179-187	nitric oxide synthase 1, neuronal	Mus musculus	128-158
16300892-1	2006	This study investigated the expression of nNOS after repeated morphine or cocaine administration in order to determine if nNOS (neuronal nitric oxide synthase) is involved in the morphine- or cocaine-induced behavioral sensitization in mu-opioid receptor knockout (MOR(-/-)) mice.	Cocaine	192-199	nitric oxide synthase 1, neuronal	Mus musculus	122-126
16300892-1	2006	This study investigated the expression of nNOS after repeated morphine or cocaine administration in order to determine if nNOS (neuronal nitric oxide synthase) is involved in the morphine- or cocaine-induced behavioral sensitization in mu-opioid receptor knockout (MOR(-/-)) mice.	Cocaine	192-199	nitric oxide synthase 1, neuronal	Mus musculus	128-158
16300892-2	2006	Higher numbers of nNOS-positive cells were observed in the dentate gyrus of the hippocampus (DG) of the wild-type (MOR(+/+)) mice repeatedly treated with either morphine or cocaine than in the saline treated MOR(+/+) mice (morphine, +122%; cocaine, +82%).	Morphine	161-169	nitric oxide synthase 1, neuronal	Mus musculus	18-22
16300892-2	2006	Higher numbers of nNOS-positive cells were observed in the dentate gyrus of the hippocampus (DG) of the wild-type (MOR(+/+)) mice repeatedly treated with either morphine or cocaine than in the saline treated MOR(+/+) mice (morphine, +122%; cocaine, +82%).	Cocaine	173-180	nitric oxide synthase 1, neuronal	Mus musculus	18-22
16300892-2	2006	Higher numbers of nNOS-positive cells were observed in the dentate gyrus of the hippocampus (DG) of the wild-type (MOR(+/+)) mice repeatedly treated with either morphine or cocaine than in the saline treated MOR(+/+) mice (morphine, +122%; cocaine, +82%).	Morphine	223-231	nitric oxide synthase 1, neuronal	Mus musculus	18-22
16300892-2	2006	Higher numbers of nNOS-positive cells were observed in the dentate gyrus of the hippocampus (DG) of the wild-type (MOR(+/+)) mice repeatedly treated with either morphine or cocaine than in the saline treated MOR(+/+) mice (morphine, +122%; cocaine, +82%).	Cocaine	240-247	nitric oxide synthase 1, neuronal	Mus musculus	18-22
16300892-3	2006	Moreover, the MOR(-/-) mice also showed significantly higher morphine- or cocaine-induced nNOS expression levels in the DG than in the saline treated MOR(+/+) mice (morphine, +234%; cocaine, +54%).	Morphine	61-69	nitric oxide synthase 1, neuronal	Mus musculus	90-94
16300892-3	2006	Moreover, the MOR(-/-) mice also showed significantly higher morphine- or cocaine-induced nNOS expression levels in the DG than in the saline treated MOR(+/+) mice (morphine, +234%; cocaine, +54%).	Cocaine	74-81	nitric oxide synthase 1, neuronal	Mus musculus	90-94
16300892-4	2006	The MOR(-/-) mice showed a significantly higher morphine-induced nNOS expression level (+103%) or a lower cocaine-induced nNOS expression level (+38%) in the DG than in the morphine- or cocaine-treated MOR(+/+) mice.	Cocaine	106-113	nitric oxide synthase 1, neuronal	Mus musculus	122-126
16300892-5	2006	These results suggest that morphine and cocaine sensitization is differentially regulated by the mu-opioid receptors in MOR(-/-) mice via the nNOS systems in the DG.	Morphine	27-35	nitric oxide synthase 1, neuronal	Mus musculus	142-146
16300892-5	2006	These results suggest that morphine and cocaine sensitization is differentially regulated by the mu-opioid receptors in MOR(-/-) mice via the nNOS systems in the DG.	Cocaine	40-47	nitric oxide synthase 1, neuronal	Mus musculus	142-146
16476419-2	2006	Considering that NMDA receptor triggers activation of neuronal nitric oxide synthase (nNOS), enzyme that produces nitric oxide (NO), this study investigated the effects of intra-PAG infusions of NPLA (Nomega-propyl-L-arginine), an nNOS inhibitor, on behavioral and antinociceptive responses induced by local injection of NMDA receptor agonist in mice.	Nitric Oxide	63-75	nitric oxide synthase 1, neuronal	Mus musculus	86-90
16385082-6	2006	In sham controls, ACh induced dose-dependent vasodilation that was blocked by the nitric oxide synthase (NOS) inhibitor L-NMMA (10 micromol/L), suggesting a key role for NO.	Acetylcholine	18-21	nitric oxide synthase 1, neuronal	Mus musculus	82-103
16385082-6	2006	In sham controls, ACh induced dose-dependent vasodilation that was blocked by the nitric oxide synthase (NOS) inhibitor L-NMMA (10 micromol/L), suggesting a key role for NO.	omega-N-Methylarginine	120-126	nitric oxide synthase 1, neuronal	Mus musculus	82-103
16431879-0	2006	Inhibition of neuronal nitric oxide synthase reduces isoflurane MAC and motor activity even in nNOS knockout mice.	nitric	23-29	nitric oxide synthase 1, neuronal	Mus musculus	95-99
16431879-2	2006	However, mice deficient in the type I NOS isoform (nNOS) are reported to have a similar MAC for isoflurane and are not affected by non-isoform specific inhibitors.	Isoflurane	96-106	nitric oxide synthase 1, neuronal	Mus musculus	51-55
16431879-3	2006	METHODS: We determined whether the nNOS specific inhibitor, 7-nitroindazole (7-NI), had an effect on isoflurane MAC and righting reflex (RRF) and investigated spontaneous motor activity in an open-field study in wild-type (WT) and knockout (KO) mice.	7-nitroindazole	60-75	nitric oxide synthase 1, neuronal	Mus musculus	35-39
16431879-3	2006	METHODS: We determined whether the nNOS specific inhibitor, 7-nitroindazole (7-NI), had an effect on isoflurane MAC and righting reflex (RRF) and investigated spontaneous motor activity in an open-field study in wild-type (WT) and knockout (KO) mice.	7-nitroindazole	77-81	nitric oxide synthase 1, neuronal	Mus musculus	35-39
16431879-3	2006	METHODS: We determined whether the nNOS specific inhibitor, 7-nitroindazole (7-NI), had an effect on isoflurane MAC and righting reflex (RRF) and investigated spontaneous motor activity in an open-field study in wild-type (WT) and knockout (KO) mice.	Isoflurane	101-111	nitric oxide synthase 1, neuronal	Mus musculus	35-39
16567525-3	2006	Hence, TDP in mouse islets may be kept suppressed by neuronal nitric oxide (NO) synthase (nNOS), an NADPH-utilizing enzyme with alkaline pH optimum.	NADP	100-105	nitric oxide synthase 1, neuronal	Mus musculus	90-94
16567525-8	2006	Remarkably, glucose produced strong TDP in NOS-KO islets and in wild-type islets treated with nNOS inhibitors.	Glucose	12-19	nitric oxide synthase 1, neuronal	Mus musculus	94-98
16567525-11	2006	Our results show that nNOS activity contributes to the absence of TDP in mouse islets putatively through depletion of intracellular arginine.	Arginine	132-140	nitric oxide synthase 1, neuronal	Mus musculus	22-26
16430790-0	2006	Inhibition of neuronal nitric oxide synthase reduces the propofol requirements in wild-type and nNOS knockout mice.	Propofol	57-65	nitric oxide synthase 1, neuronal	Mus musculus	14-44
16430790-0	2006	Inhibition of neuronal nitric oxide synthase reduces the propofol requirements in wild-type and nNOS knockout mice.	Propofol	57-65	nitric oxide synthase 1, neuronal	Mus musculus	96-100
16430790-3	2006	We hypothesized that the neuronal nitric oxide synthase selective inhibitor, 7-nitroindazole, would also reduce the propofol requirements in wild-type mice but would have no effect in neuronal nitric oxide synthase knockout mice.	7-nitroindazole	77-92	nitric oxide synthase 1, neuronal	Mus musculus	25-55
16430790-3	2006	We hypothesized that the neuronal nitric oxide synthase selective inhibitor, 7-nitroindazole, would also reduce the propofol requirements in wild-type mice but would have no effect in neuronal nitric oxide synthase knockout mice.	Propofol	116-124	nitric oxide synthase 1, neuronal	Mus musculus	25-55
16430790-4	2006	METHODS: We determined the time to loss of righting reflex, time to painful stimulus and time to regaining the righting reflex in neuronal nitric oxide synthase knockout and wild-type mice following the intraperitoneal injection of propofol in untreated, 7-nitroindazole and vehicle only treated animals (n = 6 per group).	Propofol	232-240	nitric oxide synthase 1, neuronal	Mus musculus	130-160
16299067-6	2006	The nitric-oxide synthase (NOS) inhibitors 7-nitroindazole (7-NI) and N-omega-nitro-L-arginine methyl ester also reduced NMDA toxicity.	7-nitroindazole	43-58	nitric oxide synthase 1, neuronal	Mus musculus	4-25
16299067-6	2006	The nitric-oxide synthase (NOS) inhibitors 7-nitroindazole (7-NI) and N-omega-nitro-L-arginine methyl ester also reduced NMDA toxicity.	7-nitroindazole	60-64	nitric oxide synthase 1, neuronal	Mus musculus	4-25
16299067-6	2006	The nitric-oxide synthase (NOS) inhibitors 7-nitroindazole (7-NI) and N-omega-nitro-L-arginine methyl ester also reduced NMDA toxicity.	NG-Nitroarginine Methyl Ester	70-107	nitric oxide synthase 1, neuronal	Mus musculus	4-25
16299067-6	2006	The nitric-oxide synthase (NOS) inhibitors 7-nitroindazole (7-NI) and N-omega-nitro-L-arginine methyl ester also reduced NMDA toxicity.	N-Methylaspartate	121-125	nitric oxide synthase 1, neuronal	Mus musculus	4-25
16303147-3	2006	Here we investigated whether arundic acid, an astrocyte-modulating agent, can protect against alterations of nitric oxide synthase (NOS) and superoxide dismutase (SOD) expression on MPTP neurotoxicity in mice, utilizing an immunohistochemistry.	ONO2506	29-41	nitric oxide synthase 1, neuronal	Mus musculus	109-130
16488973-4	2006	We show that the beta splice variant of nNOS elicits normal erection despite a decrease in stimulus-response characteristics and a 5-fold increased sensitivity to the NOS inhibitor, l-NAME.	NG-Nitroarginine Methyl Ester	182-188	nitric oxide synthase 1, neuronal	Mus musculus	40-44
16310374-1	2006	We examined whether nitric oxide (NO), derived from constitutive NO synthase (NOS) and/or inducible NOS (iNOS), could contribute to endotoxin-induced inflammatory hyperalgesia via interacting with nuclear factor-kappaB (NF-kappaB), inducible cyclooxygenase (COX-2) and/or polyADP-ribose synthase (PARS).	Nitric Oxide	20-32	nitric oxide synthase 1, neuronal	Mus musculus	65-76
16406488-6	2006	Combination of per se non-effective doses of melatonin (10 and 20 mg/kg) and nitric oxide synthase (NOS) substrate L-arginine (30, 60 mg/kg) showed a significant anticonvulsant activity.	Arginine	115-125	nitric oxide synthase 1, neuronal	Mus musculus	77-98
16380099-7	2006	Furthermore, the potentiative effect of bLF was partially blocked by pre-treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and completely blocked by 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor.	CHEMBL2024323	40-43	nitric oxide synthase 1, neuronal	Mus musculus	148-169
16380099-7	2006	Furthermore, the potentiative effect of bLF was partially blocked by pre-treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and completely blocked by 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor.	CHEMBL2024323	40-43	nitric oxide synthase 1, neuronal	Mus musculus	249-261
16380099-7	2006	Furthermore, the potentiative effect of bLF was partially blocked by pre-treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and completely blocked by 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor.	CHEMBL2024323	40-43	nitric oxide synthase 1, neuronal	Mus musculus	263-267
16380099-7	2006	Furthermore, the potentiative effect of bLF was partially blocked by pre-treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and completely blocked by 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor.	NG-Nitroarginine Methyl Ester	88-122	nitric oxide synthase 1, neuronal	Mus musculus	148-169
16380099-7	2006	Furthermore, the potentiative effect of bLF was partially blocked by pre-treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and completely blocked by 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor.	NG-Nitroarginine Methyl Ester	88-122	nitric oxide synthase 1, neuronal	Mus musculus	249-261
16380099-7	2006	Furthermore, the potentiative effect of bLF was partially blocked by pre-treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and completely blocked by 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor.	NG-Nitroarginine Methyl Ester	88-122	nitric oxide synthase 1, neuronal	Mus musculus	263-267
16380099-7	2006	Furthermore, the potentiative effect of bLF was partially blocked by pre-treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and completely blocked by 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor.	NG-Nitroarginine Methyl Ester	124-130	nitric oxide synthase 1, neuronal	Mus musculus	148-169
16380099-7	2006	Furthermore, the potentiative effect of bLF was partially blocked by pre-treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and completely blocked by 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor.	NG-Nitroarginine Methyl Ester	124-130	nitric oxide synthase 1, neuronal	Mus musculus	249-261
16380099-7	2006	Furthermore, the potentiative effect of bLF was partially blocked by pre-treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and completely blocked by 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor.	NG-Nitroarginine Methyl Ester	124-130	nitric oxide synthase 1, neuronal	Mus musculus	263-267
16380099-11	2006	We conclude that bLF may block the development of tolerance to morphine in mice, possibly via the selective activation of nNOS.	CHEMBL2024323	17-20	nitric oxide synthase 1, neuronal	Mus musculus	122-126
16380099-11	2006	We conclude that bLF may block the development of tolerance to morphine in mice, possibly via the selective activation of nNOS.	Morphine	63-71	nitric oxide synthase 1, neuronal	Mus musculus	122-126
16226732-7	2006	The nNOS inhibitor 7-nitroindazole or NO scavenger HbO2 restored CR500 in septic WT mice, but blockade of soluble guanylate cyclase had no effect.	7-nitroindazole	19-34	nitric oxide synthase 1, neuronal	Mus musculus	4-8
16182446-3	2006	Phosphorylated Ng reduces the affinity of Ng to bind CaM, which may affect the activities of calmodulin-dependent downstream enzymes, such as nitric oxide synthase (NOS), CaM-dependent protein kinase II (CaMKII) and adenylate cyclase (AC).	Nitroglycerin	15-17	nitric oxide synthase 1, neuronal	Mus musculus	142-163
16182446-3	2006	Phosphorylated Ng reduces the affinity of Ng to bind CaM, which may affect the activities of calmodulin-dependent downstream enzymes, such as nitric oxide synthase (NOS), CaM-dependent protein kinase II (CaMKII) and adenylate cyclase (AC).	Nitroglycerin	42-44	nitric oxide synthase 1, neuronal	Mus musculus	142-163
16045907-2	2006	To begin to address the mechanistic basis of this "ischemic tolerance", we used genetic and pharmacologic approaches to test the hypothesis that nitric oxide (NO) derived from one of the three NO synthase (NOS) isoforms was responsible for triggering the adaptive response to brief preconditioning ischemia.	Nitric Oxide	145-157	nitric oxide synthase 1, neuronal	Mus musculus	193-204
16845179-6	2006	Arsenic exposure also increases leukotriene E4 (LTE4) formation in both the mice and BAECs, an effect that is partially reversed by the addition of Nomega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor.	Arsenic	0-7	nitric oxide synthase 1, neuronal	Mus musculus	197-218
16845179-6	2006	Arsenic exposure also increases leukotriene E4 (LTE4) formation in both the mice and BAECs, an effect that is partially reversed by the addition of Nomega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor.	Leukotriene E4	48-52	nitric oxide synthase 1, neuronal	Mus musculus	197-218
16365445-6	2006	In contrast, neuronal NOS (NOS1)-deficient mice and wild-type mice treated with the nonspecific NOS inhibitor NG-nitro-L-arginine methyl ester and the NOS1-specific inhibitor 7-nitroindazole all had delayed parasite clearance.	NG-Nitroarginine Methyl Ester	110-142	nitric oxide synthase 1, neuronal	Mus musculus	27-31
16365445-6	2006	In contrast, neuronal NOS (NOS1)-deficient mice and wild-type mice treated with the nonspecific NOS inhibitor NG-nitro-L-arginine methyl ester and the NOS1-specific inhibitor 7-nitroindazole all had delayed parasite clearance.	7-nitroindazole	175-190	nitric oxide synthase 1, neuronal	Mus musculus	151-155
17051348-2	2006	Since L-Arg supply may limit nitric oxide synthase (NOS) activity in endothelial cells, we examined L-Arg supplementation in differentiating mouse myoblasts and tested the hypothesis that L-Arg exerts direct effects on myoblast fusion via augmentation of endogenous nitric oxide production.	Arginine	6-11	nitric oxide synthase 1, neuronal	Mus musculus	29-50
16174992-7	2006	The selective inhibition of neuronal isoform of nitric oxide synthase (N-NOS) activity by 7-nitroindazole significantly reduced the levels of COX-2 mRNA in Atg-/- mice by 54.1%.	7-nitroindazole	90-105	nitric oxide synthase 1, neuronal	Mus musculus	71-76
16483891-3	2006	Testosterone is necessary, but not sufficient, for evoking the persistent aggression, and that serotonin (5-HT) metabolism is altered in male nNOS-1-/- mice.	Serotonin	95-104	nitric oxide synthase 1, neuronal	Mus musculus	142-146
16483891-9	2006	Because of reduced serotonin turnover, the excessive aggressiveness displayed by nNOS-1-/- mice may be symptomatic of a depressive-like syndrome.	Serotonin	19-28	nitric oxide synthase 1, neuronal	Mus musculus	81-85
16836960-5	2006	Treatment with DHEA increased ovarian oxidative stress and diminished uterine nitric oxide synthase (NOS) activity; however, when metformin was administered together with DHEA, both ovarian oxidative stress and uterine NOS activity were not different from controls.	Dehydroepiandrosterone	15-19	nitric oxide synthase 1, neuronal	Mus musculus	78-99
16598948-0	2006	[Effects of taurine and zinc on activity of NOS and expression of nNOS in cerebral cortex of acute hypoxic mice].	Taurine	12-19	nitric oxide synthase 1, neuronal	Mus musculus	66-70
16598948-1	2006	OBJECTIVE: To explore the effect of taurine and zinc on vigor of nitric oxide synthase (NOS) and the expression level of neuronal nitric oxide synthase (nNOS) in the cerebral cortex of acute hypoxic mice and the their neuroprotective effects.	Taurine	36-43	nitric oxide synthase 1, neuronal	Mus musculus	65-86
16598948-4	2006	Compared with the NS group, the number of NADPH-d positive neurons and nNOS positive neurons in cerebral cortex of zinc sulfate group were significantly decreased, while those of the taurine and zinc sulfate group were significantly decreased than the zinc sulfate group (P &lt; 0.05).	Zinc Sulfate	115-127	nitric oxide synthase 1, neuronal	Mus musculus	71-75
16598948-5	2006	CONCLUSION: Both taurine and zinc could prolong the anoxia endurance, perhaps they might play an important role in decreasing the level of nitric oxide synthase to protect the brain against hypoxic damage.	Taurine	17-24	nitric oxide synthase 1, neuronal	Mus musculus	139-160
16836960-5	2006	Treatment with DHEA increased ovarian oxidative stress and diminished uterine nitric oxide synthase (NOS) activity; however, when metformin was administered together with DHEA, both ovarian oxidative stress and uterine NOS activity were not different from controls.	Metformin	130-139	nitric oxide synthase 1, neuronal	Mus musculus	78-99
16182432-4	2005	IN VITRO STUDIES: Cell viability and levels of p-nNOS expression were observed in PCB-treated (Aroclor 1254, 5 microg/ml) immortalized dopaminergic cell line (CATH.a cells).	Chlorodiphenyl (54% Chlorine)	95-107	nitric oxide synthase 1, neuronal	Mus musculus	49-53
16344403-5	2005	Sham-operated nNOS(-/-) mice showed enhanced basal LV contractility (P&lt;0.03 versus WT, as evaluated by preload-recruitable stroke work) but an attenuated inotropic response to dobutamine infusion (P&lt;0.01 versus WT).	Dobutamine	179-189	nitric oxide synthase 1, neuronal	Mus musculus	14-18
16297560-6	2005	Furthermore, intrathecal injection of either L-NAME or 7-nitroindazole, a selective nNOS inhibitor, markedly attenuated mechanical pain hypersensitivity at both 2 and 24h after CFA injection.	NG-Nitroarginine Methyl Ester	45-51	nitric oxide synthase 1, neuronal	Mus musculus	84-88
16297560-6	2005	Furthermore, intrathecal injection of either L-NAME or 7-nitroindazole, a selective nNOS inhibitor, markedly attenuated mechanical pain hypersensitivity at both 2 and 24h after CFA injection.	7-nitroindazole	55-70	nitric oxide synthase 1, neuronal	Mus musculus	84-88
16344403-10	2005	In contrast, infarcted nNOS(-/-) mice responded to dobutamine with a dramatic fall in LV contractility (P&lt;0.01 for preload-recruitable stroke work).	Dobutamine	51-61	nitric oxide synthase 1, neuronal	Mus musculus	23-27
16303975-2	2005	One factor involves excitatory amino acid stimulation of N-methyl-D-aspartate (NMDA)-type glutamate receptors, excessive Ca2+ influx, and formation of nitric oxide (NO) via neuronal NO synthase (nNOS).	Nitric Oxide	151-163	nitric oxide synthase 1, neuronal	Mus musculus	195-199
16303975-0	2005	Activation of matrix metalloproteinase-9 via neuronal nitric oxide synthase contributes to NMDA-induced retinal ganglion cell death.	N-Methylaspartate	91-95	nitric oxide synthase 1, neuronal	Mus musculus	45-75
16303975-2	2005	One factor involves excitatory amino acid stimulation of N-methyl-D-aspartate (NMDA)-type glutamate receptors, excessive Ca2+ influx, and formation of nitric oxide (NO) via neuronal NO synthase (nNOS).	Excitatory Amino Acids	20-41	nitric oxide synthase 1, neuronal	Mus musculus	195-199
16412259-6	2005	The established cell line (NE-MD) showed a time-dependent increase in signals of the nNOS protein when they were incubated with 12 microM furosemide (an inhibitor of Na(+)-K(+)-2Cl(-) symporter) for 5 h. In conclusion, this newly developed macula densa cell line will be useful in studies of the TGF stem.	Furosemide	138-148	nitric oxide synthase 1, neuronal	Mus musculus	85-89
16412259-6	2005	The established cell line (NE-MD) showed a time-dependent increase in signals of the nNOS protein when they were incubated with 12 microM furosemide (an inhibitor of Na(+)-K(+)-2Cl(-) symporter) for 5 h. In conclusion, this newly developed macula densa cell line will be useful in studies of the TGF stem.	+)-k(+)-2cl	169-180	nitric oxide synthase 1, neuronal	Mus musculus	85-89
16301341-6	2005	Superoxide production increased after MI in both NOS1(-/-) and WT animals, although NO increased only in WT.	Superoxides	0-10	nitric oxide synthase 1, neuronal	Mus musculus	49-53
16845179-6	2006	Arsenic exposure also increases leukotriene E4 (LTE4) formation in both the mice and BAECs, an effect that is partially reversed by the addition of Nomega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor.	NG-Nitroarginine Methyl Ester	186-192	nitric oxide synthase 1, neuronal	Mus musculus	197-218
16303975-10	2005	NMDA-induced MMP activation was diminished in the retina of nNOS-/- mice, implying that S-nitrosylation of MMP had indeed occurred.	N-Methylaspartate	0-4	nitric oxide synthase 1, neuronal	Mus musculus	60-64
16139176-2	2005	Recent studies show that several behavioural effects of the psychotomimetic drug, phencyclidine (PCP), in rodents are blocked by nitric oxide synthase (NOS) inhibitors suggesting that NO plays an important role in the pharmacological effects of PCP.	Phencyclidine	82-95	nitric oxide synthase 1, neuronal	Mus musculus	129-150
16244452-3	2005	Iron-containing heme is required as a cofactor for nitric oxide synthase (NOS) which produces nitric oxide (NO).	Iron	0-4	nitric oxide synthase 1, neuronal	Mus musculus	51-72
16244452-3	2005	Iron-containing heme is required as a cofactor for nitric oxide synthase (NOS) which produces nitric oxide (NO).	Heme	16-20	nitric oxide synthase 1, neuronal	Mus musculus	51-72
16214135-0	2005	Inhibition of neuronal nitric-oxide synthase by phosphorylation at Threonine1296 in NG108-15 neuronal cells.	threonine1296	67-80	nitric oxide synthase 1, neuronal	Mus musculus	14-44
16214135-2	2005	Treatment of NG108-15 cells expressing nNOS with calyculin A, an inhibitor of protein phosphatase 1 and 2A, revealed a dose-dependent inhibition of nNOS enzyme activity with concomitant phosphorylation of Thr(1296) residue.	Threonine	205-208	nitric oxide synthase 1, neuronal	Mus musculus	39-43
16214135-5	2005	These data suggest that phosphorylation of nNOS at Thr(1296) may involve the attenuation of nitric oxide production in neuronal cells through the decrease of NADPH-binding to the enzyme.	Threonine	51-54	nitric oxide synthase 1, neuronal	Mus musculus	43-47
16214135-5	2005	These data suggest that phosphorylation of nNOS at Thr(1296) may involve the attenuation of nitric oxide production in neuronal cells through the decrease of NADPH-binding to the enzyme.	Nitric Oxide	92-104	nitric oxide synthase 1, neuronal	Mus musculus	43-47
16139176-2	2005	Recent studies show that several behavioural effects of the psychotomimetic drug, phencyclidine (PCP), in rodents are blocked by nitric oxide synthase (NOS) inhibitors suggesting that NO plays an important role in the pharmacological effects of PCP.	pcp	97-100	nitric oxide synthase 1, neuronal	Mus musculus	129-150
16139176-2	2005	Recent studies show that several behavioural effects of the psychotomimetic drug, phencyclidine (PCP), in rodents are blocked by nitric oxide synthase (NOS) inhibitors suggesting that NO plays an important role in the pharmacological effects of PCP.	pcp	245-248	nitric oxide synthase 1, neuronal	Mus musculus	129-150
16139176-4	2005	PCP treatment caused a significant and dose-related increase in prepulse inhibition in nNOS-/- mice whereas prepulse inhibition was not significantly affected in +/+ and +/- mice.	pcp	0-3	nitric oxide synthase 1, neuronal	Mus musculus	87-91
16139176-8	2005	It is concluded that nNOS plays a role in the NO-sensitive effects of PCP.	pcp	70-73	nitric oxide synthase 1, neuronal	Mus musculus	21-25
16180097-8	2005	A significant increase in the NO production by MAECs was noticed 1 h after treatment with LPS and was inhibited by L-NAME, further suggesting the involvement of nitric oxide synthase (NOS).	NG-Nitroarginine Methyl Ester	115-121	nitric oxide synthase 1, neuronal	Mus musculus	161-182
16733795-1	2005	We determined the cellular mRNA expression of all intrarenal nitric oxide (NO)-producing NO synthase (NOS) isoforms, endothelial NOS (eNOS) and neuronal NOS (nNOS) and inducible NOS (iNOS) in kidneys from wild-type mice (WT) and immune deficient Toll-like receptor 4 (TLR4) mutant mice, during normal physiological conditions and during a short-term (6-16 h) endotoxic condition caused by systemically administered lipopolysaccaride (LPS).	Nitric Oxide	61-73	nitric oxide synthase 1, neuronal	Mus musculus	89-100
16144633-7	2005	On the basis of previous data regarding the colocalization between nNOS and GABA in the mouse claustrum, we suggest that nNOS expressing neurons in the basolateral amygdalar complex are both GABAergic and non-GABAergic.	gamma-Aminobutyric Acid	76-80	nitric oxide synthase 1, neuronal	Mus musculus	121-125
16304839-6	2005	After treating the cocultures with single dose of L-NAME at the end of 1-day [corrected] coculturing, only slight effect on AChR aggregation could be found indicating that nNOS is not related to the initial formation of AChR aggregates.	NG-Nitroarginine Methyl Ester	50-56	nitric oxide synthase 1, neuronal	Mus musculus	172-176
16304839-7	2005	In contrast, when L-NAME treatment was given at the end of a 3-day coculturing, the day just before reaching the maximum extent of AChR aggregation, new AChR aggregates were hardly formed and the preformed AChR aggregates were even dispersed indicating that the enlargement of AChR aggregates is highly dependent on the nNOS activity.	NG-Nitroarginine Methyl Ester	18-24	nitric oxide synthase 1, neuronal	Mus musculus	320-324
16103686-1	2005	BACKGROUND: Although increased nitric oxide (NO) production in asthma is mediated largely by upregulation of the inducible form of nitric oxide synthase (iNOS, or NOS 2), some studies have suggested an important role for the usually constitutive neural NOS isoform (nNOS, or NOS 1).	Nitric Oxide	31-43	nitric oxide synthase 1, neuronal	Mus musculus	266-270
16087361-1	2005	Nitric oxide (NO), which is produced from l-arginine by three isoforms of NO synthase (NOS), has been implicated in reproductive functions.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	74-85
16087361-1	2005	Nitric oxide (NO), which is produced from l-arginine by three isoforms of NO synthase (NOS), has been implicated in reproductive functions.	Arginine	42-52	nitric oxide synthase 1, neuronal	Mus musculus	74-85
16103686-1	2005	BACKGROUND: Although increased nitric oxide (NO) production in asthma is mediated largely by upregulation of the inducible form of nitric oxide synthase (iNOS, or NOS 2), some studies have suggested an important role for the usually constitutive neural NOS isoform (nNOS, or NOS 1).	Nitric Oxide	31-43	nitric oxide synthase 1, neuronal	Mus musculus	275-280
16103686-4	2005	RESULTS: In addition to expected increases in NOS 2 activity, OVA challenge led to increases in calcium-dependent NOS activity, which was accounted for by increased expression of NOS 1 at both mRNA (n = 5, p &lt; 0.001) and protein levels (n = 5, p &lt; 0.01).	Calcium	96-103	nitric oxide synthase 1, neuronal	Mus musculus	179-184
15774769-1	2005	Decreased levels of tetrahydrobiopterin (BH4), an absolute cofactor for nitric oxide synthase (NOS), lead to uncoupling of NOS into a superoxide v. nitric oxide producing enzyme, and it is this uncoupling that links it to the development of vascular disease.	sapropterin	20-39	nitric oxide synthase 1, neuronal	Mus musculus	72-93
16098672-6	2005	Pretreatment with L-arginine (30-300 mg/kg, s.c.), a substrate of NO synthase (NOS), dose-dependently increased the tail-flick latencies in vincristine-treated mice.	Arginine	18-28	nitric oxide synthase 1, neuronal	Mus musculus	66-77
16098672-6	2005	Pretreatment with L-arginine (30-300 mg/kg, s.c.), a substrate of NO synthase (NOS), dose-dependently increased the tail-flick latencies in vincristine-treated mice.	Vincristine	140-151	nitric oxide synthase 1, neuronal	Mus musculus	66-77
15774769-1	2005	Decreased levels of tetrahydrobiopterin (BH4), an absolute cofactor for nitric oxide synthase (NOS), lead to uncoupling of NOS into a superoxide v. nitric oxide producing enzyme, and it is this uncoupling that links it to the development of vascular disease.	sapropterin	41-44	nitric oxide synthase 1, neuronal	Mus musculus	72-93
15774769-1	2005	Decreased levels of tetrahydrobiopterin (BH4), an absolute cofactor for nitric oxide synthase (NOS), lead to uncoupling of NOS into a superoxide v. nitric oxide producing enzyme, and it is this uncoupling that links it to the development of vascular disease.	Superoxides	134-144	nitric oxide synthase 1, neuronal	Mus musculus	72-93
15845873-7	2005	L-arginine administered rectally, but not intravenously, decreased the basal tone in wild-type, nNOS-/-, and W/W(v) mice.	Arginine	0-10	nitric oxide synthase 1, neuronal	Mus musculus	96-100
15845873-9	2005	In vitro, L-arginine decreased basal tone in wild-type and nNOS-/- IAS but not in eNOS-/- or wild-type IAS without mucosa.	Arginine	10-20	nitric oxide synthase 1, neuronal	Mus musculus	59-63
15993935-0	2005	Correlation of inbred mouse sensitivity to nitrous oxide antinociception with brain nitric oxide synthase activity following exposure to nitrous oxide.	Nitrous Oxide	43-56	nitric oxide synthase 1, neuronal	Mus musculus	84-105
16179515-13	2005	Baicalein treatment also downregulated tumor necrosis factor receptor (TNFRp55) and upregulated noninducible nitric oxide synthase (nNOS) and glutamine synthase (GS).	baicalein	0-9	nitric oxide synthase 1, neuronal	Mus musculus	96-130
16179515-13	2005	Baicalein treatment also downregulated tumor necrosis factor receptor (TNFRp55) and upregulated noninducible nitric oxide synthase (nNOS) and glutamine synthase (GS).	baicalein	0-9	nitric oxide synthase 1, neuronal	Mus musculus	132-136
15890548-1	2005	The action of nitric oxide (NO) synthesized by NO synthases (NOS) is spatially restricted.	Nitric Oxide	14-26	nitric oxide synthase 1, neuronal	Mus musculus	47-59
15890548-11	2005	Surprisingly, in nNOS-/--mice the skeletal muscle showed patterns of significant nNOS-immunoreactivity and NADPH-d activity possibly due to alternative nNOS-splice isoforms, which might be up-regulated to compensate for decreased NO formation.	NADP	107-112	nitric oxide synthase 1, neuronal	Mus musculus	17-21
15993935-0	2005	Correlation of inbred mouse sensitivity to nitrous oxide antinociception with brain nitric oxide synthase activity following exposure to nitrous oxide.	Nitrous Oxide	137-150	nitric oxide synthase 1, neuronal	Mus musculus	84-105
15993935-1	2005	Inhibition of nitric oxide synthase (NOS) antagonizes nitrous oxide (N2O)-induced antinociception in mice.	Nitrous Oxide	54-67	nitric oxide synthase 1, neuronal	Mus musculus	14-35
15993935-1	2005	Inhibition of nitric oxide synthase (NOS) antagonizes nitrous oxide (N2O)-induced antinociception in mice.	Nitrous Oxide	69-72	nitric oxide synthase 1, neuronal	Mus musculus	14-35
15983249-8	2005	Akt inhibition independently reduced neuronal nitric oxide synthase expression in Schwann cells in low-glucose cultures.	Glucose	103-110	nitric oxide synthase 1, neuronal	Mus musculus	37-67
16000635-10	2005	DNA damage, assessed as 8-hydroxy-2-deoxyguanosine and single-stranded DNA, accumulated within injured MNs and was attenuated by nNOS and iNOS deficiency.	8-ohdg	24-50	nitric oxide synthase 1, neuronal	Mus musculus	129-133
15983249-4	2005	Neuronal nitric oxide synthase expression in sciatic nerves was reduced in diabetic mice but was preserved by rosuvastatin.	Rosuvastatin Calcium	110-122	nitric oxide synthase 1, neuronal	Mus musculus	0-30
15983249-6	2005	In vitro, rosuvastatin inhibited downregulation of neuronal nitric oxide synthase expression induced by high-glucose conditions in cultured Schwann cells.	Rosuvastatin Calcium	10-22	nitric oxide synthase 1, neuronal	Mus musculus	51-81
15983249-6	2005	In vitro, rosuvastatin inhibited downregulation of neuronal nitric oxide synthase expression induced by high-glucose conditions in cultured Schwann cells.	high-glucose	104-116	nitric oxide synthase 1, neuronal	Mus musculus	51-81
15983249-7	2005	Furthermore, Akt phosphorylation in Schwann cells, downregulated by high-glucose conditions, was also restored by rosuvastatin, consistent with the change of neuronal nitric oxide synthase expression.	Rosuvastatin Calcium	114-126	nitric oxide synthase 1, neuronal	Mus musculus	158-188
15988129-0	2005	Long-term effects of high doses of nicotine on feeding behavior and brain nitric oxide synthase activity in female mice.	Nicotine	35-43	nitric oxide synthase 1, neuronal	Mus musculus	74-95
15721868-6	2005	RESULTS: Benidipine significantly inhibited protein synthesis by cardiac myocytes stimulated with phenylephrine (PE), and this effect was partially abolished by cotreatment with a nitric oxide synthase (NOS) inhibitor [N(G)-nitro-l-arginine methylester (l-NAME)].	benidipine	9-19	nitric oxide synthase 1, neuronal	Mus musculus	180-201
15979286-3	2005	KA was administered to mice with or without pretreatment with one of the following: N(G)-nitro-l-arginine methyl ester (l-NAME), an NO synthase (NOS) inhibitor that acts on both endothelial NOS (eNOS) and neuronal NOS (nNOS); 7-nitroindazole (7-NI), which acts more selectively on nNOS in vivo; or the anti-epileptic drug, phenobarbital.	NG-Nitroarginine Methyl Ester	84-118	nitric oxide synthase 1, neuronal	Mus musculus	132-143
15979286-3	2005	KA was administered to mice with or without pretreatment with one of the following: N(G)-nitro-l-arginine methyl ester (l-NAME), an NO synthase (NOS) inhibitor that acts on both endothelial NOS (eNOS) and neuronal NOS (nNOS); 7-nitroindazole (7-NI), which acts more selectively on nNOS in vivo; or the anti-epileptic drug, phenobarbital.	NG-Nitroarginine Methyl Ester	84-118	nitric oxide synthase 1, neuronal	Mus musculus	205-217
15979286-3	2005	KA was administered to mice with or without pretreatment with one of the following: N(G)-nitro-l-arginine methyl ester (l-NAME), an NO synthase (NOS) inhibitor that acts on both endothelial NOS (eNOS) and neuronal NOS (nNOS); 7-nitroindazole (7-NI), which acts more selectively on nNOS in vivo; or the anti-epileptic drug, phenobarbital.	NG-Nitroarginine Methyl Ester	84-118	nitric oxide synthase 1, neuronal	Mus musculus	219-223
15979286-3	2005	KA was administered to mice with or without pretreatment with one of the following: N(G)-nitro-l-arginine methyl ester (l-NAME), an NO synthase (NOS) inhibitor that acts on both endothelial NOS (eNOS) and neuronal NOS (nNOS); 7-nitroindazole (7-NI), which acts more selectively on nNOS in vivo; or the anti-epileptic drug, phenobarbital.	NG-Nitroarginine Methyl Ester	84-118	nitric oxide synthase 1, neuronal	Mus musculus	281-285
15979286-3	2005	KA was administered to mice with or without pretreatment with one of the following: N(G)-nitro-l-arginine methyl ester (l-NAME), an NO synthase (NOS) inhibitor that acts on both endothelial NOS (eNOS) and neuronal NOS (nNOS); 7-nitroindazole (7-NI), which acts more selectively on nNOS in vivo; or the anti-epileptic drug, phenobarbital.	NG-Nitroarginine Methyl Ester	120-126	nitric oxide synthase 1, neuronal	Mus musculus	132-143
15854753-0	2005	Reduced nNOS expression induced by repeated nicotine treatment in mu-opioid receptor knockout mice.	Nicotine	44-52	nitric oxide synthase 1, neuronal	Mus musculus	8-12
15854753-1	2005	To determine whether neuronal nitric oxide synthase (nNOS) is involved in nicotine-induced behavioral sensitization in mu-opioid receptor knockout mice we adopted an immunohistochemical approach.	Nicotine	74-82	nitric oxide synthase 1, neuronal	Mus musculus	21-51
15854753-1	2005	To determine whether neuronal nitric oxide synthase (nNOS) is involved in nicotine-induced behavioral sensitization in mu-opioid receptor knockout mice we adopted an immunohistochemical approach.	Nicotine	74-82	nitric oxide synthase 1, neuronal	Mus musculus	53-57
15854753-3	2005	Higher numbers of nNOS-positive cells were observed in the striatum of wild-type mice repeatedly treated with nicotine than in saline-treated wild-type mice.	Nicotine	110-118	nitric oxide synthase 1, neuronal	Mus musculus	18-22
15854753-3	2005	Higher numbers of nNOS-positive cells were observed in the striatum of wild-type mice repeatedly treated with nicotine than in saline-treated wild-type mice.	Sodium Chloride	127-133	nitric oxide synthase 1, neuronal	Mus musculus	18-22
15854753-4	2005	However, mu-opioid receptor knockout mice showed significantly lower nicotine-induced nNOS expression in the striatum versus wild-type mice.	Nicotine	69-77	nitric oxide synthase 1, neuronal	Mus musculus	86-90
15854753-6	2005	These findings demonstrate that the absence of mu-opioid receptors can cause a significant reduction in the expression of nNOS in the striatum, as induced by repeated nicotine treatment.	Nicotine	167-175	nitric oxide synthase 1, neuronal	Mus musculus	122-126
15824199-1	2005	BACKGROUND: GTP-cyclohydrolase 1 (GTP-CH1) catalyzes the first step for the de novo production of tetrahydrobiopterin (BH4), a cofactor for nitric oxide synthase (NOS).	sapropterin	98-117	nitric oxide synthase 1, neuronal	Mus musculus	140-161
15836918-8	2005	Provision of unspecific NOS-antagonists to TB mice increased nNOS, eNOS and iNOS in several brain nuclei (PVN, LHA, VMH), but left tumor-induced anorexia unchanged.	Terbium	43-45	nitric oxide synthase 1, neuronal	Mus musculus	61-65
15668244-9	2005	The increase of Bcl-2 expression by sildenafil was inhibited by nitric-oxide synthase (NOS) inhibitor, L-nitro-amino-methyl-ester.	Sildenafil Citrate	36-46	nitric oxide synthase 1, neuronal	Mus musculus	64-85
15546957-1	2005	The balance of arginine metabolism via nitric oxide synthase (NOS) or arginase is an important determinant of the inflammatory response of murine macrophages and dendritic cells.	Arginine	15-23	nitric oxide synthase 1, neuronal	Mus musculus	39-60
15729148-4	2005	These results suggest that neuronal nitric-oxide-synthase-derived nitric oxide may be involved in the regulation of oxytocin gene expression in the anterior commissural nucleus.	Nitric Oxide	66-78	nitric oxide synthase 1, neuronal	Mus musculus	27-57
15806417-0	2005	Combined treatment of ascorbic acid or alpha-tocopherol with dopamine receptor antagonist or nitric oxide synthase inhibitor potentiates cataleptic effect in mice.	Ascorbic Acid	22-35	nitric oxide synthase 1, neuronal	Mus musculus	93-114
15806417-0	2005	Combined treatment of ascorbic acid or alpha-tocopherol with dopamine receptor antagonist or nitric oxide synthase inhibitor potentiates cataleptic effect in mice.	alpha-Tocopherol	39-55	nitric oxide synthase 1, neuronal	Mus musculus	93-114
15956724-4	2005	The nitric oxide synthase (NOS) inhibitor L-N(G)-nitroarginine reverted this effect.	l-n(g)-nitroarginine	42-62	nitric oxide synthase 1, neuronal	Mus musculus	4-25
15824199-1	2005	BACKGROUND: GTP-cyclohydrolase 1 (GTP-CH1) catalyzes the first step for the de novo production of tetrahydrobiopterin (BH4), a cofactor for nitric oxide synthase (NOS).	sapropterin	119-122	nitric oxide synthase 1, neuronal	Mus musculus	140-161
15689952-4	2005	Similarly, treatment with the nNOS inhibitor (7-nitroindozole, 25 mg/kg) increased infarction in female C57Bl6 WT mice, but protected male mice.	7-nitroindozole	46-61	nitric oxide synthase 1, neuronal	Mus musculus	30-34
15781754-1	2005	BACKGROUND: This study was designed to determine whether overexpression of the enzyme dimethylarginine dimethylaminohydrolase (DDAH) could enhance angiogenesis by reducing levels of the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA).	dimethylarginine	86-102	nitric oxide synthase 1, neuronal	Mus musculus	197-218
15781754-1	2005	BACKGROUND: This study was designed to determine whether overexpression of the enzyme dimethylarginine dimethylaminohydrolase (DDAH) could enhance angiogenesis by reducing levels of the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA).	N,N-dimethylarginine	264-268	nitric oxide synthase 1, neuronal	Mus musculus	197-218
15721868-6	2005	RESULTS: Benidipine significantly inhibited protein synthesis by cardiac myocytes stimulated with phenylephrine (PE), and this effect was partially abolished by cotreatment with a nitric oxide synthase (NOS) inhibitor [N(G)-nitro-l-arginine methylester (l-NAME)].	Phenylephrine	113-115	nitric oxide synthase 1, neuronal	Mus musculus	180-201
15721868-6	2005	RESULTS: Benidipine significantly inhibited protein synthesis by cardiac myocytes stimulated with phenylephrine (PE), and this effect was partially abolished by cotreatment with a nitric oxide synthase (NOS) inhibitor [N(G)-nitro-l-arginine methylester (l-NAME)].	Nitroarginine	219-240	nitric oxide synthase 1, neuronal	Mus musculus	180-201
15686955-2	2005	A second group of WT mice received the nNOS inhibitor, 7-nitroindazole (WT-7NI).	7-nitroindazole	55-70	nitric oxide synthase 1, neuronal	Mus musculus	39-43
15459896-1	2005	Fas-induced death of motoneurons in vitro has been shown to involve two signaling cascades that act together to execute the death program: a Fas-Daxx-ASK-1-p38 kinase-nNOS branch, which controls transcriptional and post-translational events, and the second classical Fas-FADD-caspase-8 branch.	ammonium ferrous sulfate	0-3	nitric oxide synthase 1, neuronal	Mus musculus	167-171
15637297-0	2005	A defect of neuronal nitric oxide synthase increases xanthine oxidase-derived superoxide anion and attenuates the control of myocardial oxygen consumption by nitric oxide derived from endothelial nitric oxide synthase.	Superoxides	78-94	nitric oxide synthase 1, neuronal	Mus musculus	12-42
15637297-0	2005	A defect of neuronal nitric oxide synthase increases xanthine oxidase-derived superoxide anion and attenuates the control of myocardial oxygen consumption by nitric oxide derived from endothelial nitric oxide synthase.	Oxygen	136-142	nitric oxide synthase 1, neuronal	Mus musculus	12-42
15637297-3	2005	However, the role of nNOS in the control of MVO2 remains unknown.	mvo2	44-48	nitric oxide synthase 1, neuronal	Mus musculus	21-25
15637297-6	2005	In contrast to WT, bradykinin- or carbachol-induced reduction in MVO2 was attenuated in nNOS-/-.	Carbachol	34-43	nitric oxide synthase 1, neuronal	Mus musculus	88-92
15637297-6	2005	In contrast to WT, bradykinin- or carbachol-induced reduction in MVO2 was attenuated in nNOS-/-.	mvo2	65-69	nitric oxide synthase 1, neuronal	Mus musculus	88-92
15637297-7	2005	S-methyl-L-thiocitrulline, a potent isoform selective inhibitor of nNOS, had no effect on bradykinin-induced reduction in MVO2 in WT.	S-methylthiocitrulline	0-25	nitric oxide synthase 1, neuronal	Mus musculus	67-71
15637297-8	2005	Bradykinin-induced reduction in MVO2 in eNOS-/- mice, in which nNOS still exists, was also attenuated.	mvo2	32-36	nitric oxide synthase 1, neuronal	Mus musculus	63-67
15637297-9	2005	The attenuated bradykinin-induced reduction in MVO2 in nNOS-/- was restored by preincubation with Tiron, ascorbic acid, Tempol, oxypurinol, or SB203850, an inhibitor of p38 kinase, but not apocynin.	mvo2	47-51	nitric oxide synthase 1, neuronal	Mus musculus	55-59
15637297-9	2005	The attenuated bradykinin-induced reduction in MVO2 in nNOS-/- was restored by preincubation with Tiron, ascorbic acid, Tempol, oxypurinol, or SB203850, an inhibitor of p38 kinase, but not apocynin.	1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt	98-103	nitric oxide synthase 1, neuronal	Mus musculus	55-59
15637297-9	2005	The attenuated bradykinin-induced reduction in MVO2 in nNOS-/- was restored by preincubation with Tiron, ascorbic acid, Tempol, oxypurinol, or SB203850, an inhibitor of p38 kinase, but not apocynin.	Ascorbic Acid	105-118	nitric oxide synthase 1, neuronal	Mus musculus	55-59
15637297-9	2005	The attenuated bradykinin-induced reduction in MVO2 in nNOS-/- was restored by preincubation with Tiron, ascorbic acid, Tempol, oxypurinol, or SB203850, an inhibitor of p38 kinase, but not apocynin.	tempol	120-126	nitric oxide synthase 1, neuronal	Mus musculus	55-59
15637297-9	2005	The attenuated bradykinin-induced reduction in MVO2 in nNOS-/- was restored by preincubation with Tiron, ascorbic acid, Tempol, oxypurinol, or SB203850, an inhibitor of p38 kinase, but not apocynin.	Oxypurinol	128-138	nitric oxide synthase 1, neuronal	Mus musculus	55-59
15637297-9	2005	The attenuated bradykinin-induced reduction in MVO2 in nNOS-/- was restored by preincubation with Tiron, ascorbic acid, Tempol, oxypurinol, or SB203850, an inhibitor of p38 kinase, but not apocynin.	sb203850	143-151	nitric oxide synthase 1, neuronal	Mus musculus	55-59
15637297-9	2005	The attenuated bradykinin-induced reduction in MVO2 in nNOS-/- was restored by preincubation with Tiron, ascorbic acid, Tempol, oxypurinol, or SB203850, an inhibitor of p38 kinase, but not apocynin.	acetovanillone	189-197	nitric oxide synthase 1, neuronal	Mus musculus	55-59
15637297-10	2005	There was an increase in lucigenin-detectable superoxide anion (O2-) in cardiac tissues from nNOS-/- compared with WT.	10,10'-dimethyl-9,9'-biacridinium	25-34	nitric oxide synthase 1, neuronal	Mus musculus	93-97
15637297-10	2005	There was an increase in lucigenin-detectable superoxide anion (O2-) in cardiac tissues from nNOS-/- compared with WT.	Superoxides	46-62	nitric oxide synthase 1, neuronal	Mus musculus	93-97
15637297-10	2005	There was an increase in lucigenin-detectable superoxide anion (O2-) in cardiac tissues from nNOS-/- compared with WT.	Oxygen	64-66	nitric oxide synthase 1, neuronal	Mus musculus	93-97
15637297-13	2005	These results indicate that a defect of nNOS increases O2- through the activation of xanthine oxidase, which is mediated by the activation of p38 kinase, and attenuates the control of MVO2 by NO derived from eNOS.	mvo2	184-188	nitric oxide synthase 1, neuronal	Mus musculus	40-44
15668387-4	2005	Erectile responses to both cavernous nerve stimulation and intracavernosal injection of the NO donor diethylamine-NONOate were augmented in eNOS-/- and nNOS-/-, eNOS-/- mice but not in WT or nNOS-/- mice.	1,1-diethyl-2-hydroxy-2-nitrosohydrazine	101-121	nitric oxide synthase 1, neuronal	Mus musculus	152-156
15920994-2	2005	Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthase (NOS).	dimethylarginine	11-27	nitric oxide synthase 1, neuronal	Mus musculus	65-76
15920994-2	2005	Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthase (NOS).	N,N-dimethylarginine	29-33	nitric oxide synthase 1, neuronal	Mus musculus	65-76
15657149-5	2005	An initial rapid increase in Thr-34 phosphorylation was NMDA/alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/metabotropic glutamate-5 receptor-dependent and was mediated through activation of a neuronal nitric oxide synthase/nitric oxide/cGMP/cGMP-dependent kinase signaling cascade.	Threonine	29-32	nitric oxide synthase 1, neuronal	Mus musculus	210-240
15657149-5	2005	An initial rapid increase in Thr-34 phosphorylation was NMDA/alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/metabotropic glutamate-5 receptor-dependent and was mediated through activation of a neuronal nitric oxide synthase/nitric oxide/cGMP/cGMP-dependent kinase signaling cascade.	N-Methylaspartate	56-60	nitric oxide synthase 1, neuronal	Mus musculus	210-240
15657149-5	2005	An initial rapid increase in Thr-34 phosphorylation was NMDA/alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/metabotropic glutamate-5 receptor-dependent and was mediated through activation of a neuronal nitric oxide synthase/nitric oxide/cGMP/cGMP-dependent kinase signaling cascade.	4-isoxazolepropionic acid	92-117	nitric oxide synthase 1, neuronal	Mus musculus	210-240
15639152-3	2005	Cyclic-GMP is synthesized by guanylyl cyclase that is directly activated by the messenger molecule, nitric oxide (NO), formed throughout the CNS by the enzyme nitric oxide synthase (NOS).	Cyclic GMP	0-10	nitric oxide synthase 1, neuronal	Mus musculus	159-180
15639152-3	2005	Cyclic-GMP is synthesized by guanylyl cyclase that is directly activated by the messenger molecule, nitric oxide (NO), formed throughout the CNS by the enzyme nitric oxide synthase (NOS).	Nitric Oxide	100-112	nitric oxide synthase 1, neuronal	Mus musculus	159-180
15548548-2	2005	In order to begin to understand this differential vulnerability we compared mRNA levels of selected genes involved in N-methyl-D-aspartate (NMDA) glutamate receptor and calcium (Ca2+) signaling pathways in MSN and nNOS-IN from 12-week-old R6/2 mice, a transgenic mouse model of HD and wild-type littermates.	Calcium	169-176	nitric oxide synthase 1, neuronal	Mus musculus	214-218
15659300-9	2005	In conclusion, decreasing nitric oxide production through inhibiting constitutive nitric oxide synthase may be a mechanism through which cyclosporin A attenuates morphine-induced place preference.	Nitric Oxide	26-38	nitric oxide synthase 1, neuronal	Mus musculus	82-103
15659300-9	2005	In conclusion, decreasing nitric oxide production through inhibiting constitutive nitric oxide synthase may be a mechanism through which cyclosporin A attenuates morphine-induced place preference.	Cyclosporine	137-150	nitric oxide synthase 1, neuronal	Mus musculus	82-103
15659300-9	2005	In conclusion, decreasing nitric oxide production through inhibiting constitutive nitric oxide synthase may be a mechanism through which cyclosporin A attenuates morphine-induced place preference.	Morphine	162-170	nitric oxide synthase 1, neuronal	Mus musculus	82-103
15721991-5	2005	Interestingly, striatal nNOS phosphorylation and dopamine turnover were elevated in obese mice after MPTP treatment, but were not observed in lean mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	101-105	nitric oxide synthase 1, neuronal	Mus musculus	24-28
15721991-8	2005	These results suggest that DIO may increase the vulnerability of dopaminergic neurons to MPTP via increased levels of reactive oxygen and nitrogen species, and the role of nNOS phosphorylation in the MPTP toxicities and dopamine homeostasis should be further evaluated.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	200-204	nitric oxide synthase 1, neuronal	Mus musculus	172-176
15668387-5	2005	PDE5A protein expression and activity and cGMP levels were significantly lower in eNOS-/- and nNOS-/-, eNOS-/- mice, and this effect was reproduced in WT corpus cavernosum exposed to NOS inhibitors.	Cyclic GMP	42-46	nitric oxide synthase 1, neuronal	Mus musculus	94-98
16206879-4	2005	For example, serotonin (5-HT) metabolism is altered in male nNOS-/- mice.	Serotonin	13-22	nitric oxide synthase 1, neuronal	Mus musculus	60-64
16181097-5	2005	The HO system shares some similarities with nitric oxide synthase (NOS), notably their syntheses of carbon monoxide (CO) and nitric oxide (NO), respectively, which are diffusible gases with numerous biological actions, including neurotransmission and vasodilation.	Carbon Monoxide	100-115	nitric oxide synthase 1, neuronal	Mus musculus	44-65
16181097-5	2005	The HO system shares some similarities with nitric oxide synthase (NOS), notably their syntheses of carbon monoxide (CO) and nitric oxide (NO), respectively, which are diffusible gases with numerous biological actions, including neurotransmission and vasodilation.	Carbon Monoxide	117-119	nitric oxide synthase 1, neuronal	Mus musculus	44-65
15572274-6	2005	The present study also showed that the immunoreactivity of parvalbumin (PV)- or neuronal nitric oxide synthase (nNOS)-positive cells in the substantia nigra was decreased 7 days after MPTP treatment, whereas no significant changes were observed in these cells of the striatum throughout the experiments.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	184-188	nitric oxide synthase 1, neuronal	Mus musculus	80-110
15572274-6	2005	The present study also showed that the immunoreactivity of parvalbumin (PV)- or neuronal nitric oxide synthase (nNOS)-positive cells in the substantia nigra was decreased 7 days after MPTP treatment, whereas no significant changes were observed in these cells of the striatum throughout the experiments.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	184-188	nitric oxide synthase 1, neuronal	Mus musculus	112-116
15572274-7	2005	The administration of perindopril significantly attenuated MPTP-induced decrease of the PV- or nNOS-immunoreactivity in the nigral cells.	Perindopril	22-33	nitric oxide synthase 1, neuronal	Mus musculus	95-99
15572274-7	2005	The administration of perindopril significantly attenuated MPTP-induced decrease of the PV- or nNOS-immunoreactivity in the nigral cells.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	59-63	nitric oxide synthase 1, neuronal	Mus musculus	95-99
16206879-5	2005	Baseline corticosterone, but not ACTH, concentrations are also altered in the nNOS-/- mice.	Corticosterone	9-23	nitric oxide synthase 1, neuronal	Mus musculus	78-82
16206879-6	2005	Despite elevated corticosterone concentrations, nNOS knockout mice are less "anxious" or "fearful" than WT mice, which may contribute to their aggressiveness.	Corticosterone	17-31	nitric oxide synthase 1, neuronal	Mus musculus	48-52
15803752-1	2004	Nitric oxide (NO) is known to be produced by macrophages, endothelial cells and neurons and synthesized by an enzyme called nitric oxide synthase (NOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	124-145
15284190-6	2004	This hypertension reversal and the bradycardia were prevented by chronic infusion of the nitric oxide synthase (NOS) blocker l-NAME.	NG-Nitroarginine Methyl Ester	125-131	nitric oxide synthase 1, neuronal	Mus musculus	89-110
15496304-0	2004	The neuronal selective nitric oxide synthase inhibitor, Nomega-propyl-L-arginine, blocks the effects of phencyclidine on prepulse inhibition and locomotor activity in mice.	N(omega)-propylarginine	56-80	nitric oxide synthase 1, neuronal	Mus musculus	23-44
15496304-0	2004	The neuronal selective nitric oxide synthase inhibitor, Nomega-propyl-L-arginine, blocks the effects of phencyclidine on prepulse inhibition and locomotor activity in mice.	Phencyclidine	104-117	nitric oxide synthase 1, neuronal	Mus musculus	23-44
15496304-2	2004	In the present study, the ability of the neuronal selective nitric oxide synthase (NOS) inhibitor, Nomega-propyl-L-arginine, to block the behavioural effects of phencyclidine in mice was investigated.	N(omega)-propylarginine	99-123	nitric oxide synthase 1, neuronal	Mus musculus	60-81
15496304-2	2004	In the present study, the ability of the neuronal selective nitric oxide synthase (NOS) inhibitor, Nomega-propyl-L-arginine, to block the behavioural effects of phencyclidine in mice was investigated.	Phencyclidine	161-174	nitric oxide synthase 1, neuronal	Mus musculus	60-81
15542708-0	2004	Differential response of nNOS knockout mice to MDMA ("ecstasy")- and methamphetamine-induced psychomotor sensitization and neurotoxicity.	N-Methyl-3,4-methylenedioxyamphetamine	47-51	nitric oxide synthase 1, neuronal	Mus musculus	25-29
15542708-0	2004	Differential response of nNOS knockout mice to MDMA ("ecstasy")- and methamphetamine-induced psychomotor sensitization and neurotoxicity.	Methamphetamine	69-84	nitric oxide synthase 1, neuronal	Mus musculus	25-29
15542708-1	2004	It has been shown that mice deficient in neuronal nitric oxide synthase (nNOS) gene are resistant to cocaine-induced psychomotor sensitization and methamphetamine (METH)-induced dopaminergic neurotoxicity.	Cocaine	101-108	nitric oxide synthase 1, neuronal	Mus musculus	41-71
15542708-1	2004	It has been shown that mice deficient in neuronal nitric oxide synthase (nNOS) gene are resistant to cocaine-induced psychomotor sensitization and methamphetamine (METH)-induced dopaminergic neurotoxicity.	Cocaine	101-108	nitric oxide synthase 1, neuronal	Mus musculus	73-77
15542708-1	2004	It has been shown that mice deficient in neuronal nitric oxide synthase (nNOS) gene are resistant to cocaine-induced psychomotor sensitization and methamphetamine (METH)-induced dopaminergic neurotoxicity.	Methamphetamine	147-162	nitric oxide synthase 1, neuronal	Mus musculus	41-71
15542708-1	2004	It has been shown that mice deficient in neuronal nitric oxide synthase (nNOS) gene are resistant to cocaine-induced psychomotor sensitization and methamphetamine (METH)-induced dopaminergic neurotoxicity.	Methamphetamine	147-162	nitric oxide synthase 1, neuronal	Mus musculus	73-77
15542708-1	2004	It has been shown that mice deficient in neuronal nitric oxide synthase (nNOS) gene are resistant to cocaine-induced psychomotor sensitization and methamphetamine (METH)-induced dopaminergic neurotoxicity.	Methamphetamine	164-168	nitric oxide synthase 1, neuronal	Mus musculus	41-71
15542708-1	2004	It has been shown that mice deficient in neuronal nitric oxide synthase (nNOS) gene are resistant to cocaine-induced psychomotor sensitization and methamphetamine (METH)-induced dopaminergic neurotoxicity.	Methamphetamine	164-168	nitric oxide synthase 1, neuronal	Mus musculus	73-77
15542708-2	2004	The present study was undertaken to investigate the hypothesis that nNOS has a major role in dopamine (DA)- but not serotonin (5-hydroxytryptamine; 5-HT)-mediated effects of psychostimulants.	Dopamine	93-101	nitric oxide synthase 1, neuronal	Mus musculus	68-72
15542708-2	2004	The present study was undertaken to investigate the hypothesis that nNOS has a major role in dopamine (DA)- but not serotonin (5-hydroxytryptamine; 5-HT)-mediated effects of psychostimulants.	Dopamine	103-105	nitric oxide synthase 1, neuronal	Mus musculus	68-72
15542708-4	2004	Repeated administration of MDMA for 5 days resulted in psychomotor sensitization in both WT and nNOS KO mice, while repeated administration of METH caused psychomotor sensitization in WT but not in KO mice.	N-Methyl-3,4-methylenedioxyamphetamine	27-31	nitric oxide synthase 1, neuronal	Mus musculus	96-100
15534476-5	2004	However, staining with nNOS and NADPH diaphorase revealed significant differences between the DBA strain and the C57BL/6J mice.	1,2,5,6-dibenzanthracene	94-97	nitric oxide synthase 1, neuronal	Mus musculus	23-27
15610930-0	2004	Litter has an effect on the behavioural changes caused by the administration of the nitric oxide synthase inhibitor NG-nitro-L-arginine and ethanol in mice.	Nitroarginine	116-135	nitric oxide synthase 1, neuronal	Mus musculus	84-105
15610930-1	2004	The aim of the work was to study the effects of litter and the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine (L-NOARG) on the behaviour of mice after acute and chronic ethanol administration and withdrawal.	Nitroarginine	101-120	nitric oxide synthase 1, neuronal	Mus musculus	63-84
15610930-1	2004	The aim of the work was to study the effects of litter and the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine (L-NOARG) on the behaviour of mice after acute and chronic ethanol administration and withdrawal.	Nitroarginine	122-129	nitric oxide synthase 1, neuronal	Mus musculus	63-84
15469894-2	2004	In addition, PRL mRNA levels increased in the hypothalamus and the brainstem of nNOS control mice after administration of 7-nitro-indazole (7-NI), a relatively selective nNOS inhibitor.	7-nitroindazole	122-138	nitric oxide synthase 1, neuronal	Mus musculus	80-84
15469894-2	2004	In addition, PRL mRNA levels increased in the hypothalamus and the brainstem of nNOS control mice after administration of 7-nitro-indazole (7-NI), a relatively selective nNOS inhibitor.	7-nitroindazole	122-138	nitric oxide synthase 1, neuronal	Mus musculus	170-174
15469894-2	2004	In addition, PRL mRNA levels increased in the hypothalamus and the brainstem of nNOS control mice after administration of 7-nitro-indazole (7-NI), a relatively selective nNOS inhibitor.	7-nitroindazole	140-144	nitric oxide synthase 1, neuronal	Mus musculus	80-84
15469894-2	2004	In addition, PRL mRNA levels increased in the hypothalamus and the brainstem of nNOS control mice after administration of 7-nitro-indazole (7-NI), a relatively selective nNOS inhibitor.	7-nitroindazole	140-144	nitric oxide synthase 1, neuronal	Mus musculus	170-174
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	N-Methyl-3,4-methylenedioxyamphetamine	86-90	nitric oxide synthase 1, neuronal	Mus musculus	29-33
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	N-Methyl-3,4-methylenedioxyamphetamine	86-90	nitric oxide synthase 1, neuronal	Mus musculus	118-122
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	N-Methyl-3,4-methylenedioxyamphetamine	86-90	nitric oxide synthase 1, neuronal	Mus musculus	118-122
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	Methamphetamine	95-99	nitric oxide synthase 1, neuronal	Mus musculus	29-33
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	Methamphetamine	95-99	nitric oxide synthase 1, neuronal	Mus musculus	118-122
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	Methamphetamine	95-99	nitric oxide synthase 1, neuronal	Mus musculus	118-122
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	Methamphetamine	201-205	nitric oxide synthase 1, neuronal	Mus musculus	29-33
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	Methamphetamine	201-205	nitric oxide synthase 1, neuronal	Mus musculus	118-122
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	Methamphetamine	201-205	nitric oxide synthase 1, neuronal	Mus musculus	118-122
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	N-Methyl-3,4-methylenedioxyamphetamine	210-214	nitric oxide synthase 1, neuronal	Mus musculus	29-33
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	N-Methyl-3,4-methylenedioxyamphetamine	210-214	nitric oxide synthase 1, neuronal	Mus musculus	118-122
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	N-Methyl-3,4-methylenedioxyamphetamine	210-214	nitric oxide synthase 1, neuronal	Mus musculus	118-122
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	N-Methyl-3,4-methylenedioxyamphetamine	210-214	nitric oxide synthase 1, neuronal	Mus musculus	29-33
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	N-Methyl-3,4-methylenedioxyamphetamine	210-214	nitric oxide synthase 1, neuronal	Mus musculus	118-122
15542708-9	2004	The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.	N-Methyl-3,4-methylenedioxyamphetamine	210-214	nitric oxide synthase 1, neuronal	Mus musculus	118-122
15465783-2	2004	Major pathways for arginine production are protein breakdown and de novo arginine production from citrulline; disposal of arginine is mainly used for protein synthesis or used by the enzymes arginase and nitric oxide synthase (NOS).	Arginine	19-27	nitric oxide synthase 1, neuronal	Mus musculus	204-225
15149340-0	2004	Nitric oxide synthase expression in AT2 receptor-deficient mice after DOCA-salt.	doca-salt	70-79	nitric oxide synthase 1, neuronal	Mus musculus	0-21
15296842-4	2004	Neuronal death was reduced when agmatine was present during OGD, and this protection was associated with a reduction of nitric oxide (NO) and neuronal nitric oxide synthase (nNOS), but not inducible NOS (iNOS).	Agmatine	32-40	nitric oxide synthase 1, neuronal	Mus musculus	142-172
15296842-4	2004	Neuronal death was reduced when agmatine was present during OGD, and this protection was associated with a reduction of nitric oxide (NO) and neuronal nitric oxide synthase (nNOS), but not inducible NOS (iNOS).	Agmatine	32-40	nitric oxide synthase 1, neuronal	Mus musculus	174-178
15296842-8	2004	Agmatine markedly reduced infarct area in all treatment groups except when treatment was delayed 5 h. The number of nNOS immunopositive cells was correlated with neuroprotection.	Agmatine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	116-120
15296842-10	2004	Our study suggests that agmatine may be a novel therapeutic strategy to reduce cerebral ischemic injury, and may act by inhibiting the detrimental effects of nNOS.	Agmatine	24-32	nitric oxide synthase 1, neuronal	Mus musculus	158-162
15491851-7	2004	Since dexamethasone prevents induction of nitric oxide synthase (NOS), we evaluated the role of NO in the effects of both PGE2 and dexamethasone.	Dexamethasone	6-19	nitric oxide synthase 1, neuronal	Mus musculus	42-63
15252770-3	2004	NO is synthesized from L-arginine by NO synthases (NOS).	Arginine	23-33	nitric oxide synthase 1, neuronal	Mus musculus	37-49
15251042-8	2004	The levels of nNOS and eNOS were increased significantly in the OVA-sensitized/ozone-exposed/OVA-challenged group and the iNOS levels were reduced compared with the OVA-sensitized/saline-challenged group.	Sodium Chloride	180-186	nitric oxide synthase 1, neuronal	Mus musculus	14-18
15148562-8	2004	A similar redistribution pattern in the ipsilateral AVCN for the N-methyl-D-aspartate (NMDA) receptor was also observed at POD 4, corresponding to the fact that the activation of nNOS is coupled to calcium influx via the NMDA-receptor.	Calcium	198-205	nitric oxide synthase 1, neuronal	Mus musculus	179-183
15148562-12	2004	Further evidence is shown by the results of fluorescent double staining; nNOS-positive cells were surrounded by GAP-43 labeled regions that appeared to be presynaptic boutons, and the vast majority of nNOS-positive cells also expressed cGMP.	Cyclic GMP	236-240	nitric oxide synthase 1, neuronal	Mus musculus	201-205
15353992-19	2004	The pro-inflammatory cytokines, IL-1beta, TNFalpha, and IFNgamma, synergistically induce nitrite production, which was abrogated by treatment with the nitric oxide synthase inhibitor, AG.	Nitrites	89-96	nitric oxide synthase 1, neuronal	Mus musculus	151-172
15317855-7	2004	Concomitant with the increase in PACAP immunoreactivity after nerve injury, NADPH-dependent nitric oxide synthase (NOS) activity visualized by NADPH diaphorase histochemistry markedly increased in the superficial layer of the spinal cord of wild-type mice, which was not observed in PACAP-/- mice.	NADP	76-81	nitric oxide synthase 1, neuronal	Mus musculus	92-113
15246834-6	2004	The NO level can be increased further by pretreatment with sepiapterin, a membrane permeable precursor for BH4 synthesis, suggesting that the BH4 levels or access required for nNOS activation is limited in CAD cells.	sepiapterin	59-70	nitric oxide synthase 1, neuronal	Mus musculus	176-180
15246834-7	2004	Reducing mitochondrial Ca2+ uptake using ruthenium red (RuR) increased ionomycin-mediated NO production over ionomycin alone and indicates a critical role for mitochondria in nNOS regulation.	Ruthenium Red	41-54	nitric oxide synthase 1, neuronal	Mus musculus	175-179
15246834-7	2004	Reducing mitochondrial Ca2+ uptake using ruthenium red (RuR) increased ionomycin-mediated NO production over ionomycin alone and indicates a critical role for mitochondria in nNOS regulation.	Ionomycin	71-80	nitric oxide synthase 1, neuronal	Mus musculus	175-179
15155789-7	2004	In vivo nNOS gene transfer using adenoviruses targeted to atrial ganglia enhanced choline acetyltransferase-nNOS co-localization (P &lt; 0.05) and increased phenylephrine-induced bradycardia in vivo and heart rate responses to vagal nerve stimulation in vitro compared to gene transfer of enhanced green fluorescent protein (eGFP, P &lt; 0.01).	Phenylephrine	157-170	nitric oxide synthase 1, neuronal	Mus musculus	8-12
15136793-5	2004	Pretreatment with the NO synthase (NOS) inhibitor L-NG-nitro arginine antagonized the effects of both chlordiazepoxide and THIP; similar pretreatment with the D-isomer, D-NG-nitro arginine, which is inactive as an NOS inhibitor, was without effect on chlordiazepoxide and THIP.	Nitroarginine	50-69	nitric oxide synthase 1, neuronal	Mus musculus	22-33
15136793-5	2004	Pretreatment with the NO synthase (NOS) inhibitor L-NG-nitro arginine antagonized the effects of both chlordiazepoxide and THIP; similar pretreatment with the D-isomer, D-NG-nitro arginine, which is inactive as an NOS inhibitor, was without effect on chlordiazepoxide and THIP.	Chlordiazepoxide	102-118	nitric oxide synthase 1, neuronal	Mus musculus	22-33
15136793-5	2004	Pretreatment with the NO synthase (NOS) inhibitor L-NG-nitro arginine antagonized the effects of both chlordiazepoxide and THIP; similar pretreatment with the D-isomer, D-NG-nitro arginine, which is inactive as an NOS inhibitor, was without effect on chlordiazepoxide and THIP.	gaboxadol	123-127	nitric oxide synthase 1, neuronal	Mus musculus	22-33
15338171-4	2004	N-omega-nitro- L-arginine methyl ester ( L-NAME) inhibits nitric oxide synthase (NOS) and NO production.	NG-Nitroarginine Methyl Ester	0-38	nitric oxide synthase 1, neuronal	Mus musculus	58-79
15338171-4	2004	N-omega-nitro- L-arginine methyl ester ( L-NAME) inhibits nitric oxide synthase (NOS) and NO production.	NG-Nitroarginine Methyl Ester	41-47	nitric oxide synthase 1, neuronal	Mus musculus	58-79
15196804-0	2004	Antagonism of nitrous oxide antinociception in mice by antisense oligodeoxynucleotide directed against neuronal nitric oxide synthase enzyme.	Nitrous Oxide	14-27	nitric oxide synthase 1, neuronal	Mus musculus	103-133
15196804-0	2004	Antagonism of nitrous oxide antinociception in mice by antisense oligodeoxynucleotide directed against neuronal nitric oxide synthase enzyme.	Oligodeoxyribonucleotides	65-85	nitric oxide synthase 1, neuronal	Mus musculus	103-133
15196804-2	2004	This study was conducted to determine the sensitivity of N2O-induced antinociception to antagonism by an antisense oligodeoxynucleotide (AS-ODN) against neuronal nitric oxide synthase (nNOS).	Nitrous Oxide	57-60	nitric oxide synthase 1, neuronal	Mus musculus	153-183
15196804-2	2004	This study was conducted to determine the sensitivity of N2O-induced antinociception to antagonism by an antisense oligodeoxynucleotide (AS-ODN) against neuronal nitric oxide synthase (nNOS).	Nitrous Oxide	57-60	nitric oxide synthase 1, neuronal	Mus musculus	185-189
15196804-2	2004	This study was conducted to determine the sensitivity of N2O-induced antinociception to antagonism by an antisense oligodeoxynucleotide (AS-ODN) against neuronal nitric oxide synthase (nNOS).	Oligodeoxyribonucleotides	115-135	nitric oxide synthase 1, neuronal	Mus musculus	153-183
15196804-2	2004	This study was conducted to determine the sensitivity of N2O-induced antinociception to antagonism by an antisense oligodeoxynucleotide (AS-ODN) against neuronal nitric oxide synthase (nNOS).	Oligodeoxyribonucleotides	115-135	nitric oxide synthase 1, neuronal	Mus musculus	185-189
15196804-2	2004	This study was conducted to determine the sensitivity of N2O-induced antinociception to antagonism by an antisense oligodeoxynucleotide (AS-ODN) against neuronal nitric oxide synthase (nNOS).	as-odn	137-143	nitric oxide synthase 1, neuronal	Mus musculus	153-183
15196804-2	2004	This study was conducted to determine the sensitivity of N2O-induced antinociception to antagonism by an antisense oligodeoxynucleotide (AS-ODN) against neuronal nitric oxide synthase (nNOS).	as-odn	137-143	nitric oxide synthase 1, neuronal	Mus musculus	185-189
15196804-4	2004	This result implicates the specific involvement of nNOS in N2O-induced antinociception.	Nitrous Oxide	59-62	nitric oxide synthase 1, neuronal	Mus musculus	51-55
15010356-0	2004	Inhibition of nNOS expression in the macula densa by COX-2-derived prostaglandin E(2).	Dinoprostone	67-85	nitric oxide synthase 1, neuronal	Mus musculus	14-18
15010356-4	2004	In additional studies, we accumulated evidence to show an inhibitory influence of PGE(2) on nNOS expression.	Prostaglandins E	82-85	nitric oxide synthase 1, neuronal	Mus musculus	92-96
15010356-5	2004	In a cultured macula densa cell line, PGE(2) significantly reduced nNOS mRNA expression, as quantified by real-time RT-PCR.	Prostaglandins E	38-41	nitric oxide synthase 1, neuronal	Mus musculus	67-71
15010356-9	2004	Furthermore, the inhibitory effect of PGE(2) on nNOS mRNA expression indicates a novel interaction between NO and prostaglandin-mediated pathways of renin regulation.	Prostaglandins E	38-41	nitric oxide synthase 1, neuronal	Mus musculus	48-52
15010356-9	2004	Furthermore, the inhibitory effect of PGE(2) on nNOS mRNA expression indicates a novel interaction between NO and prostaglandin-mediated pathways of renin regulation.	Prostaglandins	114-127	nitric oxide synthase 1, neuronal	Mus musculus	48-52
15213153-6	2004	Increased transcription of NOS1 or NOS3 is not found in iNOS-knockout (KO) mice, indicating that the absence of nitric oxide production through iNOS is not compensated for by increased production of other NOS isoforms.	Nitric Oxide	112-124	nitric oxide synthase 1, neuronal	Mus musculus	27-31
15016479-1	2004	Several studies have demonstrated the involvement of reactive nitrogen and oxygen species (RNOS) in the neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydro-pyridin (MPTP) and methamphetamine (METH), so the contribution of altered nitric oxide synthase (NOS) enzyme function can be suspected.	reactive nitrogen and oxygen species	53-89	nitric oxide synthase 1, neuronal	Mus musculus	237-258
15016479-1	2004	Several studies have demonstrated the involvement of reactive nitrogen and oxygen species (RNOS) in the neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydro-pyridin (MPTP) and methamphetamine (METH), so the contribution of altered nitric oxide synthase (NOS) enzyme function can be suspected.	rnos	91-95	nitric oxide synthase 1, neuronal	Mus musculus	237-258
15016479-1	2004	Several studies have demonstrated the involvement of reactive nitrogen and oxygen species (RNOS) in the neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydro-pyridin (MPTP) and methamphetamine (METH), so the contribution of altered nitric oxide synthase (NOS) enzyme function can be suspected.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	172-176	nitric oxide synthase 1, neuronal	Mus musculus	237-258
15126916-7	2004	FDD was no longer different between TK and TK mice when experiments were performed in the presence of the nitric oxide synthase (NOS) inhibitor N-nitro-l-arginine methyl ester (l-NAME; P = 0.26), l-NAME plus diclofenac (P = 0.73), or l-NAME plus diclofenac plus potassium chloride (P = 0.31), indicating that inactivation of tissue kallikrein preferentially affects the contribution of nitric oxide to flow response.	NG-Nitroarginine Methyl Ester	177-183	nitric oxide synthase 1, neuronal	Mus musculus	106-127
15075180-5	2004	In the isolated kidney preparation, bumetanide caused similar relative increases in renin secretion in kidneys of wild-type, nNOS-/-, and eNOS-/- mice.	Bumetanide	36-46	nitric oxide synthase 1, neuronal	Mus musculus	125-129
14722775-3	2004	In aortas from nNOS-/- mice, contraction responses to phenylephrine were increased.	Phenylephrine	54-67	nitric oxide synthase 1, neuronal	Mus musculus	15-19
14722775-6	2004	In cavernosum from eNOS-/- and nNOS-/- mice, maximum contractions to phenylephrine and EFS, and relaxation responses to nitroprusside, were increased.	Phenylephrine	69-82	nitric oxide synthase 1, neuronal	Mus musculus	31-35
14722775-6	2004	In cavernosum from eNOS-/- and nNOS-/- mice, maximum contractions to phenylephrine and EFS, and relaxation responses to nitroprusside, were increased.	Nitroprusside	120-133	nitric oxide synthase 1, neuronal	Mus musculus	31-35
15063141-5	2004	Pharmacological inhibition of inducible nitric oxide synthase (NOS) with guanidinoethyldisulfide (GED) or stimulation of the breakdown of the nitrogen reactive species peroxynitrite using a potent decomposition catalyst, FP 15, reduced both the intestinal tumor load and the oxidative stress associated with intestinal polyposis in Apc(min/+) mice.	bis(2-guanidinoethyl)disulfide	73-96	nitric oxide synthase 1, neuronal	Mus musculus	40-61
15063141-6	2004	Surprisingly, pharmacological inhibition of poly(ADP-ribose) synthetase by the phenanthridinone derivative PJ 34 also reduced the intestinal polyposis and oxidative stress in these mice, possibly through the inhibition of induction of nitric oxide synthase.	phenanthridone	79-95	nitric oxide synthase 1, neuronal	Mus musculus	235-256
14980445-1	2004	Tetrahydrobiopterin is an essential cofactor for nitric oxide synthase (NOS).	sapropterin	0-19	nitric oxide synthase 1, neuronal	Mus musculus	49-70
15013024-3	2004	In the present study, we further examined whether 7-nitroindazole can also protect against the alterations of TH-, microtubule-associated protein 2a,b (MAP2)-, glial fibrillary acidic protein (GFAP)-, parvalbumin (PV)-, dopamine transporter (DAT)-, nNOS- or endothelial NOS (eNOS)-positive cells, in comparison with pargyline as a relatively selective inhibitor of the monoamine oxidase-B (MAO-B).	7-nitroindazole	50-65	nitric oxide synthase 1, neuronal	Mus musculus	249-253
15013024-4	2004	The present study showed that nNOS inhibitor as well as MAO-B inhibitor has a dose-dependent protective effect against MPTP-induced striatal dopamine and DOPAC depletion in mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	119-123	nitric oxide synthase 1, neuronal	Mus musculus	30-34
15013024-4	2004	The present study showed that nNOS inhibitor as well as MAO-B inhibitor has a dose-dependent protective effect against MPTP-induced striatal dopamine and DOPAC depletion in mice.	Dopamine	141-149	nitric oxide synthase 1, neuronal	Mus musculus	30-34
15013024-4	2004	The present study showed that nNOS inhibitor as well as MAO-B inhibitor has a dose-dependent protective effect against MPTP-induced striatal dopamine and DOPAC depletion in mice.	3,4-Dihydroxyphenylacetic Acid	154-159	nitric oxide synthase 1, neuronal	Mus musculus	30-34
15013024-0	2004	Protective effects of neuronal nitric oxide synthase inhibitor in mouse brain against MPTP neurotoxicity: an immunohistological study.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	86-90	nitric oxide synthase 1, neuronal	Mus musculus	22-52
15013024-1	2004	We recently reported that neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole, can protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in mice.	7-nitroindazole	75-90	nitric oxide synthase 1, neuronal	Mus musculus	26-56
15013024-1	2004	We recently reported that neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole, can protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in mice.	7-nitroindazole	75-90	nitric oxide synthase 1, neuronal	Mus musculus	58-62
15013024-1	2004	We recently reported that neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole, can protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	112-156	nitric oxide synthase 1, neuronal	Mus musculus	26-56
15013024-1	2004	We recently reported that neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole, can protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	112-156	nitric oxide synthase 1, neuronal	Mus musculus	58-62
15013024-1	2004	We recently reported that neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole, can protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	158-162	nitric oxide synthase 1, neuronal	Mus musculus	26-56
15013024-1	2004	We recently reported that neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole, can protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	158-162	nitric oxide synthase 1, neuronal	Mus musculus	58-62
14757173-2	2004	This study was conducted to establish the role of specific isoforms of NO synthase (NOS) in morphine tolerance development using genetically modified mice.	Morphine	92-100	nitric oxide synthase 1, neuronal	Mus musculus	71-82
14757173-7	2004	RESULTS: Following sustained morphine administration, nNOS-deficient mice exhibited less tolerance development when compared to the control group, although measurable tolerance still occurred.	Morphine	29-37	nitric oxide synthase 1, neuronal	Mus musculus	54-58
14748849-4	2004	This effect is blocked by nitric oxide synthase (NOS) inhibitors, suggesting that nitric oxide plays an important role in this effect of phencyclidine.	Phencyclidine	137-150	nitric oxide synthase 1, neuronal	Mus musculus	26-47
14748849-11	2004	The results from the present study further support the suggestion that the nitric oxide synthase/guanylate cyclase pathway is involved in pharmacological and behavioural effects of phencyclidine.	Phencyclidine	181-194	nitric oxide synthase 1, neuronal	Mus musculus	75-96
14748849-12	2004	Since phencyclidine as well exerts psychotomimetic characteristics, agents that interfere with the nitric oxide synthase/guanylate cyclase pathway may be of therapeutic value also in the treatment of schizophrenia.	Phencyclidine	6-19	nitric oxide synthase 1, neuronal	Mus musculus	99-120
14665440-1	2004	Nitric oxide (NO) is a free radical that is largely produced by three isoforms of NO synthase (NOS): neuronal (nNOS), endothelial (eNOS), and inducible (iNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	82-93
14978361-4	2004	The NO synthase 1 (NOS1) inhibitor 7-nitroindazole (1 nmol/site) decreased SP-induced scratching and NO production.	7-nitroindazole	35-50	nitric oxide synthase 1, neuronal	Mus musculus	4-17
14978361-4	2004	The NO synthase 1 (NOS1) inhibitor 7-nitroindazole (1 nmol/site) decreased SP-induced scratching and NO production.	7-nitroindazole	35-50	nitric oxide synthase 1, neuronal	Mus musculus	19-23
14978361-5	2004	Repeated administration of Unsei-in (300 mg/kg) reduced the cutaneous NOS1 level.	unsei-	27-33	nitric oxide synthase 1, neuronal	Mus musculus	70-74
14698461-0	2004	Agmatine reduces only peripheral-related behavioral signs, not the central signs, of morphine withdrawal in nNOS deficient transgenic mice.	Agmatine	0-8	nitric oxide synthase 1, neuronal	Mus musculus	108-112
14665440-1	2004	Nitric oxide (NO) is a free radical that is largely produced by three isoforms of NO synthase (NOS): neuronal (nNOS), endothelial (eNOS), and inducible (iNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	111-115
15320741-1	2004	Nitric oxide (NO) is generated by a family of NO synthase (NOS) enzymes, including endothelial (eNOS), inducible (iNOS) and neuronal (nNOS).	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	46-57
14688153-2	2004	NO is formed from L-arginine by isoforms of nitric oxide synthase (NOS) via NG-hydroxy-L-arginine, with L-citrulline as a byproduct.	Arginine	18-28	nitric oxide synthase 1, neuronal	Mus musculus	44-65
14688153-2	2004	NO is formed from L-arginine by isoforms of nitric oxide synthase (NOS) via NG-hydroxy-L-arginine, with L-citrulline as a byproduct.	N(omega)-hydroxyarginine	76-97	nitric oxide synthase 1, neuronal	Mus musculus	44-65
14688153-2	2004	NO is formed from L-arginine by isoforms of nitric oxide synthase (NOS) via NG-hydroxy-L-arginine, with L-citrulline as a byproduct.	Citrulline	104-116	nitric oxide synthase 1, neuronal	Mus musculus	44-65
14587983-1	2003	Nitric oxide (NO), which is produced by nitric oxide synthase (NOS), has been recently identified as a multifunctional mediator.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	40-61
15302995-5	2004	In addition, nitric oxide synthase (NOS) inhibitors, Nomega monomethyl L-arginine and aminoguanidine, also reduced LMM3-induced angiogenesis and nitric oxide (NO) synthesis as well.	omega-N-Methylarginine	53-81	nitric oxide synthase 1, neuronal	Mus musculus	13-34
15302995-5	2004	In addition, nitric oxide synthase (NOS) inhibitors, Nomega monomethyl L-arginine and aminoguanidine, also reduced LMM3-induced angiogenesis and nitric oxide (NO) synthesis as well.	pimagedine	86-100	nitric oxide synthase 1, neuronal	Mus musculus	13-34
15033804-6	2003	Cerebellar extracts from both nTg and Tg mice displayed the highest level of nNOS activity, which was fourfold higher than cortical extracts.	Nitroglycerin	30-33	nitric oxide synthase 1, neuronal	Mus musculus	77-81
15320493-2	2003	Immunophilin-binding agents like FK506 are known to inactivate neuronal nitric oxide synthase (nNOS) by inhibiting calcineurin and decrease the production of nitric oxide.	Tacrolimus	33-38	nitric oxide synthase 1, neuronal	Mus musculus	63-93
15320493-2	2003	Immunophilin-binding agents like FK506 are known to inactivate neuronal nitric oxide synthase (nNOS) by inhibiting calcineurin and decrease the production of nitric oxide.	Tacrolimus	33-38	nitric oxide synthase 1, neuronal	Mus musculus	95-99
15320493-2	2003	Immunophilin-binding agents like FK506 are known to inactivate neuronal nitric oxide synthase (nNOS) by inhibiting calcineurin and decrease the production of nitric oxide.	Nitric Oxide	72-84	nitric oxide synthase 1, neuronal	Mus musculus	95-99
15320493-6	2003	Nitric oxide synthase (NOS) inhibitor L-NAME significantly and dose dependently (10-40 mg/kg, ip) potentiated the FK506 (0.5 mg/kg)-induced antinociception.	NG-Nitroarginine Methyl Ester	38-44	nitric oxide synthase 1, neuronal	Mus musculus	0-21
15320493-6	2003	Nitric oxide synthase (NOS) inhibitor L-NAME significantly and dose dependently (10-40 mg/kg, ip) potentiated the FK506 (0.5 mg/kg)-induced antinociception.	Tacrolimus	114-119	nitric oxide synthase 1, neuronal	Mus musculus	0-21
14675208-2	2003	As NO is synthesized from L-arginine by NO synthases (NOS), the availability of L-arginine might be one rate-limiting factor of NO production at the wound site.	Arginine	26-36	nitric oxide synthase 1, neuronal	Mus musculus	40-52
14675208-2	2003	As NO is synthesized from L-arginine by NO synthases (NOS), the availability of L-arginine might be one rate-limiting factor of NO production at the wound site.	Arginine	80-90	nitric oxide synthase 1, neuronal	Mus musculus	40-52
12966566-5	2003	We described two populations of nitric oxide-producing neurons in the mouse claustrum on the basis of a different level of nNOS expression.	Nitric Oxide	32-44	nitric oxide synthase 1, neuronal	Mus musculus	123-127
12966566-6	2003	Densely nNOS-stained neurons were mostly GABA immunoreactive, displayed ultrastructural features typically seen in aspiny neurons, and may originate in the subpallium; they were first seen in the claustrum at embryonic stage 17.5 and probably represent local inhibitory interneurons.	gamma-Aminobutyric Acid	41-45	nitric oxide synthase 1, neuronal	Mus musculus	8-12
12900399-7	2003	Preincubation of de-endothelialized vessels with the nitric oxide synthase (NOS) inhibitor l-NAME (l-N(G)-nitroarginine methyl ester) (10-5 mol/liter) resulted in a stronger contraction to KCl (p &lt;0.05 versus without l-NAME), thus unmasking vasodilatory effects of inherent NO production.	NG-Nitroarginine Methyl Ester	91-97	nitric oxide synthase 1, neuronal	Mus musculus	53-74
12900399-7	2003	Preincubation of de-endothelialized vessels with the nitric oxide synthase (NOS) inhibitor l-NAME (l-N(G)-nitroarginine methyl ester) (10-5 mol/liter) resulted in a stronger contraction to KCl (p &lt;0.05 versus without l-NAME), thus unmasking vasodilatory effects of inherent NO production.	l-n(g)-nitroarginine methyl ester	99-132	nitric oxide synthase 1, neuronal	Mus musculus	53-74
12900399-7	2003	Preincubation of de-endothelialized vessels with the nitric oxide synthase (NOS) inhibitor l-NAME (l-N(G)-nitroarginine methyl ester) (10-5 mol/liter) resulted in a stronger contraction to KCl (p &lt;0.05 versus without l-NAME), thus unmasking vasodilatory effects of inherent NO production.	Potassium Chloride	189-192	nitric oxide synthase 1, neuronal	Mus musculus	53-74
12900399-7	2003	Preincubation of de-endothelialized vessels with the nitric oxide synthase (NOS) inhibitor l-NAME (l-N(G)-nitroarginine methyl ester) (10-5 mol/liter) resulted in a stronger contraction to KCl (p &lt;0.05 versus without l-NAME), thus unmasking vasodilatory effects of inherent NO production.	NG-Nitroarginine Methyl Ester	220-226	nitric oxide synthase 1, neuronal	Mus musculus	53-74
14551528-1	2003	PURPOSE: Nitric oxide formation by nitric oxide synthase (NOS) has been implicated in vascular injury and retinal neovascularization during oxygen-induced retinopathy.	Nitric Oxide	9-21	nitric oxide synthase 1, neuronal	Mus musculus	35-56
14551528-1	2003	PURPOSE: Nitric oxide formation by nitric oxide synthase (NOS) has been implicated in vascular injury and retinal neovascularization during oxygen-induced retinopathy.	Oxygen	140-146	nitric oxide synthase 1, neuronal	Mus musculus	35-56
14766771-2	2004	We hypothesized that episodic hypoxia (EH) promotes inflammation in the cerebral microcirculation and that nitric oxide (NO) produced by the endothelial and neuronal isoforms of NO synthase (eNOS and nNOS, respectively) modulates this response.	Nitric Oxide	107-119	nitric oxide synthase 1, neuronal	Mus musculus	200-204
14749478-7	2004	Aminoguanidine, an inducible nitric oxide synthase (NOS) inhibitor, given before C5aAP returned VP to control levels.	pimagedine	0-14	nitric oxide synthase 1, neuronal	Mus musculus	29-50
12971910-9	2004	Similarly, the neuronal form of nitric oxide synthase (NOS) inhibitor 7-nitroindazole (7-NI) as well as the nonselective NOS inhibitor L-NMMA, but not the inducible NOS inhibitor 1400W, partially prevented the death of mice and prolonged the period of death.	7-nitroindazole	70-85	nitric oxide synthase 1, neuronal	Mus musculus	32-53
12971910-9	2004	Similarly, the neuronal form of nitric oxide synthase (NOS) inhibitor 7-nitroindazole (7-NI) as well as the nonselective NOS inhibitor L-NMMA, but not the inducible NOS inhibitor 1400W, partially prevented the death of mice and prolonged the period of death.	7-nitroindazole	87-91	nitric oxide synthase 1, neuronal	Mus musculus	32-53
14645704-4	2003	Here, we demonstrate a significant enhancement of these measures of muscle performance at low physiological pO2 and an inhibitory influence at higher physiological pO2, which depend on endogenous nNOS.	PO-2	164-167	nitric oxide synthase 1, neuronal	Mus musculus	196-200
14645704-6	2003	In addition, responsivity to pO2 is altered significantly in nNOS mutant muscle.	PO-2	29-32	nitric oxide synthase 1, neuronal	Mus musculus	61-65
15048017-9	2003	We have shown that the administration of tetrahydrobiopterin, an important co-factor for nitric oxide synthase (NOS) partially restores endothelial function (1) in leptin-deficient mice (db/db) with spontaneous type II diabetes, as well as (2) in human vascular tissue harvested for coronary artery bypass grafting (CABG).	sapropterin	41-60	nitric oxide synthase 1, neuronal	Mus musculus	89-110
14660920-12	2003	There was increased immunoreactivity of neuronal NOS (nNOS) in the surviving cells after SO2 exposure.	Sulfur Dioxide	89-92	nitric oxide synthase 1, neuronal	Mus musculus	40-52
14660920-12	2003	There was increased immunoreactivity of neuronal NOS (nNOS) in the surviving cells after SO2 exposure.	Sulfur Dioxide	89-92	nitric oxide synthase 1, neuronal	Mus musculus	54-58
14660920-14	2003	In Western blot analysis, nNOS expression increased 4 hours after SO2 exposure.	Sulfur Dioxide	66-69	nitric oxide synthase 1, neuronal	Mus musculus	26-30
14996426-1	2003	Nitric oxide (NO), produced by NO-synthase (NOS), serves as an important vasodilator and inhibitory neurotransmitter.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	31-42
12913056-2	2003	l-Arginine, the substrate for nitric oxide synthase (NOS), decreases NaCl absorption by THALs.	Arginine	0-10	nitric oxide synthase 1, neuronal	Mus musculus	30-51
12966566-3	2003	We also analyzed colocalization of nNOS with the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) as well as the ontogenesis of the nNOS-immunoreactive neurons, providing evidence for different populations of nitrergic neurons in the mouse claustrum.	gamma-Aminobutyric Acid	77-100	nitric oxide synthase 1, neuronal	Mus musculus	35-39
12966566-3	2003	We also analyzed colocalization of nNOS with the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) as well as the ontogenesis of the nNOS-immunoreactive neurons, providing evidence for different populations of nitrergic neurons in the mouse claustrum.	gamma-Aminobutyric Acid	102-106	nitric oxide synthase 1, neuronal	Mus musculus	35-39
14526232-6	2003	In response to hyperbaric oxygen (HBO2) at 5 ATA, WT and nNOS-/- mice showed decreases in rCBF over 30 minutes, but eNOS-/- mice did not.	Oxygen	26-32	nitric oxide synthase 1, neuronal	Mus musculus	57-61
14523625-5	2003	In the substantia nigra, intense immunoreactivity of nNOS-positive cells increased 5 hr after MPTP treatment.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	94-98	nitric oxide synthase 1, neuronal	Mus musculus	53-57
14523625-6	2003	Thereafter, the immunoreactivity of nNOS-positive cells decreased gradually from 1 day up to 7 days after MPTP treatment.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	106-110	nitric oxide synthase 1, neuronal	Mus musculus	36-40
12913056-2	2003	l-Arginine, the substrate for nitric oxide synthase (NOS), decreases NaCl absorption by THALs.	Sodium Chloride	69-73	nitric oxide synthase 1, neuronal	Mus musculus	30-51
14568310-3	2003	Food intake, measured at 1, 2, and 4 h following injection of 70 mg/kg of MA, was attenuated in a dose related manner with increasing pretreatment dose (1,10, 25 and 50 mg/kg sc) of the NO-synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), reaching statistical significance at 10 mg/kg of L-NAME at h1 when compared to vehicle control condition.	NG-Nitroarginine Methyl Ester	215-249	nitric oxide synthase 1, neuronal	Mus musculus	186-197
14568310-3	2003	Food intake, measured at 1, 2, and 4 h following injection of 70 mg/kg of MA, was attenuated in a dose related manner with increasing pretreatment dose (1,10, 25 and 50 mg/kg sc) of the NO-synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), reaching statistical significance at 10 mg/kg of L-NAME at h1 when compared to vehicle control condition.	NG-Nitroarginine Methyl Ester	251-257	nitric oxide synthase 1, neuronal	Mus musculus	186-197
14568310-3	2003	Food intake, measured at 1, 2, and 4 h following injection of 70 mg/kg of MA, was attenuated in a dose related manner with increasing pretreatment dose (1,10, 25 and 50 mg/kg sc) of the NO-synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), reaching statistical significance at 10 mg/kg of L-NAME at h1 when compared to vehicle control condition.	NG-Nitroarginine Methyl Ester	309-315	nitric oxide synthase 1, neuronal	Mus musculus	186-197
12950342-1	2003	Nitric oxide (NO) is a free radical synthesized from l-arginine by a family of NO synthase (NOS) enzymes, all of which are present in the skin, and also by reduction of sweat nitrate.	Nitric Oxide	0-12	nitric oxide synthase 1, neuronal	Mus musculus	79-90
12845643-1	2003	Using clonal derivatives of spontaneous mammary tumours in C3H/HeJ mice, we had earlier shown that tumour-derived nitric oxide (NO), resulting from endothelial type (e) NO synthase (NOS) expression by tumour cells, promoted tumour growth and metastasis by multiple mechanisms: stimulation of tumour cell invasiveness, migration and angiogenesis.	Nitric Oxide	114-126	nitric oxide synthase 1, neuronal	Mus musculus	169-180
13129835-8	2003	The results of the present study suggest that quercetin reversal of morphine tolerance and dependence may involve its ability to suppress nitric oxide synthase (NOS) activity.	Quercetin	46-55	nitric oxide synthase 1, neuronal	Mus musculus	138-159
13129835-8	2003	The results of the present study suggest that quercetin reversal of morphine tolerance and dependence may involve its ability to suppress nitric oxide synthase (NOS) activity.	Morphine	68-76	nitric oxide synthase 1, neuronal	Mus musculus	138-159
12970039-4	2003	STUDY DESIGN: In this study, we compared the neurogenic (tetrodotoxin-sensitive) NANC relaxation of tracheal segments from nNOS-/- mice and control wild-type mice (nNOS(+/+)), induced by electrical field stimulation (EFS).	Tetrodotoxin	57-69	nitric oxide synthase 1, neuronal	Mus musculus	123-127
12970039-4	2003	STUDY DESIGN: In this study, we compared the neurogenic (tetrodotoxin-sensitive) NANC relaxation of tracheal segments from nNOS-/- mice and control wild-type mice (nNOS(+/+)), induced by electrical field stimulation (EFS).	Tetrodotoxin	57-69	nitric oxide synthase 1, neuronal	Mus musculus	164-168
12970039-8	2003	Methacholine induced concentration-dependent contractions that were consistently higher in the nNOS-/- tracheas relative to wild-type mice tracheas (p &gt; 0.05).	Methacholine Chloride	0-12	nitric oxide synthase 1, neuronal	Mus musculus	95-99
12969273-3	2003	In the first experiment, the effect of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI; 25 mg/kg x 4) on fenfluramine (25 mg/kg x 4)-induced serotonergic neurotoxicity in Swiss Webster mice was investigated.	7-nitroindazole	91-106	nitric oxide synthase 1, neuronal	Mus musculus	43-73
12969273-3	2003	In the first experiment, the effect of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI; 25 mg/kg x 4) on fenfluramine (25 mg/kg x 4)-induced serotonergic neurotoxicity in Swiss Webster mice was investigated.	7-nitroindazole	91-106	nitric oxide synthase 1, neuronal	Mus musculus	75-79
12969273-3	2003	In the first experiment, the effect of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI; 25 mg/kg x 4) on fenfluramine (25 mg/kg x 4)-induced serotonergic neurotoxicity in Swiss Webster mice was investigated.	Fenfluramine	131-143	nitric oxide synthase 1, neuronal	Mus musculus	43-73
14656046-2	2003	NO is synthesized from L-arginine by NO synthase occurring in three isoforms of (neuronal, nNOS; endothelial, eNOS; inducible, iNOS).	Arginine	23-33	nitric oxide synthase 1, neuronal	Mus musculus	91-95
12950342-1	2003	Nitric oxide (NO) is a free radical synthesized from l-arginine by a family of NO synthase (NOS) enzymes, all of which are present in the skin, and also by reduction of sweat nitrate.	Arginine	53-63	nitric oxide synthase 1, neuronal	Mus musculus	79-90
12950342-1	2003	Nitric oxide (NO) is a free radical synthesized from l-arginine by a family of NO synthase (NOS) enzymes, all of which are present in the skin, and also by reduction of sweat nitrate.	Nitrates	175-182	nitric oxide synthase 1, neuronal	Mus musculus	79-90
12928013-9	2003	Responses to bPTH(1-34) were also inhibited by both non-selective and selective neuronal nitric oxide synthase (NOS) inhibitors N(omega)-nitro-L-arginine methyl ester (0.01-1mM) and 7-nitroindazole (0.01-10 microM), respectively.	bpth	13-17	nitric oxide synthase 1, neuronal	Mus musculus	80-110
12928013-9	2003	Responses to bPTH(1-34) were also inhibited by both non-selective and selective neuronal nitric oxide synthase (NOS) inhibitors N(omega)-nitro-L-arginine methyl ester (0.01-1mM) and 7-nitroindazole (0.01-10 microM), respectively.	NG-Nitroarginine Methyl Ester	128-166	nitric oxide synthase 1, neuronal	Mus musculus	80-110
12907314-6	2003	The nitric oxide synthase (NOS) substrate, L-arginine (60 mg/kg), inhibited the anticonvulsant property of agmatine and this effect was significantly reversed by NOS inhibitor N(G)-nitro-L-arginine (L-NAME, 30 mg/kg), implying an NO-dependent mechanism for L-arginine effect.	Arginine	43-53	nitric oxide synthase 1, neuronal	Mus musculus	4-25
14609545-3	2003	Recently, the excessive aggressive and impulsive traits of neuronal NO synthase knockout (nNOS-/-) mice were shown to be caused by reductions in serotonin (5-HT) turnover and deficient 5-HT1A and 5-HT1B receptor function in brain regions regulating emotion.	Serotonin	145-154	nitric oxide synthase 1, neuronal	Mus musculus	90-94
12907314-6	2003	The nitric oxide synthase (NOS) substrate, L-arginine (60 mg/kg), inhibited the anticonvulsant property of agmatine and this effect was significantly reversed by NOS inhibitor N(G)-nitro-L-arginine (L-NAME, 30 mg/kg), implying an NO-dependent mechanism for L-arginine effect.	Agmatine	107-115	nitric oxide synthase 1, neuronal	Mus musculus	4-25
12907314-6	2003	The nitric oxide synthase (NOS) substrate, L-arginine (60 mg/kg), inhibited the anticonvulsant property of agmatine and this effect was significantly reversed by NOS inhibitor N(G)-nitro-L-arginine (L-NAME, 30 mg/kg), implying an NO-dependent mechanism for L-arginine effect.	Nitroarginine	176-197	nitric oxide synthase 1, neuronal	Mus musculus	4-25
12907314-6	2003	The nitric oxide synthase (NOS) substrate, L-arginine (60 mg/kg), inhibited the anticonvulsant property of agmatine and this effect was significantly reversed by NOS inhibitor N(G)-nitro-L-arginine (L-NAME, 30 mg/kg), implying an NO-dependent mechanism for L-arginine effect.	NG-Nitroarginine Methyl Ester	199-205	nitric oxide synthase 1, neuronal	Mus musculus	4-25
12907314-6	2003	The nitric oxide synthase (NOS) substrate, L-arginine (60 mg/kg), inhibited the anticonvulsant property of agmatine and this effect was significantly reversed by NOS inhibitor N(G)-nitro-L-arginine (L-NAME, 30 mg/kg), implying an NO-dependent mechanism for L-arginine effect.	Arginine	187-197	nitric oxide synthase 1, neuronal	Mus musculus	4-25
14559429-0	2003	Inhibition of neuronal nitric oxide synthase suppresses the maintenance but not the induction of psychomotor sensitization to MDMA ("Ecstasy") and p-chloroamphetamine in mice.	p-Chloroamphetamine	147-166	nitric oxide synthase 1, neuronal	Mus musculus	14-44
12721331-0	2003	Role of nitric-oxide synthase isoforms in nitrous oxide antinociception in mice.	Nitrous Oxide	42-55	nitric oxide synthase 1, neuronal	Mus musculus	8-29
12721331-1	2003	Exposure of mice to the anesthetic gas N2O evokes a prominent antinociceptive effect that is sensitive to antagonism by nonselective nitric-oxide synthase (NOS) inhibitors.	Nitrous Oxide	39-42	nitric oxide synthase 1, neuronal	Mus musculus	133-154
14559429-2	2003	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co-administration of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI).	Cocaine	105-112	nitric oxide synthase 1, neuronal	Mus musculus	220-250
14559429-2	2003	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co-administration of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI).	Cocaine	105-112	nitric oxide synthase 1, neuronal	Mus musculus	252-256
14559429-2	2003	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co-administration of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI).	Methamphetamine	114-129	nitric oxide synthase 1, neuronal	Mus musculus	220-250
14559429-2	2003	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co-administration of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI).	Methamphetamine	114-129	nitric oxide synthase 1, neuronal	Mus musculus	252-256
14559429-2	2003	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co-administration of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI).	Methylphenidate	135-150	nitric oxide synthase 1, neuronal	Mus musculus	220-250
14559429-2	2003	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co-administration of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI).	Methylphenidate	135-150	nitric oxide synthase 1, neuronal	Mus musculus	252-256
14559429-2	2003	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co-administration of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI).	Dopamine	161-169	nitric oxide synthase 1, neuronal	Mus musculus	220-250
14559429-2	2003	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co-administration of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI).	Dopamine	161-169	nitric oxide synthase 1, neuronal	Mus musculus	252-256
14559429-2	2003	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co-administration of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI).	7-nitroindazole	268-283	nitric oxide synthase 1, neuronal	Mus musculus	220-250
14559429-2	2003	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co-administration of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI).	7-nitroindazole	285-289	nitric oxide synthase 1, neuronal	Mus musculus	220-250