PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
25453793-2	2014	The present study aimed to investigate that AE could attenuate scopolamine-induced cognitive deficits via inhibiting acetylcholinesterase (AChE) activity and modulating oxidative stress.	Scopolamine	63-74	acetylcholinesterase	Rattus norvegicus	117-137
25453793-2	2014	The present study aimed to investigate that AE could attenuate scopolamine-induced cognitive deficits via inhibiting acetylcholinesterase (AChE) activity and modulating oxidative stress.	Scopolamine	63-74	acetylcholinesterase	Rattus norvegicus	139-143
25121635-4	2014	The increase of acetylcholinesterase activity caused by scopolamine was significantly attenuated by RCM treatment.	Scopolamine	56-67	acetylcholinesterase	Mus musculus	16-36
25419365-7	2014	Compared with saline group, scopolamine administered significantly decreased the cognitive performance of rats during the Morris water maze test and changed Abeta, Beclin-1 and mTOR levels in rat prefrontal cortex and hippocampus (P<0.05); In addition, rats in sirolimus plus scopolamine group significantly reversed scopolamine-induced effects (P<0.05).	Scopolamine	28-39	amyloid beta precursor protein	Rattus norvegicus	157-162
25419365-7	2014	Compared with saline group, scopolamine administered significantly decreased the cognitive performance of rats during the Morris water maze test and changed Abeta, Beclin-1 and mTOR levels in rat prefrontal cortex and hippocampus (P<0.05); In addition, rats in sirolimus plus scopolamine group significantly reversed scopolamine-induced effects (P<0.05).	Scopolamine	28-39	beclin 1	Rattus norvegicus	164-172
25419365-7	2014	Compared with saline group, scopolamine administered significantly decreased the cognitive performance of rats during the Morris water maze test and changed Abeta, Beclin-1 and mTOR levels in rat prefrontal cortex and hippocampus (P<0.05); In addition, rats in sirolimus plus scopolamine group significantly reversed scopolamine-induced effects (P<0.05).	Scopolamine	28-39	mechanistic target of rapamycin kinase	Rattus norvegicus	177-181
25061594-8	2014	Inhibition of cell proliferation and suppression of BDNF and TrkB expressions were observed in the scopolamine-induced amnesia mice.	Scopolamine	99-110	brain derived neurotrophic factor	Mus musculus	52-56
25086267-0	2014	Novel peptide VIP-TAT with higher affinity for PAC1 inhibited scopolamine induced amnesia.	Scopolamine	62-73	vasoactive intestinal polypeptide	Mus musculus	14-17
25086267-0	2014	Novel peptide VIP-TAT with higher affinity for PAC1 inhibited scopolamine induced amnesia.	Scopolamine	62-73	adenylate cyclase activating polypeptide 1 receptor 1	Mus musculus	47-51
25231482-0	2014	Acupuncture stimulation improves scopolamine-induced cognitive impairment via activation of cholinergic system and regulation of BDNF and CREB expressions in rats.	Scopolamine	33-44	brain-derived neurotrophic factor	Rattus norvegicus	129-133
25231482-0	2014	Acupuncture stimulation improves scopolamine-induced cognitive impairment via activation of cholinergic system and regulation of BDNF and CREB expressions in rats.	Scopolamine	33-44	cAMP responsive element binding protein 1	Rattus norvegicus	138-142
24948063-9	2014	The impact on BDNF synthesis was mimicked by muscarinic receptor agonist pilocarpine and abolished by selective muscarinic antagonist scopolamine.	Scopolamine	134-145	brain-derived neurotrophic factor	Rattus norvegicus	14-18
24836869-4	2014	Mice that received scopolamine alone showed impaired learning and memory retention and considerably decreased cholinergic system reactivity in the hippocampus and frontal cortex, as indicated by a decreased acetylcholine (ACh) level and an increased acetylcholinesterase (AChE) activity.	Scopolamine	19-30	acetylcholinesterase	Mus musculus	250-270
24836869-4	2014	Mice that received scopolamine alone showed impaired learning and memory retention and considerably decreased cholinergic system reactivity in the hippocampus and frontal cortex, as indicated by a decreased acetylcholine (ACh) level and an increased acetylcholinesterase (AChE) activity.	Scopolamine	19-30	acetylcholinesterase	Mus musculus	272-276
24836869-5	2014	Sulforaphane significantly attenuated the scopolamine-induced memory impairment and improved cholinergic system reactivity, as indicated by an increased ACh level, decreased AChE activity, and increased choline acetyltransferase (ChAT) expression in the hippocampus and frontal cortex.	Scopolamine	42-53	acetylcholinesterase	Mus musculus	174-178
25061594-8	2014	Inhibition of cell proliferation and suppression of BDNF and TrkB expressions were observed in the scopolamine-induced amnesia mice.	Scopolamine	99-110	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	61-65
23797156-0	2014	Secreted calmodulin-like skin protein ameliorates scopolamine-induced memory impairment.	Scopolamine	50-61	predicted gene 1123	Mus musculus	9-37
24857631-4	2014	Benzo[h][1,6]naphthyridine derivatives showed the highest H3R affinity, and compound 17 (H3R Ki = 41.6 nM; 5-HT4R Ki = 208 nM) completely reversed the amnesiant effect of scopolamine at 3 mg/kg in a spatial working memory experiment.	Scopolamine	171-182	histamine receptor H3	Homo sapiens	89-92
23797156-6	2014	In this study, we show that recombinant CLSP, administered intracerebroventricularly or intraperitoneally, ameliorates scopolamine-induced dementia in mice.	Scopolamine	119-130	predicted gene 1123	Mus musculus	40-44
24708927-0	2014	CDP-choline attenuates scopolamine induced disruption of prepulse inhibition in rats: involvement of central nicotinic mechanism.	Scopolamine	23-34	cut-like homeobox 1	Rattus norvegicus	0-3
24936785-3	2014	However, according to the literature, the most frequently used doses of scopolamine efficient on memory consolidation, are 1 and 30 mg/kg, low and high doses, respectively.	Scopolamine	72-83	VPS52 subunit of GARP complex	Rattus norvegicus	119-124
24813882-11	2014	DPH6 was capable to significantly decrease scopolamine-induced learning deficits in healthy adult mice.	Scopolamine	43-54	diphthamine biosynthesis 6	Mus musculus	0-4
24325271-1	2014	Scopolamine (Sco) can induce amyloid beta (Abeta) deposition, oxidative stress, synaptic dysfunction, and learning/memory impairment as observed in Alzheimer"s disease (AD), the most common form of dementia affecting more than 25 million elderly people worldwide.	Scopolamine	0-11	amyloid beta precursor protein	Homo sapiens	29-41
24325271-1	2014	Scopolamine (Sco) can induce amyloid beta (Abeta) deposition, oxidative stress, synaptic dysfunction, and learning/memory impairment as observed in Alzheimer"s disease (AD), the most common form of dementia affecting more than 25 million elderly people worldwide.	Scopolamine	0-11	amyloid beta precursor protein	Homo sapiens	43-48
24325271-1	2014	Scopolamine (Sco) can induce amyloid beta (Abeta) deposition, oxidative stress, synaptic dysfunction, and learning/memory impairment as observed in Alzheimer"s disease (AD), the most common form of dementia affecting more than 25 million elderly people worldwide.	Scopolamine	0-3	amyloid beta precursor protein	Homo sapiens	29-41
24325271-1	2014	Scopolamine (Sco) can induce amyloid beta (Abeta) deposition, oxidative stress, synaptic dysfunction, and learning/memory impairment as observed in Alzheimer"s disease (AD), the most common form of dementia affecting more than 25 million elderly people worldwide.	Scopolamine	0-3	amyloid beta precursor protein	Homo sapiens	43-48
24325271-2	2014	Herein we explored the protective effect of 7,8-dihydroxyflavone (7,8-DHF) on Sco-induced Abeta deposition, oxidative stress, synaptic dysfunction, and learning/memory defects.	Scopolamine	78-81	amyloid beta precursor protein	Homo sapiens	90-95
24708927-3	2014	In this study, prepulse inhibition (PPI) of the acoustic startle reflex was used to test the sensorimotor gating functioning, and the effects of CDP-choline on scopolamine induced PPI disruption were evaluated in rats.	Scopolamine	160-171	cut-like homeobox 1	Rattus norvegicus	145-148
24708927-6	2014	Scopolamine (0.4mg/kg; s.c.) significantly decreased the PPI levels and intraperitoneal administration of CDP-choline (250mg/kg) attenuated the effects of scopolamine.	Scopolamine	155-166	cut-like homeobox 1	Rattus norvegicus	106-109
24708927-9	2014	completely blocked the reversal effects of CDP-choline on scopolamine induced disruption of PPI.	Scopolamine	58-69	cut-like homeobox 1	Rattus norvegicus	43-46
24708927-10	2014	These results demonstrate that exogenous administration of CDP-choline attenuates scopolamine induced PPI disruption and show that the activation of central alpha7-nAChR may play a critical role in this effect.	Scopolamine	82-93	cut-like homeobox 1	Rattus norvegicus	59-62
24578344-11	2014	VIP (100 nM) induced longitudinal muscle contraction that was inhibited by TTX (1 muM), PG97-269 (VPAC1 antagonist; 1 muM), and hyoscine (10 muM), but not by hexamethonium (200 muM).	Scopolamine	128-136	VIP peptides	Cavia porcellus	0-3
24690775-8	2014	Scopolamine-induced changes in reactive oxygen species (ROS), malondialehyde (MDA), and AChE activity were significantly attenuated in mice pretreated with Myelophil.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	88-92
24578344-12	2014	VIP (50 nM)-evoked secretion was depressed by hyoscine or PG97-269 and involved a small TTX-sensitive component.	Scopolamine	46-54	VIP peptides	Cavia porcellus	0-3
24231553-6	2014	Scopolamine-induced increases in hippocampal ACh efflux was significantly reduced in SAP lesioned Tg2576 mice compared to sham lesioned Tg2576 mice.	Scopolamine	0-11	amyloid P component, serum	Mus musculus	85-88
25657779-9	2014	Also, inhibition of AChE activity was observed in both naive and scopolamine-induced memory-impaired rats.	Scopolamine	65-76	acetylcholinesterase	Rattus norvegicus	20-24
24534175-1	2014	AIMS: The aim of the present study was to investigate the effect of swimming exercise on elevated plus-maze (EPM)-associated memory deficit induced by intra-CA1 injection of scopolamine (a muscarinic acetylcholine receptor antagonist used to model Alzheimer"s disease in rodents) in male mice.	Scopolamine	174-185	carbonic anhydrase 1	Mus musculus	157-160
24534175-5	2014	On the other hand, pretest intra-CA1 injection of scopolamine at the doses of 2 and 3 but not 1 mug/mouse reduced the emotional memory.	Scopolamine	50-61	carbonic anhydrase 1	Mus musculus	33-36
24534175-6	2014	Our results demonstrated that 20 days of swimming by itself and without any drug injection restored the emotional memory deficit induced by intra-CA1 injection of scopolamine, only at the dose of 2 but not 3 mug/mouse.	Scopolamine	163-174	carbonic anhydrase 1	Mus musculus	146-149
24534175-10	2014	SIGNIFICANCE: Swimming improved the emotional memory by itself and restored the emotional memory deficit induced by the intra-CA1 injection of scopolamine.	Scopolamine	143-154	carbonic anhydrase 1	Mus musculus	126-129
24729923-7	2014	RESULTS: Short-term memory deteriorated in the mice with scopolamine-induced amnesia, concomitant with enhanced AChE expression and suppression of angiogenesis in the hippocampus.	Scopolamine	57-68	acetylcholinesterase	Mus musculus	112-116
24729923-8	2014	Critically, treadmill exercise ameliorated short-term memory impairment, suppressed AChE expression, and enhanced angiogenesis in the mice with scopolamine-induced amnesia.	Scopolamine	144-155	acetylcholinesterase	Mus musculus	84-88
24315930-10	2014	Scopolamine resulted in memory impairment that was coupled by alterations in the estimated neurotransmitters, heat shock protein 70, acetylcholinesterase activity, oxidative stress as well as inflammatory biomarkers.	Scopolamine	0-11	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	110-131
24315930-10	2014	Scopolamine resulted in memory impairment that was coupled by alterations in the estimated neurotransmitters, heat shock protein 70, acetylcholinesterase activity, oxidative stress as well as inflammatory biomarkers.	Scopolamine	0-11	acetylcholinesterase	Rattus norvegicus	133-153
24012657-0	2014	Acetyl-L-carnitine rescues scopolamine-induced memory deficits by restoring insulin-like growth factor II via decreasing p53 oxidation.	Scopolamine	27-38	insulin like growth factor 2	Homo sapiens	76-105
24993630-9	2014	In trained animals, scopolamine decreased the fEPSP amplitude in the hippocampal CA1 area during first 1.5 h after the injection.	Scopolamine	20-31	carbonic anhydrase 1	Rattus norvegicus	81-84
24989012-7	2014	Finally, the memory ameliorating effects of alpha- or beta-amyrin on the scopolamine-induced cognitive impairments were significantly blocked by ERK inhibitor U0126.	Scopolamine	73-84	mitogen-activated protein kinase 1	Mus musculus	145-148
24938777-6	2014	Scopolamine administration induced a significant impairment of central cholinergic activity in rats, as indicated by a marked increase in AChE activity.	Scopolamine	0-11	acetylcholinesterase	Rattus norvegicus	138-142
24938777-9	2014	Pretreatment of MPME (250 mg/kg, orally administered) significantly reduced scopolamine-induced alternation in brain monoamines with an attenuation of scopolamine-induced rise in brain AChE activity and brain oxidative stress.	Scopolamine	151-162	acetylcholinesterase	Rattus norvegicus	185-189
25031604-7	2014	Interestingly, the level of CREB phosphorylation and BDNF expression in hippocampal tissue of scopolamine-treated mice was significantly increased by the administration of fermented C. lanceolata.	Scopolamine	94-105	cAMP responsive element binding protein 1	Mus musculus	28-32
25031604-7	2014	Interestingly, the level of CREB phosphorylation and BDNF expression in hippocampal tissue of scopolamine-treated mice was significantly increased by the administration of fermented C. lanceolata.	Scopolamine	94-105	brain derived neurotrophic factor	Mus musculus	53-57
24012657-0	2014	Acetyl-L-carnitine rescues scopolamine-induced memory deficits by restoring insulin-like growth factor II via decreasing p53 oxidation.	Scopolamine	27-38	tumor protein p53	Homo sapiens	121-124
24386444-9	2013	The increase in ROS level and caspase-3 activity in the brain of scopolamine-treated mice were antagonized by the ME treatment.	Scopolamine	65-76	caspase 3	Mus musculus	30-39
24135200-9	2013	Modulation of scopolamine-induced impulsivity by olanzapine could be partly due to its antagonistic action at 5-HT2a and 5-HT6 receptors, respectively.	Scopolamine	14-25	5-hydroxytryptamine receptor 2A	Rattus norvegicus	110-136
23751205-3	2013	METHODS: The influence of scopolamine on mTORC1 signaling was determined by analysis of the phosphorylated and activated forms of mTORC1 signaling proteins in the prefrontal cortex (PFC).	Scopolamine	26-37	CREB regulated transcription coactivator 1	Mus musculus	41-47
23751205-3	2013	METHODS: The influence of scopolamine on mTORC1 signaling was determined by analysis of the phosphorylated and activated forms of mTORC1 signaling proteins in the prefrontal cortex (PFC).	Scopolamine	26-37	CREB regulated transcription coactivator 1	Mus musculus	130-136
23751205-6	2013	RESULTS: The results demonstrate that a single, low dose of scopolamine rapidly increases mTORC1 signaling and the number and function of spine synapses in layer V pyramidal neurons in the PFC.	Scopolamine	60-71	CREB regulated transcription coactivator 1	Mus musculus	90-96
23751205-7	2013	Scopolamine administration also produces an antidepressant response in the forced swim test that is blocked by pretreatment with the mTORC1 inhibitor or by a glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor antagonist.	Scopolamine	0-11	CREB regulated transcription coactivator 1	Mus musculus	133-139
23751205-8	2013	CONCLUSIONS: Taken together, the results demonstrate that the antidepressant actions of scopolamine require mTORC1 signaling and are associated with increased glutamate transmission, and synaptogenesis, similar to N-methyl-D-aspartate receptor antagonists.	Scopolamine	88-99	CREB regulated transcription coactivator 1	Mus musculus	108-114
23748234-7	2013	CCh-stimulated [(35)S]GTPgammaS binding to Galphaq was inhibited by mAChR antagonists, including scopolamine, ipratropium, atropine, 4-DAMP, pirenzepine, and AF-DX 116, with a rank order of potency consistent with previous studies of M1-expressing cells.	Scopolamine	97-108	G protein subunit alpha q	Rattus norvegicus	43-50
24404337-8	2013	EUE also markedly increased brain-derived neurotrophic factor (BDNF) and phosphorylation of cAMP element binding protein (CREB) in the hippocampus of scopolamine-induced mice.	Scopolamine	150-161	brain derived neurotrophic factor	Mus musculus	28-61
24404337-8	2013	EUE also markedly increased brain-derived neurotrophic factor (BDNF) and phosphorylation of cAMP element binding protein (CREB) in the hippocampus of scopolamine-induced mice.	Scopolamine	150-161	cAMP responsive element binding protein 1	Mus musculus	122-126
23933216-1	2013	In the present study, we investigated the possible role of the dorsal hippocampal (CA1) dopamine D1 receptors on scopolamine-induced amnesia as well as scopolamine state-dependent memory in adult male Wistar rats.	Scopolamine	113-124	carbonic anhydrase 1	Rattus norvegicus	83-86
23933216-3	2013	Results indicated that pre-training or pre-test intra-CA1 administration of scopolamine (1.5 and 3 mug/rat) dose-dependently reduced the step-through latency, showing an amnestic response.	Scopolamine	76-87	carbonic anhydrase 1	Rattus norvegicus	54-57
23933216-8	2013	These results indicate that the CA1 dopamine D1 receptors may potentially play an important role in scopolamine-induced amnesia as well as the scopolamine state-dependent memory.	Scopolamine	100-111	carbonic anhydrase 1	Rattus norvegicus	32-35
23933216-8	2013	These results indicate that the CA1 dopamine D1 receptors may potentially play an important role in scopolamine-induced amnesia as well as the scopolamine state-dependent memory.	Scopolamine	143-154	carbonic anhydrase 1	Rattus norvegicus	32-35
23651687-3	2013	METHODS: Scopolamine was subcutaneously administered for 28 days via an Alzet minipump (44 mg/ml delivered at 2 5 mul/h) along with a daily intraperitoneal administration of vehicle (saline) 10 mg/kg luteolin or 5 mg/kg galantamine (GAL) (a control drug for acetylcholinesterase (AChE) inhibitor) for 28 days.	Scopolamine	9-20	acetylcholinesterase	Rattus norvegicus	258-278
23722831-0	2013	Chronic scopolamine-injection-induced cognitive deficit on reward-directed instrumental learning in rat is associated with CREB signaling activity in the cerebral cortex and dorsal hippocampus.	Scopolamine	8-19	cAMP responsive element binding protein 1	Rattus norvegicus	123-127
23722831-10	2013	Furthermore, CREB signaling was inactivated by pretraining scopolamine treatment in both the DH and CCx.	Scopolamine	59-70	cAMP responsive element binding protein 1	Rattus norvegicus	13-17
23722831-12	2013	CONCLUSIONS: The results suggest that scopolamine-induced cognitive deficits on RDIL are related to the distinguishing alteration of CREB signaling in the DH and CCx.	Scopolamine	38-49	cAMP responsive element binding protein 1	Rattus norvegicus	133-137
23651687-3	2013	METHODS: Scopolamine was subcutaneously administered for 28 days via an Alzet minipump (44 mg/ml delivered at 2 5 mul/h) along with a daily intraperitoneal administration of vehicle (saline) 10 mg/kg luteolin or 5 mg/kg galantamine (GAL) (a control drug for acetylcholinesterase (AChE) inhibitor) for 28 days.	Scopolamine	9-20	acetylcholinesterase	Rattus norvegicus	280-284
23946693-0	2013	Neuroprotective Effects of AMP-Activated Protein Kinase on Scopolamine Induced Memory Impairment.	Scopolamine	59-70	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	27-55
23916742-0	2013	Tetramethylpyrazine protects against scopolamine-induced memory impairments in rats by reversing the cAMP/PKA/CREB pathway.	Scopolamine	37-48	cAMP responsive element binding protein 1	Rattus norvegicus	110-114
23946693-4	2013	The AMPK WT-injected rats showed significant reversal of the scopolamine induced cognitive deficit as evaluated by escape latency in the Morris water maze.	Scopolamine	61-72	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	4-8
23627469-4	2013	OBJECTIVE: The present study investigates the effect of methanol root extract of C. ferruginea and its active constituent amentoflavone (CF-2) on memory, oxidative stress and acetylcholinesterase (AChE) activity in scopolamine-induced amnesia.	Scopolamine	215-226	coagulation factor II	Mus musculus	137-141
23677777-5	2013	Scopolamine also decreased the activity of 5"-nucleotidase (43 %) and ADA (91 %) in hippocampus.	Scopolamine	0-11	5'-nucleotidase ecto	Homo sapiens	43-58
23677777-5	2013	Scopolamine also decreased the activity of 5"-nucleotidase (43 %) and ADA (91 %) in hippocampus.	Scopolamine	0-11	adenosine deaminase	Homo sapiens	70-73
23627469-8	2013	RESULTS: Scopolamine caused memory impairment along with increased AChE activity and oxidative stress in mice brain.	Scopolamine	9-20	acetylcholinesterase	Mus musculus	67-71
23627469-9	2013	Oral administration of CF and CF-2 significantly prevented scopolamine-induced memory impairment, inhibited AChE and enhanced antioxidant enzyme activity in the brain following scopolamine injection as compared to vehicle administration in scopolamine (i.p.	Scopolamine	59-70	coagulation factor II	Mus musculus	30-34
23627469-9	2013	Oral administration of CF and CF-2 significantly prevented scopolamine-induced memory impairment, inhibited AChE and enhanced antioxidant enzyme activity in the brain following scopolamine injection as compared to vehicle administration in scopolamine (i.p.	Scopolamine	177-188	coagulation factor II	Mus musculus	30-34
23627469-9	2013	Oral administration of CF and CF-2 significantly prevented scopolamine-induced memory impairment, inhibited AChE and enhanced antioxidant enzyme activity in the brain following scopolamine injection as compared to vehicle administration in scopolamine (i.p.	Scopolamine	177-188	coagulation factor II	Mus musculus	30-34
23313392-11	2013	These ginsenosides also reversed hippocampal brain-derived neurotrophic factor (BDNF) expression and cAMP response element-binding protein (CREB) phosphorylation reduced by scopolamine.	Scopolamine	173-184	cAMP responsive element binding protein 1	Mus musculus	101-138
23415910-7	2013	Instant decaffeinated coffee suppressed scopolamine-mediated elevation of tumor necrosis factor-alpha (TNF-alpha) and stimulation of nuclear factor-kappaB (NF-kappaB) pathway (i.e., phosphorylation of IkappaBalpha and p65) in the rat hippocampus.	Scopolamine	40-51	tumor necrosis factor	Rattus norvegicus	74-101
23415910-7	2013	Instant decaffeinated coffee suppressed scopolamine-mediated elevation of tumor necrosis factor-alpha (TNF-alpha) and stimulation of nuclear factor-kappaB (NF-kappaB) pathway (i.e., phosphorylation of IkappaBalpha and p65) in the rat hippocampus.	Scopolamine	40-51	tumor necrosis factor	Rattus norvegicus	103-112
23415910-7	2013	Instant decaffeinated coffee suppressed scopolamine-mediated elevation of tumor necrosis factor-alpha (TNF-alpha) and stimulation of nuclear factor-kappaB (NF-kappaB) pathway (i.e., phosphorylation of IkappaBalpha and p65) in the rat hippocampus.	Scopolamine	40-51	NFKB inhibitor alpha	Rattus norvegicus	201-213
23415910-7	2013	Instant decaffeinated coffee suppressed scopolamine-mediated elevation of tumor necrosis factor-alpha (TNF-alpha) and stimulation of nuclear factor-kappaB (NF-kappaB) pathway (i.e., phosphorylation of IkappaBalpha and p65) in the rat hippocampus.	Scopolamine	40-51	synaptotagmin 1	Rattus norvegicus	218-221
23313392-11	2013	These ginsenosides also reversed hippocampal brain-derived neurotrophic factor (BDNF) expression and cAMP response element-binding protein (CREB) phosphorylation reduced by scopolamine.	Scopolamine	173-184	cAMP responsive element binding protein 1	Mus musculus	140-144
23054680-0	2013	Melatonin attenuates scopolamine-induced memory/synaptic disorder by rescuing EPACs/miR-124/Egr1 pathway.	Scopolamine	21-32	early growth response 1	Homo sapiens	92-96
23154841-7	2013	In addition, they also significantly increased the reduced activities of glutathione reductase and superoxide dismutase and the glutathione content in the hippocampus and cortex of scopolamine-induced amnesic mice.	Scopolamine	181-192	glutathione reductase	Mus musculus	73-94
23000530-4	2013	Interestingly, histamine H(3) receptor (H(3)R) antagonists/inverse agonists stimulate acetylcholine transmission in different brain areas, facilitate memory in animal models and can reverse learning deficits induced by drugs such as scopolamine, dizocilpine and alcohol.	Scopolamine	233-244	histamine receptor H3	Homo sapiens	15-46
23606881-10	2013	Furthermore, BMX ameliorates scopolamine-(Sco-) induced learning and memory impairment in animals, indicating a novel role of BMX in learning and memory.	Scopolamine	29-40	BMX non-receptor tyrosine kinase	Rattus norvegicus	13-16
23606881-10	2013	Furthermore, BMX ameliorates scopolamine-(Sco-) induced learning and memory impairment in animals, indicating a novel role of BMX in learning and memory.	Scopolamine	29-40	BMX non-receptor tyrosine kinase	Rattus norvegicus	126-129
22909986-4	2012	Moreover, intra-CA1/MS administration of a subthreshold dose of muscimol or bicuculline increased and reversed the impairment induced by scopolamine in MS/CA1 respectively (cross injection).	Scopolamine	137-148	carbonic anhydrase 1	Rattus norvegicus	16-19
23469045-7	2013	Co-administration of rivastigmine (1 mg/kg) with the muscarinic antagonist scopolamine significantly increased the number of CD11b expressing cells in the colon but did not change DAI compared to those treated with rivastigmine alone.	Scopolamine	75-86	integrin subunit alpha M	Homo sapiens	125-130
23948897-3	2013	We found that scopolamine caused spatial learning and memory deficits that involved activation of glycogen synthase kinase-3beta (GSK-3beta) and impairments of dendrite arborization and spine formation/maturation associated with alterations of AMPAR, Homer1, and CREB.	Scopolamine	14-25	glycogen synthase kinase 3 beta	Rattus norvegicus	98-128
23948897-3	2013	We found that scopolamine caused spatial learning and memory deficits that involved activation of glycogen synthase kinase-3beta (GSK-3beta) and impairments of dendrite arborization and spine formation/maturation associated with alterations of AMPAR, Homer1, and CREB.	Scopolamine	14-25	glycogen synthase kinase 3 beta	Rattus norvegicus	130-139
23948897-3	2013	We found that scopolamine caused spatial learning and memory deficits that involved activation of glycogen synthase kinase-3beta (GSK-3beta) and impairments of dendrite arborization and spine formation/maturation associated with alterations of AMPAR, Homer1, and CREB.	Scopolamine	14-25	homer scaffold protein 1	Rattus norvegicus	251-257
23948897-3	2013	We found that scopolamine caused spatial learning and memory deficits that involved activation of glycogen synthase kinase-3beta (GSK-3beta) and impairments of dendrite arborization and spine formation/maturation associated with alterations of AMPAR, Homer1, and CREB.	Scopolamine	14-25	cAMP responsive element binding protein 1	Rattus norvegicus	263-267
23080310-8	2012	In terms of receptor expressions, 0.8 and 2 mg/kg scopolamine administration significantly decreased NR2A protein expression, which corroborates suggestions of an interaction between cholinergic and glutamatergic receptors in the hippocampus.	Scopolamine	50-61	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	101-105
22909986-4	2012	Moreover, intra-CA1/MS administration of a subthreshold dose of muscimol or bicuculline increased and reversed the impairment induced by scopolamine in MS/CA1 respectively (cross injection).	Scopolamine	137-148	carbonic anhydrase 1	Rattus norvegicus	155-158
22362194-4	2012	METHODS: Scopolamine was given to male Swiss albino mice to induce memory impairment tested in passive avoidance and Morris water maze tests after a week long administration of blocker of AT1 receptor, candesartan, and AT2 receptor, PD123, 319.	Scopolamine	9-20	angiotensin II receptor, type 1a	Mus musculus	188-191
23079232-2	2012	The present study aimed to determine the effect of the standardized extract of B. platyphylla bark and its major diarylheptanoids in scopolamine-induced amnesic mice through cyclic AMP response element-binding protein (CREB) activation.	Scopolamine	133-144	cAMP responsive element binding protein 1	Mus musculus	174-217
23079232-2	2012	The present study aimed to determine the effect of the standardized extract of B. platyphylla bark and its major diarylheptanoids in scopolamine-induced amnesic mice through cyclic AMP response element-binding protein (CREB) activation.	Scopolamine	133-144	cAMP responsive element binding protein 1	Mus musculus	219-223
23079232-4	2012	CREB phosphorylation and brain-derived neurotrophic factor (BDNF) expression in the cortex and hippocampus of the scopolamine-treated mice were markedly increased by the treatment of the standardized extract of B. platyphylla bark and platyphylloside.	Scopolamine	114-125	cAMP responsive element binding protein 1	Mus musculus	0-4
23079232-4	2012	CREB phosphorylation and brain-derived neurotrophic factor (BDNF) expression in the cortex and hippocampus of the scopolamine-treated mice were markedly increased by the treatment of the standardized extract of B. platyphylla bark and platyphylloside.	Scopolamine	114-125	brain derived neurotrophic factor	Mus musculus	25-58
23079232-4	2012	CREB phosphorylation and brain-derived neurotrophic factor (BDNF) expression in the cortex and hippocampus of the scopolamine-treated mice were markedly increased by the treatment of the standardized extract of B. platyphylla bark and platyphylloside.	Scopolamine	114-125	brain derived neurotrophic factor	Mus musculus	60-64
23214261-2	2012	Scopolamine administration resulted in an increase in acetylcholinesterase (AChE) activity (approximately 9% with respect to the control group) and malonaldehyde (MDA) content.	Scopolamine	0-11	acetylcholinesterase	Rattus norvegicus	54-74
23214261-2	2012	Scopolamine administration resulted in an increase in acetylcholinesterase (AChE) activity (approximately 9% with respect to the control group) and malonaldehyde (MDA) content.	Scopolamine	0-11	acetylcholinesterase	Rattus norvegicus	76-80
23112420-0	2012	Supplementation of Convolvulus pluricaulis attenuates scopolamine-induced increased tau and amyloid precursor protein (AbetaPP) expression in rat brain.	Scopolamine	54-65	amyloid beta precursor protein	Rattus norvegicus	92-117
23112420-2	2012	The present study investigated the potential of Convolvulus pluricaulis (CP) to attenuate scopolamine (2 mg/kg, i.p) induced increased protein and mRNA levels of tau, amyloid precursor protein (AbetaPP), amyloid beta (Abeta) levels and histopathological changes in rat cerebral cortex.	Scopolamine	90-101	amyloid beta precursor protein	Rattus norvegicus	167-192
22362194-13	2012	CONCLUSION: The study suggests that activation of AT1 receptors appears to be involved in the scopolamine-induced amnesia and that AT2 receptors contribute to the beneficial effects of candesartan.	Scopolamine	94-105	angiotensin II receptor, type 1a	Mus musculus	50-53
22475379-8	2012	to scopolamine induced rats significantly (p<0.05) decreased TBARS levels which was accompanied by an increase in the activities of SOD and Catalase.	Scopolamine	3-14	catalase	Rattus norvegicus	143-151
22609381-7	2012	Ketanserin and scopolamine each prevented the ability of SERT knockout or inhibition to increase mucosal growth and proliferation.	Scopolamine	15-26	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	57-61
22362194-4	2012	METHODS: Scopolamine was given to male Swiss albino mice to induce memory impairment tested in passive avoidance and Morris water maze tests after a week long administration of blocker of AT1 receptor, candesartan, and AT2 receptor, PD123, 319.	Scopolamine	9-20	angiotensin II receptor, type 2	Mus musculus	219-231
22367167-6	2012	In contrast, SB-271046 was able to reverse the scopolamine-induced deficits in working memory (only at 30 mg kg-1) and those of acquisition and retrieval of aversive learning (dose-dependent effect); scopolamine-induced deficits in episodic-like memory (acquisition and retrieval) were partially counteracted by 5-HT6R blockade.	Scopolamine	47-58	5-hydroxytryptamine receptor 6	Homo sapiens	312-318
22367167-6	2012	In contrast, SB-271046 was able to reverse the scopolamine-induced deficits in working memory (only at 30 mg kg-1) and those of acquisition and retrieval of aversive learning (dose-dependent effect); scopolamine-induced deficits in episodic-like memory (acquisition and retrieval) were partially counteracted by 5-HT6R blockade.	Scopolamine	200-211	5-hydroxytryptamine receptor 6	Homo sapiens	312-318
22362194-7	2012	RESULTS: Scopolamine caused memory impairment, reduced CBF, acetylcholine (ACh) level, elevated acetylcholinesterase (AChE) activity, and malondialdehyde (MDA).	Scopolamine	9-20	acetylcholinesterase	Mus musculus	118-122
22362194-9	2012	Candesartan prevented scopolamine-induced amnesia, restored CBF and ACh level, and decreased AChE activity and MDA level.	Scopolamine	22-33	acetylcholinesterase	Mus musculus	93-97
22460064-8	2012	Scopolamine caused impairment in memory which was associated with reduced CBF, acetylcholine (ACh) level and elevated acetylcholinesterase (AChE) activity and malondialdehyde (MDA) level.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	140-144
22421366-9	2012	On the other hand, co-administration subthreshold doses of D-AP7 and scopolamine into CA1 and/or MS induced amnesia.	Scopolamine	69-80	carbonic anhydrase 1	Rattus norvegicus	86-89
22460064-0	2012	Inhibition of central angiotensin converting enzyme ameliorates scopolamine induced memory impairment in mice: role of cholinergic neurotransmission, cerebral blood flow and brain energy metabolism.	Scopolamine	64-75	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	22-51
22426465-13	2012	This suggests that the positive effect of UK-343,664 on scopolamine-induced memory decay might arise from peripheral PDE5 inhibition.	Scopolamine	56-67	phosphodiesterase 5A	Homo sapiens	117-121
22328573-6	2012	In vivo effects of PDE9A inhibition included reversal of the respective disruptions of working memory by ketamine, episodic and spatial memory by scopolamine, and auditory gating by amphetamine, as well as potentiation of risperidone-induced improvements in sensorimotor gating and reversal of the stereotypic scratching response to the hallucinogenic 5-hydroxytryptamine 2A agonist mescaline.	Scopolamine	146-157	phosphodiesterase 9A	Homo sapiens	19-24
22145985-6	2012	In aerosolized AMB and scopolamine-treated animals the remaining AChE activity was significantly higher (45-60%) compared to sarin-exposed animals (p < 0.05).	Scopolamine	23-34	acetylcholinesterase	Cavia porcellus	65-69
22226623-3	2012	The results showed that in the animals that received post-training intra-MS injections of saline, intra-CA1 administrations of scopolamine (0.75, 1, and 2 mug/rat) decreased inhibitory avoidance (IA) memory consolidation as evidenced by a decrease in step-through latency on the test day, which was suggestive of drug-induced amnesia.	Scopolamine	127-138	carbonic anhydrase 1	Rattus norvegicus	104-107
22226623-5	2012	Interestingly, intra-MS injections of SKF38393 (0.15, 0.3 and 0.5 mug/rat) significantly prevented amnesia induced by intra-CA1 injections of scopolamine (1 mug/rat).	Scopolamine	142-153	carbonic anhydrase 1	Rattus norvegicus	124-127
22248637-10	2012	Scopolamine treatment not only impaired water maze learning and memory, but also decreased the amount of phosphorylated (activated) ERK and Akt.	Scopolamine	0-11	Eph receptor B1	Rattus norvegicus	132-135
22420664-0	2012	PPARgamma agonist pioglitazone improves scopolamine-induced memory impairment in mice.	Scopolamine	40-51	peroxisome proliferator activated receptor gamma	Mus musculus	0-9
22420664-5	2012	KEY FINDINGS: Scopolamine injection induced impaired performance in the passive avoidance test and the water maze test and severe decrease of cholinergic system reactivity, as indicated by reduced acetylcholine levels, decreased choline acetyltransferase activity and increased acetylcholinesterase activity.	Scopolamine	14-25	choline acetyltransferase	Mus musculus	229-254
22420664-5	2012	KEY FINDINGS: Scopolamine injection induced impaired performance in the passive avoidance test and the water maze test and severe decrease of cholinergic system reactivity, as indicated by reduced acetylcholine levels, decreased choline acetyltransferase activity and increased acetylcholinesterase activity.	Scopolamine	14-25	acetylcholinesterase	Mus musculus	278-298
22420664-7	2012	Pioglitazone also protected against scopolamine-induced cholinergic system deficit, including reduced acetylcholine levels, decreased choline acetyltransferase activity and increased acetylcholinesterase activity in the hippocampus or cortex.	Scopolamine	36-47	choline acetyltransferase	Mus musculus	134-159
22420664-7	2012	Pioglitazone also protected against scopolamine-induced cholinergic system deficit, including reduced acetylcholine levels, decreased choline acetyltransferase activity and increased acetylcholinesterase activity in the hippocampus or cortex.	Scopolamine	36-47	acetylcholinesterase	Mus musculus	183-203
24250476-6	2012	Intra-CA1 injection of scopolamine abolished the memory performance in rats.	Scopolamine	23-34	carbonic anhydrase 1	Rattus norvegicus	6-9
22248637-10	2012	Scopolamine treatment not only impaired water maze learning and memory, but also decreased the amount of phosphorylated (activated) ERK and Akt.	Scopolamine	0-11	AKT serine/threonine kinase 1	Rattus norvegicus	140-143
22248637-11	2012	Agmatine pre-treatment prevented both the learning impairment and hippocampal ERK and Akt inactivation induced by scopolamine.	Scopolamine	114-125	AKT serine/threonine kinase 1	Rattus norvegicus	86-89
22173129-8	2012	In addition, the expression levels of phosphorylated ERK and CREB in the hippocampus were significantly increased by stigmasterol, which was blocked by tamoxifen or MK-801 with scopolamine.	Scopolamine	177-188	mitogen-activated protein kinase 1	Mus musculus	53-56
22173129-8	2012	In addition, the expression levels of phosphorylated ERK and CREB in the hippocampus were significantly increased by stigmasterol, which was blocked by tamoxifen or MK-801 with scopolamine.	Scopolamine	177-188	cAMP responsive element binding protein 1	Mus musculus	61-65
22209911-6	2012	The aim of this study was to ascertain the effect of the NK3-R agonist, senktide, in the scopolamine-induced deficit model.	Scopolamine	89-100	tachykinin receptor 3	Rattus norvegicus	57-62
22107832-10	2012	RESULTS: Scopolamine caused memory impairment along with reduced CBF, increased AChE activity and oxidative stress in mice brain.	Scopolamine	9-20	acetylcholinesterase	Mus musculus	80-84
22209911-0	2012	The NK3 receptor agonist senktide ameliorates scopolamine-induced deficits in memory for object, place and temporal order.	Scopolamine	46-57	tachykinin receptor 3	Rattus norvegicus	4-16
22107832-13	2012	Further, increased oxidative stress and AChE activity following scopolamine was significantly attenuated by ethanolic extract of Noni and its fractions.	Scopolamine	64-75	acetylcholinesterase	Mus musculus	40-44
23238464-6	2012	In turn, scopolamine, an antagonist of cholinergic receptors (0.3 and 1.0 mg/kg, ip), significantly increased TL2 values, impairing cognition.	Scopolamine	9-20	brachyury, T-box transcription factor T	Mus musculus	110-113
22878197-5	2012	The mice treated with Scopolamine showed increased activity of AChE, MDA and SOD levels in both the Hippo and the CC area.	Scopolamine	22-33	acetylcholinesterase	Mus musculus	63-67
21867720-7	2012	Finally, reserved monkeys showed a lower phMRI response to the muscarinic receptor antagonist scopolamine compared to the bold monkeys.	Scopolamine	94-105	cholinergic receptor muscarinic 5	Macaca mulatta	63-82
22567130-6	2012	In scopolamine post-treated animals with extinguished seizures the striatal synaptotagmin7 mRNA levels (at 12 h after the onset of seizures) were not different from the levels in control animals without seizures, while in rats with attenuated seizures, the upregulation closely resembled kainate seizures-like pattern of striatal upregulation.	Scopolamine	3-14	synaptotagmin 7	Rattus norvegicus	76-90
21960666-5	2011	The BAL fluid acetylcholinesterase and butyrylcholinesterase levels were also increased by scopolamine treatment.	Scopolamine	91-102	cholinesterase	Cavia porcellus	39-60
22384146-7	2012	At the day of retrieval, hippocampal levels for M1, Nic7 and NR1 were higher in the scopolamine treated groups than in vehicle-treated groups.The concerted action, i.e. the pattern of four brain receptor complexes regulated by the anticholinergic compound scopolamine, is shown.	Scopolamine	84-95	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	61-64
21839753-6	2011	Scopolamine (10 muM) restored DLL in strychnine-treated slices, suggesting that inhibition of glycine receptors on cholinergic interneurons could modulate eCB signaling by enhancing muscarinic receptor activation and reducing the opening of L-type calcium channels in response to depolarization.	Scopolamine	0-11	latexin	Homo sapiens	16-19
21644059-0	2011	Additive effects of a cholinesterase inhibitor and a histamine inverse agonist on scopolamine deficits in humans.	Scopolamine	82-93	butyrylcholinesterase	Homo sapiens	22-36
21871530-6	2011	On the other hand, intra-CA1 co-administration of an ineffective dose of scopolamine (3mug/rat), but not mecamylamine (1mug/rat), with an ineffective dose of MK-801 (0.5mug/rat) increased %OAT and %OAE and decreased %CAT and %CAE.	Scopolamine	73-84	carbonic anhydrase 1	Rattus norvegicus	25-28
22021993-8	2011	Reduced activities or contents of glutathione reductase, superoxide dismutase, and reduced glutathione within the cortex and hippocampus induced by scopolamine were elevated by the extract.	Scopolamine	148-159	glutathione-disulfide reductase	Rattus norvegicus	34-55
22260011-8	2011	CONCLUSION: CSE can significantly improve the learning and memory impairment in mice induced by scopolamine, which may be correlated with the inhibition of activity of AchE.	Scopolamine	96-107	cystathionase (cystathionine gamma-lyase)	Mus musculus	12-15
22260011-8	2011	CONCLUSION: CSE can significantly improve the learning and memory impairment in mice induced by scopolamine, which may be correlated with the inhibition of activity of AchE.	Scopolamine	96-107	acetylcholinesterase	Mus musculus	168-172
21615274-5	2011	Further, the scopolamine-induced increase in AChE activity was significantly suppressed and the level of acetylcholine was maintained as normal by Sch B treatment.	Scopolamine	13-24	acetylcholinesterase	Mus musculus	45-49
22201090-1	2011	Animal model of depression was developed by means of chronic exposure of rat pups to anticholinergic drugs (Atropine, Scopolamine) during the early life period from postnatal day 7 (P7) and/or 14 (P14) to P21 and/or P28, respectively.	Scopolamine	118-129	S100 calcium binding protein A9	Rattus norvegicus	197-200
22201090-1	2011	Animal model of depression was developed by means of chronic exposure of rat pups to anticholinergic drugs (Atropine, Scopolamine) during the early life period from postnatal day 7 (P7) and/or 14 (P14) to P21 and/or P28, respectively.	Scopolamine	118-129	KRAS proto-oncogene, GTPase	Rattus norvegicus	205-208
21771623-5	2011	The administration of scopolamine significantly decreased the mean number of Ki67- and DCX-immunoreactive cells in the dentate gyrus.	Scopolamine	22-33	doublecortin	Homo sapiens	87-90
21771623-8	2011	These results suggest that the BuChE inhibitor, HBU-39, can ameliorate the scopolamine-induced reductions of cell proliferation and neuroblast differentiation, and HBU-39 may be applicable to amnesia patients to promote memory functions.	Scopolamine	75-86	butyrylcholinesterase	Homo sapiens	31-36
21430646-0	2011	Muscarinic receptor occupancy and cognitive impairment: a PET study with [11C](+)3-MPB and scopolamine in conscious monkeys.	Scopolamine	91-102	cholinergic receptor muscarinic 5	Macaca mulatta	0-19
21554136-9	2011	The activity of AChE was decreased in scopolamine-treated mice but was inhibited significantly by SMS treatment (4 or 8 g/kg) in both salt- and detergent-soluble fractions of brain homogenates.	Scopolamine	38-49	acetylcholinesterase	Mus musculus	16-20
21167182-7	2011	The effects of scopolamine were attenuated by CART, and potentiated by CART-antibody.	Scopolamine	15-26	CART prepropeptide	Rattus norvegicus	46-50
21333723-8	2011	TN-2 also markedly increased BNDF expression and activated the transcription factor CREB in the hippocampi of scopolamine-treated mice.	Scopolamine	110-121	cAMP responsive element binding protein 1	Mus musculus	84-88
21301326-0	2011	MK-7128, a novel CB1 receptor inverse agonist, improves scopolamine-induced learning and memory deficits in mice.	Scopolamine	56-67	cannabinoid receptor 1 (brain)	Mus musculus	17-20
21167182-7	2011	The effects of scopolamine were attenuated by CART, and potentiated by CART-antibody.	Scopolamine	15-26	CART prepropeptide	Rattus norvegicus	71-75
20971004-3	2010	Especially the compounds bearing a para-pyridine consistently showed in vivo activity in rat behavioral models after oral administration, for example, blockade of the mGluR2/3 agonist LY354740-induced hypoactivity and improvement of a working memory deficit induced either by LY354740 or scopolamine in the delayed match to position task (DMTP).	Scopolamine	288-299	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	167-173
19178986-7	2011	Scopolamine had a small effect on delay eyeblink classical conditioning in wild type mice but a large effect in mice lacking apoE.	Scopolamine	0-11	apolipoprotein E	Mus musculus	125-129
19178986-9	2011	These results support a role for apoE in ACh function and suggest that modulation of cortical and hippocampal mAChRs might contribute to genotype differences in scopolamine sensitivity and task acquisition.	Scopolamine	161-172	apolipoprotein E	Mus musculus	33-37
22358085-5	2011	Treatment with scopolamine (0.3 or 1.0 mg/kg, ip) significantly increased TL2 values, thus impairing cognitive processes.	Scopolamine	15-26	brachyury, T-box transcription factor T	Mus musculus	74-77
22358085-6	2011	Moreover, we found that treatment with nicotine, at the non-effective doses used during testing, prevented scopolamine-induced memory impairment by inducing a decrease in TL2 values.	Scopolamine	107-118	brachyury, T-box transcription factor T	Mus musculus	171-174
20971004-4	2010	Moreover, combination studies with a cholinesterase inhibitor show apparent synergistic effects on working memory impairment induced by scopolamine.	Scopolamine	136-147	butyrylcholinesterase	Rattus norvegicus	37-51
20064624-3	2010	Results indicate that post-training or pre-test intra-CA1 administration of scopolamine (1 and 2 microg/rat) dose-dependently reduced the step-through latency, showing an amnestic response.	Scopolamine	76-87	carbonic anhydrase 1	Rattus norvegicus	54-57
20816712-5	2010	We also demonstrated that subsequent intrahippocampal infusions of Norleucine1-Angiotensin IV (Nle1-AngIV) significantly prevented the scopolamine-induced deficit.	Scopolamine	135-146	notchless homolog 1	Rattus norvegicus	95-99
21165335-8	2010	Scopolamine/streptozotocin administration also produced a significant enhancement of brain AChE activity and brain oxidative stress (an increase in TBARS and a decrease in GSH) levels.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	91-95
20685338-4	2010	Moreover, scopolamine infusions attenuated phosphorylation of extracellular signal-regulated kinase (ERK) in the amygdala, indicating that cholinergic signals in the DH are important for trace fear conditioning.	Scopolamine	10-21	Eph receptor B1	Rattus norvegicus	62-99
20685338-4	2010	Moreover, scopolamine infusions attenuated phosphorylation of extracellular signal-regulated kinase (ERK) in the amygdala, indicating that cholinergic signals in the DH are important for trace fear conditioning.	Scopolamine	10-21	Eph receptor B1	Rattus norvegicus	101-104
20188767-11	2010	NNZ-2591 also counteracted the scopolamine-induced up-regulation of choline-acetyltransferase positive neurons in the striatum and similarly counteracted the increased synaptophysin density in the hippocampus.	Scopolamine	31-42	choline O-acetyltransferase	Rattus norvegicus	68-93
20188767-11	2010	NNZ-2591 also counteracted the scopolamine-induced up-regulation of choline-acetyltransferase positive neurons in the striatum and similarly counteracted the increased synaptophysin density in the hippocampus.	Scopolamine	31-42	synaptophysin	Rattus norvegicus	168-181
20564503-0	2010	Comparison of ginsenosides Rg1 and Rb1 for their effects on improving scopolamine-induced learning and memory impairment in mice.	Scopolamine	70-81	protein phosphatase 1, regulatory subunit 3A	Mus musculus	27-30
20564503-0	2010	Comparison of ginsenosides Rg1 and Rb1 for their effects on improving scopolamine-induced learning and memory impairment in mice.	Scopolamine	70-81	RB transcriptional corepressor 1	Mus musculus	35-38
20564503-7	2010	Both Rg1 and Rb1 inhibited the decrease of 5-HT induced by scopolamine, but Rb1 was more active than the same dose of Rg1.	Scopolamine	59-70	protein phosphatase 1, regulatory subunit 3A	Mus musculus	5-8
20564503-7	2010	Both Rg1 and Rb1 inhibited the decrease of 5-HT induced by scopolamine, but Rb1 was more active than the same dose of Rg1.	Scopolamine	59-70	RB transcriptional corepressor 1	Mus musculus	13-16
20564503-8	2010	These results demonstrate that multiple administrations of Rg1 and Rb1 are effective in improving memory deficiency induced by scopolamine.	Scopolamine	127-138	protein phosphatase 1, regulatory subunit 3A	Mus musculus	59-62
20564503-8	2010	These results demonstrate that multiple administrations of Rg1 and Rb1 are effective in improving memory deficiency induced by scopolamine.	Scopolamine	127-138	RB transcriptional corepressor 1	Mus musculus	67-70
20861374-2	2010	Using DNA microarray, we demonstrated the overexpression of quinone reductase 2 (QR2) in the hippocampus in two models of learning deficits, namely the aged memory impaired rats and the scopolamine-induced amnesia model.	Scopolamine	186-197	N-ribosyldihydronicotinamide:quinone reductase 2	Rattus norvegicus	60-79
20861374-2	2010	Using DNA microarray, we demonstrated the overexpression of quinone reductase 2 (QR2) in the hippocampus in two models of learning deficits, namely the aged memory impaired rats and the scopolamine-induced amnesia model.	Scopolamine	186-197	N-ribosyldihydronicotinamide:quinone reductase 2	Rattus norvegicus	81-84
20600432-8	2010	Post-trial treatments with SP 1-11, SP 1-7 or ChCl blocked the amnesic effects of SCP and DZP.	Scopolamine	82-85	Sp1 transcription factor	Rattus norvegicus	27-34
20064624-5	2010	Interestingly, pre-test intra-CA1 microinjection of alpha1-adrenergic agonist, phenylephrine (1 and 2 microg/rat) or alpha2-adrenergic agonist, clonidine improved post-training scopolamine (2 microg/rat)-induced retrieval impairment.	Scopolamine	177-188	carbonic anhydrase 1	Rattus norvegicus	30-33
20064624-9	2010	These results suggest that alpha1- and alpha2-adrenergic receptors of the dorsal hippocampal CA1 regions may play an important role in scopolamine-induced amnesia and scopolamine state-dependent memory.	Scopolamine	135-146	carbonic anhydrase 1	Rattus norvegicus	93-96
20064624-9	2010	These results suggest that alpha1- and alpha2-adrenergic receptors of the dorsal hippocampal CA1 regions may play an important role in scopolamine-induced amnesia and scopolamine state-dependent memory.	Scopolamine	167-178	carbonic anhydrase 1	Rattus norvegicus	93-96
19774505-0	2010	Cryptotanshinone, an acetylcholinesterase inhibitor from Salvia miltiorrhiza, ameliorates scopolamine-induced amnesia in Morris water maze task.	Scopolamine	90-101	acetylcholinesterase	Rattus norvegicus	21-41
19744535-0	2010	The nitric oxide-releasing derivative of ferulic acid NCX 2057 antagonized delay-dependent and scopolamine-induced performance deficits in a recognition memory task in the rat.	Scopolamine	95-106	solute carrier family 8 member A1	Rattus norvegicus	54-57
19744535-10	2010	In addition, NCX 2057 (3 and 10 mg/kg, i.p) reversed the scopolamine (0.2 mg/kg, s.c.)-induced performance deficits in this recognition memory task.	Scopolamine	57-68	solute carrier family 8 member A1	Rattus norvegicus	13-16
19657331-6	2009	Consistent with its ability to enhance the learning-associated, post-training increases in NCAM PSA state, GSK189254 (0.3 mg/kg) reversed the amnesia induced by scopolamine given in the 6-h post-training period after training in an odor discrimination paradigm.	Scopolamine	161-172	neural cell adhesion molecule 1	Rattus norvegicus	91-95
19766675-11	2010	Scopolamine impaired learning at both doses in AChE+/+ mice, but only at the highest dose in AChE+/- mice.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	47-51
19941887-0	2010	Vitamin C deficiency increases basal exploratory activity but decreases scopolamine-induced activity in APP/PSEN1 transgenic mice.	Scopolamine	72-83	presenilin 1	Mus musculus	108-113
19426756-3	2009	Among saponins, timosaponin AIII (TA3) significantly reversed the scopolamine-induced deficits in a passive avoidance test and in the Morris water maze test.	Scopolamine	66-77	RIKEN cDNA 2700049A03 gene	Mus musculus	34-37
19463889-0	2009	Nelumbo nucifera semen extract improves memory in rats with scopolamine-induced amnesia through the induction of choline acetyltransferase expression.	Scopolamine	60-71	choline O-acetyltransferase	Rattus norvegicus	113-138
19694610-8	2009	As shown by the passive avoidance reflex (PAR) test, the intravenous administration of the nanoparticle-bound NGF successfully reversed scopolamine-induced amnesia and improved recognition and memory.	Scopolamine	136-147	nerve growth factor	Rattus norvegicus	110-113
19639304-0	2009	The role of nicotinic receptors in the amelioration of cholinesterase inhibitors in scopolamine-induced memory deficits.	Scopolamine	84-95	butyrylcholinesterase	Homo sapiens	55-69
19639304-2	2009	OBJECTIVE: The present study was undertaken to clarify the role of nicotinic receptors in the ameliorative effects of cholinesterase inhibitors on scopolamine-induced memory deficit.	Scopolamine	147-158	butyrylcholinesterase	Homo sapiens	118-132
19639304-9	2009	CONCLUSION: These results indicate that nicotinic receptors have an essential role in the ameliorative effects of cholinesterase inhibitors in both scopolamine-induced memory deficit and the increase in hippocampal theta activity.	Scopolamine	148-159	butyrylcholinesterase	Homo sapiens	114-128
19426756-4	2009	TA3 also increased hippocampal acetylcholine levels in scopolamine-treated mice and dose-dependently inhibited acetylcholinesterase (AChE) activity (IC(50) value, 35.4 microM).	Scopolamine	55-66	RIKEN cDNA 2700049A03 gene	Mus musculus	0-3
19426756-7	2009	Scopolamine treatment in mice increased brain levels of TNF-alpha and IL-1beta expression.	Scopolamine	0-11	tumor necrosis factor	Mus musculus	56-65
19426756-7	2009	Scopolamine treatment in mice increased brain levels of TNF-alpha and IL-1beta expression.	Scopolamine	0-11	interleukin 1 beta	Mus musculus	70-78
19426756-8	2009	However, treatment with TA3 and scopolamine inhibited the increase of TNF-alpha and IL-1beta expression.	Scopolamine	32-43	tumor necrosis factor	Mus musculus	70-79
19426756-8	2009	However, treatment with TA3 and scopolamine inhibited the increase of TNF-alpha and IL-1beta expression.	Scopolamine	32-43	interleukin 1 beta	Mus musculus	84-92
19426756-10	2009	TA3 also inhibited the activation of NF-kappaB signaling in BV-2 microglia and in SK-N-SH neuroblastoma cells induced with TNF-alpha or scopolamine.	Scopolamine	136-147	trace amine associated receptor 9	Homo sapiens	0-3
18687163-6	2009	We recently showed that LI was disrupted by scopolamine at low doses, and this was reversed by typical and atypical antipsychotic drugs (APDs) and the acetylcholinesterase inhibitor physostigmine.	Scopolamine	44-55	acetylcholinesterase	Rattus norvegicus	151-171
19343477-7	2009	The ethanol extract of Magnolia officinalis and 4-O-methylhonokiol also dose-dependently attenuated the scopolamine-induced increase of acetylcholinesterase (AChE) activity in the cortex and hippocampus of mice, and inhibited AChE activity in vitro with IC(50) (12 nM).	Scopolamine	104-115	acetylcholinesterase	Mus musculus	158-162
19343477-7	2009	The ethanol extract of Magnolia officinalis and 4-O-methylhonokiol also dose-dependently attenuated the scopolamine-induced increase of acetylcholinesterase (AChE) activity in the cortex and hippocampus of mice, and inhibited AChE activity in vitro with IC(50) (12 nM).	Scopolamine	104-115	acetylcholinesterase	Mus musculus	226-230
19191026-5	2009	Highly selective muscarinic toxins MT1 and MT2-affinity order M(1) > or = M(4) >> others-and MT3-highly selective M(4) antagonist-did not show significant effects on basal or forskolin-stimulated cyclic AMP production but, like scopolamine, counteracted oxotremorine inhibition.	Scopolamine	237-248	metallothionein 2A	Rattus norvegicus	43-46
19022248-4	2009	The reinnervated vas deferens produced good contractile responses to transmural stimulation, and these were substantially reduced by a cholinergic muscarinic blocking agent, hyoscine, as compared to only a small reduction in the control vas deferens.	Scopolamine	174-182	arginine vasopressin	Rattus norvegicus	17-20
19182383-7	2009	Mangiferin also reduced acetylcholine and tumor necrosis factor (TNF)-alpha levels induced by scopolamine in mice brain (p<0.05) and inhibited nuclear factor (NF)-kappaB activation in scopolamine or TNF-alpha-stimulated BV-2 microglial cells.	Scopolamine	94-105	tumor necrosis factor	Mus musculus	42-75
19182383-7	2009	Mangiferin also reduced acetylcholine and tumor necrosis factor (TNF)-alpha levels induced by scopolamine in mice brain (p<0.05) and inhibited nuclear factor (NF)-kappaB activation in scopolamine or TNF-alpha-stimulated BV-2 microglial cells.	Scopolamine	187-198	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	146-172
21204339-18	2009	Studies with the centrally acting cholinesterase inhibitor physostigmine demonstrated consistent but partial reversal of scopolamine-induced memory deficits [11,12].	Scopolamine	121-132	butyrylcholinesterase	Homo sapiens	34-48
18996178-7	2009	Moreover, the reduced activities or contents of glutathione reductase, superoxide dismutase (SOD) and reduced GSH within the cortex and hippocampus caused by scopolamine were elevated by the treatment of KD-501.	Scopolamine	158-169	glutathione reductase	Mus musculus	48-69
19010431-2	2009	The present study was outlined to investigate if the association between coffee odor (CS1) and electrical footshock (US) would be an effective model for the study of fear-induced behavior and whether compounds used in humans for emotional-related disorders such as midazolam, propranolol, or scopolamine, applied during the different stages of fear conditioning (acquisition, consolidation and expression), affect the defensive responses to both, the olfactory CS1, and the context (CS2) where the CS1 had been presented (second order conditioning).	Scopolamine	292-303	chorionic somatomammotropin hormone 1	Homo sapiens	86-89
18493749-9	2009	CONCLUSIONS: Histamine H3 receptor antagonists restore the performance of rats impaired by scopolamine and enhance recognition memory after acute administration before the retrieval phase via a mechanism dependent on H1 and H2 receptor activation.	Scopolamine	91-102	histamine receptor H3	Rattus norvegicus	13-34
18501884-11	2008	We also found that chronic treatment of donepezil enhanced, and scopolamine suppressed phosphorylation of cAMP response element binding protein (CREB), which was involved in cell survival, in the DG.	Scopolamine	64-75	cAMP responsive element binding protein 1	Rattus norvegicus	106-143
18976034-8	2008	On the other hand, intra-CA1 administration of scopolamine (0.5, 1, and 2 microg/mouse) after training or injection of the drug (2 microg/mouse) before testing impaired memory when retrieval was tested 24 hours later.	Scopolamine	47-58	carbonic anhydrase 1	Mus musculus	25-28
18533140-3	2008	However, when treated with the muscarinic receptor antagonist scopolamine (0.5, 5mg/kg s.c.) 20 min before each water-maze training session, learning impairments were observed at both doses in AChE(+/+) mice, but only at the highest dose in AChE(+/-) mice.	Scopolamine	62-73	acetylcholinesterase	Mus musculus	241-250
18501884-11	2008	We also found that chronic treatment of donepezil enhanced, and scopolamine suppressed phosphorylation of cAMP response element binding protein (CREB), which was involved in cell survival, in the DG.	Scopolamine	64-75	cAMP responsive element binding protein 1	Rattus norvegicus	145-149
18336929-11	2008	AChE activity in DS fraction of scopolamine amnesic mice was inhibited by donepezil, insulin and melatonin with varying extent in different brain regions, whereas AChE activity in SS fraction was not much affected.	Scopolamine	32-43	acetylcholinesterase	Mus musculus	0-4
18485465-11	2008	As a result, WSDP (100 mg/kg) significantly inhibited AChE activity in the hippocampus of scopolamine-treated mice.	Scopolamine	90-101	acetylcholinesterase	Mus musculus	54-58
18779669-3	2008	METHODS: Aqueous tear production of C57BL/6J Jms Slc male mice aged 10 to 12 weeks were inhibited by subcutaneous scopolamine injection and mice were placed in a continuous airflow blower to create desiccating environmental stress.	Scopolamine	114-125	chemokine (C-C motif) ligand 21A (serine)	Mus musculus	49-52
18515016-8	2008	The results demonstrated that patterned stimulation elicited a significant increase in c-Fos immunolabeled neurons in layer IV of the contralateral primary visual cortex to the stimulated eye which was completely abolished by cholinergic fibers lesion as well as scopolamine administration.	Scopolamine	263-274	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
18384867-7	2008	Acetylcholinesterase inhibitors and anticholinergics used as prophylactics can offset each other, but exceptions are observed in a previous study when a very potent anticholinergic (scopolamine) or a high dose of procyclidine still results in cognitive deficits in spite of coadministration with physostigmine.	Scopolamine	182-193	acetylcholinesterase	Rattus norvegicus	0-20
18357464-9	2008	RESULTS: Daily scopolamine doses of 12.5 mg and 25 mg applied for a 28-day period induced keratitis, a decrease in Muc5AC immunostaining density in the conjunctival epithelium, and modifications in the fatty acid composition of the exorbital LG.	Scopolamine	15-26	mucin 5AC, oligomeric mucus/gel-forming	Rattus norvegicus	115-121
18357464-13	2008	The levels of TNF-alpha, IL-1beta and IL-6 mRNA were increased with scopolamine treatment in both conjunctiva and exorbital LG.	Scopolamine	68-79	tumor necrosis factor	Rattus norvegicus	14-23
18357464-13	2008	The levels of TNF-alpha, IL-1beta and IL-6 mRNA were increased with scopolamine treatment in both conjunctiva and exorbital LG.	Scopolamine	68-79	interleukin 1 beta	Rattus norvegicus	25-33
18357464-13	2008	The levels of TNF-alpha, IL-1beta and IL-6 mRNA were increased with scopolamine treatment in both conjunctiva and exorbital LG.	Scopolamine	68-79	interleukin 6	Rattus norvegicus	38-42
18023504-10	2008	Infusion of scopolamine (1 microM) caused a fivefold increase of ACh levels in wild-type animals but only a 50% increase in AChE-deficient mice.	Scopolamine	12-23	acetylcholinesterase	Mus musculus	124-128
18191820-2	2008	We previously reported that low doses of nociceptin improved the scopolamine-induced impairment of learning and memory in the passive avoidance test and the spontaneous Y-maze alternation task in mice.	Scopolamine	65-76	prepronociceptin	Rattus norvegicus	41-51
18256461-2	2008	Zeatin mitigated cognitive deficits and showed AChE inhibition in scopolamine (Scop)-induced mice following 21 d of zeatin treatment.	Scopolamine	66-77	acetylcholinesterase	Mus musculus	47-51
18256461-2	2008	Zeatin mitigated cognitive deficits and showed AChE inhibition in scopolamine (Scop)-induced mice following 21 d of zeatin treatment.	Scopolamine	79-83	acetylcholinesterase	Mus musculus	47-51
18218192-1	2008	In vivo and in vitro metabolism of scopolamine is investigated using a highly specific and sensitive liquid chromatography-mass spectrometry (LC-MSn) method.	Scopolamine	35-46	moesin	Rattus norvegicus	145-148
17267053-7	2007	Scopolamine or dizocilpine decreased 5-HT(6) receptors expression in nine different brain areas and increased it in CA3 hippocampus or other eight areas, respectively.	Scopolamine	0-11	carbonic anhydrase 3	Rattus norvegicus	116-119
17350296-5	2007	Scopolamine infusions into dorsal CA3 caused deficits for both spatial and nonspatial (visual object) novelty detection.	Scopolamine	0-11	carbonic anhydrase 3	Rattus norvegicus	34-37
17350296-9	2007	These deficits were similar to the deficits caused by scopolamine infusions into dorsal CA3.	Scopolamine	54-65	carbonic anhydrase 3	Rattus norvegicus	88-91
17368430-3	2007	As previously reported ketamine (glutamatergic antagonist) and two well-known amnesic drugs, scopolamine (cholinergic antagonist) and dizocilpine (NMDA antagonist) impaired STM but not LTM; dizocilpine even improved the latter.	Scopolamine	93-104	sulfotransferase family 1A member 3	Homo sapiens	173-176
17920665-8	2008	Additionally, we mapped Fos induction in rats treated with scopolamine and/or Ro 4368554; scopolamine increased Fos expression in the central nucleus of the amygdala and this was attenuated by Ro 4368554.	Scopolamine	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
17920665-8	2008	Additionally, we mapped Fos induction in rats treated with scopolamine and/or Ro 4368554; scopolamine increased Fos expression in the central nucleus of the amygdala and this was attenuated by Ro 4368554.	Scopolamine	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
17920665-8	2008	Additionally, we mapped Fos induction in rats treated with scopolamine and/or Ro 4368554; scopolamine increased Fos expression in the central nucleus of the amygdala and this was attenuated by Ro 4368554.	Scopolamine	90-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
17920665-8	2008	Additionally, we mapped Fos induction in rats treated with scopolamine and/or Ro 4368554; scopolamine increased Fos expression in the central nucleus of the amygdala and this was attenuated by Ro 4368554.	Scopolamine	90-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
17540011-0	2007	Hippocampal gene expression profiling reveals the possible involvement of Homer1 and GABA(B) receptors in scopolamine-induced amnesia.	Scopolamine	106-117	homer scaffold protein 1	Rattus norvegicus	74-80
17010154-6	2007	However, CHT+/- mice display impaired performance as a result of physical challenge in the treadmill paradigm, as well as reduced sensitivity to challenge with the muscarinic receptor antagonist scopolamine in the open field paradigm.	Scopolamine	195-206	solute carrier family 5 (choline transporter), member 7	Mus musculus	9-12
16971898-0	2007	Scopolamine induces disruption of latent inhibition which is prevented by antipsychotic drugs and an acetylcholinesterase inhibitor.	Scopolamine	0-11	acetylcholinesterase (Cartwright blood group)	Homo sapiens	101-121
17004056-1	2007	The cDNA from Nicotiana tabacum encoding Putrescine N-methyltransferase (PMT), which catalyzes the first committed step in the biosynthesis of tropane alkaloids, has been introduced into the genome of a scopolamine-producing Hyoscyamus niger mediated by the disarmed Agrobacterium tumefaciens strain C58C1, which also carries Agrobacterium rhizogenes Ri plasmid pRiA4, and expressed under the control of the CaMV 35S promoter.	Scopolamine	203-214	putrescine N-methyltransferase 1	Nicotiana tabacum	41-71
17004056-1	2007	The cDNA from Nicotiana tabacum encoding Putrescine N-methyltransferase (PMT), which catalyzes the first committed step in the biosynthesis of tropane alkaloids, has been introduced into the genome of a scopolamine-producing Hyoscyamus niger mediated by the disarmed Agrobacterium tumefaciens strain C58C1, which also carries Agrobacterium rhizogenes Ri plasmid pRiA4, and expressed under the control of the CaMV 35S promoter.	Scopolamine	203-214	putrescine N-methyltransferase 1	Nicotiana tabacum	73-76
16774840-5	2006	Scopolamine produced a dose-dependent reduction in responding to the trace CS1, regardless of whether subjects were trained with standard trace (CS1-->trace interval-->US) or serial (CS1-->CS2-->US) trials.	Scopolamine	0-11	catalase	Rattus norvegicus	75-78
17318785-4	2007	The results suggest that psoralen and isopsoralen are the major active ingredients of Psoraleae Fructus responsible for the progressive reversal of scopolamine-induced amnesia, whose effects are partially associated with inhibition of AchE activity and hence activation of the central cholinergic neuronal system.	Scopolamine	148-159	acetylcholinesterase	Rattus norvegicus	235-239
16845528-1	2006	Tropinone reductases (TRs) are essential enzymes in the tropane alkaloid biosynthesis, providing either tropine for hyoscyamine and scopolamine formation or providing pseudotropine for calystegines.	Scopolamine	132-143	tropinone reductase 1-like	Solanum tuberosum	0-20
16774840-5	2006	Scopolamine produced a dose-dependent reduction in responding to the trace CS1, regardless of whether subjects were trained with standard trace (CS1-->trace interval-->US) or serial (CS1-->CS2-->US) trials.	Scopolamine	0-11	catalase	Rattus norvegicus	145-148
16774840-5	2006	Scopolamine produced a dose-dependent reduction in responding to the trace CS1, regardless of whether subjects were trained with standard trace (CS1-->trace interval-->US) or serial (CS1-->CS2-->US) trials.	Scopolamine	0-11	catalase	Rattus norvegicus	145-148
16774840-5	2006	Scopolamine produced a dose-dependent reduction in responding to the trace CS1, regardless of whether subjects were trained with standard trace (CS1-->trace interval-->US) or serial (CS1-->CS2-->US) trials.	Scopolamine	0-11	calsyntenin 2	Rattus norvegicus	198-201
16828889-3	2006	Aged F-344 rats and young mice over-expressing the Swedish mutation in the human amyloid precursor protein (APPsw; Tg2576+) had elevated levels of soluble Abeta, and were more vulnerable to scopolamine challenge in the Morris water maze (MWM), relative to young rats and Tg2576- mice; but, among individual animals, higher levels of soluble Abeta were not correlated with vulnerability to scopolamine.	Scopolamine	190-201	amyloid beta precursor protein	Homo sapiens	81-106
16889901-8	2006	We also found that donepezil enhanced, and scopolamine suppressed, the expression level of phosphorylated cAMP response element binding protein (CREB), which is related to cell survival, in the DG.	Scopolamine	43-54	cAMP responsive element binding protein 1	Rattus norvegicus	106-143
16889901-8	2006	We also found that donepezil enhanced, and scopolamine suppressed, the expression level of phosphorylated cAMP response element binding protein (CREB), which is related to cell survival, in the DG.	Scopolamine	43-54	cAMP responsive element binding protein 1	Rattus norvegicus	145-149
16889901-9	2006	These results indicate that donepezil enhances and scopolamine suppresses the survival of newborn cells in the DG via CREB signaling without affecting neural progenitor cell proliferation and the neuronal differentiation.	Scopolamine	51-62	cAMP responsive element binding protein 1	Rattus norvegicus	118-122
16828889-3	2006	Aged F-344 rats and young mice over-expressing the Swedish mutation in the human amyloid precursor protein (APPsw; Tg2576+) had elevated levels of soluble Abeta, and were more vulnerable to scopolamine challenge in the Morris water maze (MWM), relative to young rats and Tg2576- mice; but, among individual animals, higher levels of soluble Abeta were not correlated with vulnerability to scopolamine.	Scopolamine	389-400	amyloid beta precursor protein	Homo sapiens	81-106
17283607-6	2006	Increased release of ACh and ERK activation are events mechanistically related to each other, as demonstrated by the use of scopolamine, a muscarinic receptor antagonist, and by inhibitors of ERK activation, which blocked memory encoding and ERK activation.	Scopolamine	124-135	mitogen-activated protein kinase 1	Homo sapiens	29-32
16472967-4	2006	PMS777, both a PAF antagonist and a new potent acetylcholinesterase inhibitor was recently demonstrated to reverse scopolamine-induced amnesia in mice without toxicity.	Scopolamine	115-126	acetylcholinesterase	Mus musculus	47-67
16423497-3	2006	Scopolamine treatment of transgenic Tg2576 mice resulted in increased levels of fibrillar Abeta(1-40) and Abeta(1-42), while the soluble, SDS-extractable Abeta level remained unchanged as compared to vehicle-injected Tg2576 mice.	Scopolamine	0-11	amyloid beta (A4) precursor protein	Mus musculus	90-95
16724513-5	2006	Systemically administered scopolamine (CAS 114-49-8) (1 mg/kg i.p.)	Scopolamine	26-37	BCAR1 scaffold protein, Cas family member	Rattus norvegicus	39-42
16914954-2	2006	A preliminary study has shown that central administration of neurotensin enhances spatial and nonspatial working memory in the presence of scopolamine, a muscarinic receptor antagonist which induces memory deficits.	Scopolamine	139-150	neurotensin	Rattus norvegicus	61-72
16914954-6	2006	The restoration effect on scopolamine-induced amnesia produced by PD149163 was blocked by SR142948A, a nonselective neurotensin receptor antagonist, at a dose of 1 mg/kg (intraperitonial) but not at 0.1 mg/kg.	Scopolamine	26-37	neurotensin	Rattus norvegicus	116-127
16364460-0	2006	Microinjection of ritanserin into the CA1 region of hippocampus improves scopolamine-induced amnesia in adult male rats.	Scopolamine	73-84	carbonic anhydrase 1	Rattus norvegicus	38-41
16364460-9	2006	Our findings show that microinjection of ritanserin into the CA1 region of the hippocampus improves the scopolamine-induced amnesia.	Scopolamine	104-115	carbonic anhydrase 1	Rattus norvegicus	61-64
16289415-0	2005	Attenuation of the effects of physostigmine by hyoscine in guinea-pig brain cholinergic enzymes: acetylcholinesterase.	Scopolamine	47-55	acetylcholinesterase	Cavia porcellus	97-117
15863234-4	2005	We reported that kappa-opioid receptor agonists such as U-50,488H and dynorphin A (1-13), improved scopolamine-induced impairment of learning and memory in mice and/or rats.	Scopolamine	99-110	prodynorphin	Mus musculus	70-87
16216227-11	2005	Microinjection of scopolamine, a cholinoceptor antagonist, into the PHN caused a small but significant decrease of firing rate of AHA angiotensin-II-sensitive neurons in SHR but not in WKY.	Scopolamine	18-29	angiotensinogen	Rattus norvegicus	134-148
19595845-0	2005	Reversal of scopolamine-induced deficits with a single dose of donepezil, an acetylcholinesterase inhibitor.	Scopolamine	12-23	acetylcholinesterase (Cartwright blood group)	Homo sapiens	77-97
15982643-2	2005	Pretreatment with the antimuscarinic drugs scopolamine and atropine was able to greatly suppress novelty-induced Fos expression at these sites.	Scopolamine	43-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
16153612-2	2005	Systemic administration of the muscarinic antagonist scopolamine (50 mg/kg) partially attenuates reserpine-mediated striatal Fos expression.	Scopolamine	53-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
16175141-19	2005	After incubation with beta-glucuronidase and sulfatase, the recovery of scopolamine in human urine increased from 3% to approximately 30% of the drug dose (intravenously administered).	Scopolamine	72-83	arylsulfatase family member H	Homo sapiens	45-54
16175141-23	2005	Scopolamine has been shown to undergo an oxidative demethylation during incubation with CYP3A (cytochrome P-450 subfamily).	Scopolamine	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	88-93
15567561-0	2005	Delayed rectifier potassium currents and Kv2.1 mRNA increase in hippocampal neurons of scopolamine-induced memory-deficient rats.	Scopolamine	87-98	potassium voltage-gated channel subfamily B member 1	Rattus norvegicus	41-46
15882896-5	2005	AChE activity was altered in both the fractions SS and DS of different brain areas following passive avoidance in control, scopolamine treated, tacrine treated and tacrine treatment in scopolamine pretreated rats.	Scopolamine	123-134	acetylcholinesterase	Rattus norvegicus	0-4
15882896-5	2005	AChE activity was altered in both the fractions SS and DS of different brain areas following passive avoidance in control, scopolamine treated, tacrine treated and tacrine treatment in scopolamine pretreated rats.	Scopolamine	185-196	acetylcholinesterase	Rattus norvegicus	0-4
15882896-10	2005	Changes in activity of G4 isoform of AChE in hippocampus could be correlated with passive avoidance learning, scopolamine induced deficit in passive avoidance and reversal of scopolamine deficit by tacrine.	Scopolamine	110-121	acetylcholinesterase	Rattus norvegicus	37-41
15882896-10	2005	Changes in activity of G4 isoform of AChE in hippocampus could be correlated with passive avoidance learning, scopolamine induced deficit in passive avoidance and reversal of scopolamine deficit by tacrine.	Scopolamine	175-186	acetylcholinesterase	Rattus norvegicus	37-41
15845095-9	2005	Pretreatment of YC-1 inhibited the scopolamine-induced learning deficit.	Scopolamine	35-46	RNA binding motif single stranded interacting protein 1	Homo sapiens	16-20
15698848-4	2005	Another noteworthy result included the fact that prolonged oral daily treatments of mice with much lower amounts of ESP-102 (1 and 10 mg/kg body weight) for ten days reversed scopolamine-induced memory deficits.	Scopolamine	175-186	exocrine gland secreted peptide 1	Mus musculus	116-133
15567561-5	2005	The mRNA level of Kv2.1 was increased (P<0.01) in the scopolamine-treated group, but there was no significant change of Kv1.5 mRNA level.	Scopolamine	57-68	potassium voltage-gated channel subfamily B member 1	Rattus norvegicus	18-23
15567561-7	2005	The increase of Kv2.1 mRNA expression in hippocampal pyramidal cells might be responsible for the enhancement of IK and could be the ionic basis of the memory deficits induced by scopolamine.	Scopolamine	179-190	potassium voltage-gated channel subfamily B member 1	Rattus norvegicus	16-21
15474645-0	2005	Effects of the cholinesterase inhibitors donepezil and metrifonate on scopolamine-induced impairments in the spatial cone field orientation task in rats.	Scopolamine	70-81	butyrylcholinesterase	Rattus norvegicus	15-29
15474645-9	2005	Thus, a cholinesterase inhibitor with proven clinical efficacy can antagonize scopolamine-induced spatial memory deficits.	Scopolamine	78-89	butyrylcholinesterase	Rattus norvegicus	8-22
15987265-9	2005	The scopolamine group had the least intense AChE staining of all groups.	Scopolamine	4-15	acetylcholinesterase	Rattus norvegicus	44-48
15620572-0	2005	The cholinesterase inhibitor, phenserine, improves Morris water maze performance of scopolamine-treated rats.	Scopolamine	84-95	butyrylcholinesterase	Rattus norvegicus	4-18
15987265-13	2005	In addition, our data suggest that the encountered changes in the AChE staining in the dentate gyrus that followed treatment with scopolamine do not help to explain its disease-modifying effects.	Scopolamine	130-141	acetylcholinesterase	Rattus norvegicus	66-70
14759502-0	2004	Heat-shock pretreatment prevents suppression of long-term potentiation induced by scopolamine in rat hippocampal CA1 synapses.	Scopolamine	82-93	carbonic anhydrase 1	Rattus norvegicus	113-116
15196678-5	2004	Hence, the present results indicate that heat shock has a protective, but not therapeutic, effect on the memory impairment induced by scopolamine by overexpression of HSP72 in rat brain.	Scopolamine	134-145	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	167-172
15246838-0	2004	Differential effects of scopolamine on in vivo binding of dopamine transporter and vesicular monoamine transporter radioligands in rat brain.	Scopolamine	24-35	solute carrier family 6 member 3	Rattus norvegicus	58-78
12646291-0	2003	Ameliorative effect of NC-1900, a new AVP4-9 analog, through vasopressin V1A receptor on scopolamine-induced impairments of spatial memory in the eight-arm radial maze.	Scopolamine	89-100	arginine vasopressin receptor 1A	Rattus norvegicus	61-85
15044039-3	2004	In contrast, the muscarinic receptor antagonist scopolamine (0.75-3.00 mg/kg) virtually abolished the Fos response at both sites.	Scopolamine	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
14643852-6	2003	In nai;ve rats, which have not been exposed to conditioned fear, scopolamine administration also increased MDA and reduced GSH levels, although with an increase in brain GSHPx activity.	Scopolamine	65-76	glutathione peroxidase 1	Rattus norvegicus	170-175
12966162-2	2003	In animals, AChE inhibitors improve learning and memory, reverse scopolamine-induced amnesia, and produce hippocampal theta rhythm.	Scopolamine	65-76	acetylcholinesterase	Rattus norvegicus	12-16
14521875-16	2003	In conclusion, the cholinergic antagonist, scopolamine, disrupts encoding in both CA3 and CA1 subregions of the hippocampus.	Scopolamine	43-54	carbonic anhydrase 3	Rattus norvegicus	82-85
14521875-16	2003	In conclusion, the cholinergic antagonist, scopolamine, disrupts encoding in both CA3 and CA1 subregions of the hippocampus.	Scopolamine	43-54	carbonic anhydrase 1	Rattus norvegicus	90-93
14513799-8	2003	CONCLUSION: The selective adenosine A1 receptor antagonist DPCPX was shown to significantly improve scopolamine but not AP5-induced memory impairment.	Scopolamine	100-111	adenosine A1 receptor	Mus musculus	26-47
12672554-0	2003	The influence of adenosine A3 receptor agonist: IB-MECA, on scopolamine- and MK-801-induced memory impairment.	Scopolamine	60-71	adenosine A3 receptor	Mus musculus	17-38
12672554-6	2003	Obtained results indicate that adenosine A3 receptor stimulation may ameliorate spatial memory and long term memory impairments in terms of cholinergic and glutamatergic deficits induced by scopolamine and MK-801, respectively.	Scopolamine	190-201	adenosine A3 receptor	Mus musculus	31-52
11909625-2	2002	The pmt gene of Nicotiana tabacum was placed under the regulation of the CaMV 35S promoter and introduced into the genome of a scopolamine-rich Duboisia hybrid by a binary vector system using the disarmed Agrobacterium tumefaciens strain C58C1 carrying the rooting plasmid pRiA4.	Scopolamine	127-138	putrescine N-methyltransferase 3	Nicotiana tabacum	4-7
12589378-0	2003	Selective 5-HT1A antagonists WAY 100635 and NAD-299 attenuate the impairment of passive avoidance caused by scopolamine in the rat.	Scopolamine	108-119	5-hydroxytryptamine receptor 1A	Rattus norvegicus	10-16
12387361-4	2002	Physostigmine and hyoscine inhibited red cell AChE by 18.7 +/- 3.7% and plasma ChE by 44.1 +/- 3.1%.	Scopolamine	18-26	acetylcholinesterase	Cavia porcellus	46-50
11954044-4	2002	The results showed that pilocarpine accelerated kindling rates and enhanced kindling-induced mossy fiber sprouting in the CA3 region of the hippocampus, whereas scopolamine retarded kindling rates and blocked kindling-induced mossy fiber sprouting in the CA3 and IML regions.	Scopolamine	161-172	carbonic anhydrase 3	Rattus norvegicus	255-258
12493848-1	2003	In order to increase the production of the pharmaceuticals hyoscyamine and scopolamine in hairy root cultures, a binary vector system was developed to introduce the T-DNA of the Ri plasmid together with the tobacco pmt gene under the control of CaMV 35S promoter, into the genome of Datura metel and Hyoscyamus muticus.	Scopolamine	75-86	putrescine N-methyltransferase 3	Nicotiana tabacum	215-218
12384257-8	2002	The pressor response to angiotensin II was inhibited by scopolamine microinjected into the RVLM, although this produced no effect on the response to carbachol.	Scopolamine	56-67	angiotensinogen	Rattus norvegicus	24-38
12164550-3	2002	scopolamine, a classical anticholinergic agent, or caramiphen, an anticonvulsant anticholinergic drug with anti-glutamatergic properties, in conjunction with pyridostigmine, a reversible cholinesterase inhibitor, were administered prior to sbman (1 LD50).	Scopolamine	0-11	butyrylcholinesterase	Rattus norvegicus	187-201
11746724-1	2001	The present study evaluated the effects of methamphetamine and scopolamine on the striatal dopamine D(1) receptor binding, measured by [(11)C]SCH23390, and D(1) receptor-coupled cAMP messenger system, determined as phosphodiesterase type-IV (PDE-IV) activity, were evaluated in the brains of conscious monkeys using positron emission tomography (PET) with microdialysis.	Scopolamine	63-74	dopamine receptor D1	Homo sapiens	91-113
11494304-6	2001	The maximum increase of LPO levels in erythrocyte membranes was observed as 32% for the Se+E-deficient group.	Scopolamine	88-92	lactoperoxidase	Gallus gallus	24-27
11814146-4	2001	Brain acetylcholinesterase activity was markedly reduced by scopolamine injection.	Scopolamine	60-71	acetylcholinesterase	Rattus norvegicus	6-26
11701197-6	2001	Use of scopolamine and/or diphenhydramine may be possible regimens to alleviate and avoid nausea and vomiting in patients with CsA therapy.	Scopolamine	7-18	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	127-130
11640976-0	2001	Histamine H(3)-receptor antagonism improves memory retention and reverses the cognitive deficit induced by scopolamine in a two-trial place recognition task.	Scopolamine	107-118	histamine receptor H3	Rattus norvegicus	0-23
11553362-0	2001	Ameliorative effect of vasopressin-(4-9) through vasopressin V(1A) receptor on scopolamine-induced impairments of rat spatial memory in the eight-arm radial maze.	Scopolamine	79-90	arginine vasopressin receptor 1A	Rattus norvegicus	49-75
11337201-4	2001	In situ hybridization histochemistry experiment was performed to study its effects on the induction of immediate early gene expression (c-fos, c-jun) by dopamine D1 receptor agonist SKF-82958 and on the augmentation of the SKF-82958-induced expression of these genes by scopolamine.	Scopolamine	270-281	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
11564462-0	2001	Posttraining administration of gastrin-releasing peptide improves memory loss in scopolamine- and hypoxia-induced amnesic mice.	Scopolamine	81-92	gastrin releasing peptide	Mus musculus	31-56
11448481-3	2001	[Arg(8)] vasopressin improved not only scopolamine--but also pyrilamine--and diphenhydramine-induced memory deficits, although a high dose of [Arg(8)] vasopressin was needed to antagonize pyrilamine-induced memory deficits.	Scopolamine	39-50	arginine vasopressin	Rattus norvegicus	9-20
11430861-9	2001	Combined treatment with scopolamine (0.5 mg/kg IP) and CRH (0.5 microg ICV) had only mild, and primarily independent, effects, but overall suggested that concomitant blockade of muscarinic receptors and activation of the CRH system would rather act synergistically to disrupt spatial discrimination learning.	Scopolamine	24-35	corticotropin releasing hormone	Mus musculus	221-224
11378256-5	2001	In somatosensory cortex, the induction of the c-fos gene by linopirdine was nearly completely blocked by atropine and scopolamine and strongly attenuated by the NMDA receptor blockers CPP and MK-801.	Scopolamine	118-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
11202614-3	2000	Pretreatment with the 5-HT1A-receptor agonists 8-OH-DPAT ((+/-)-8-hydroxy-dipropylaminotetralin) and 5-CT (5-carboxamidotryptamine) dose-dependently prevented the amnesia induced by 5-HT1A antagonists, scopolamine, dicyclomine and exposure to an hypoxic environment.	Scopolamine	202-213	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	22-37
11223008-0	2001	Comparative effects of scopolamine and quinpirole on the striatal fos expression induced by stimulation of D(1) dopamine receptors in the rat.	Scopolamine	23-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
11223008-7	2001	These findings demonstrate that there are both differences and similarities between the effects of scopolamine and quinpirole on D(1) agonist-induced Fos expression and suggest that although inhibition of cholinergic neurons may be one of the mechanisms through which the effects of quinpirole are produced, other factors must also contribute.	Scopolamine	99-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
11166120-5	2001	Selective inhibition with pharmacological agents revealed that the constitutive hippocampal cholinergic neurostimulating peptide precursor protein messenger RNA level can be up-regulated by D-(-)-2-amino-5-phosphono-valeric acid, and that activity-dependent transcription can be inhibited by tetrodotoxin, nifedipine, 6-cyano-7-nitroquinoxaline-2,3-dione, and scopolamine, but not by mecamylamine.	Scopolamine	360-371	phosphatidylethanolamine binding protein 1	Rattus norvegicus	80-128
11202614-3	2000	Pretreatment with the 5-HT1A-receptor agonists 8-OH-DPAT ((+/-)-8-hydroxy-dipropylaminotetralin) and 5-CT (5-carboxamidotryptamine) dose-dependently prevented the amnesia induced by 5-HT1A antagonists, scopolamine, dicyclomine and exposure to an hypoxic environment.	Scopolamine	202-213	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	22-28
10995853-4	2000	Systemic administration of scopolamine at doses of 10 and 100 microg/kg dose-dependently increased both dopamine synthesis and DAT availability as measured by l-[beta-(11)C]DOPA and [beta-(11)C]CFT, respectively.	Scopolamine	27-38	solute carrier family 6 member 3	Homo sapiens	127-130
11059909-2	2000	In the present study, the muscarinic (M) receptor antagonists atropine and scopolamine as well as the M2 receptor antagonist AF-DX 116, but not the preferential M1 receptor antagonist pirenzepine, reduced the suppressant effect of the 5-HT1A receptor agonist 8-OH-DPAT on the spontaneous firing activity of rat dorsal raphe 5-HT neurons.	Scopolamine	75-86	5-hydroxytryptamine receptor 1A	Rattus norvegicus	235-241
11501041-1	2000	AIM: The effect of histamine H3-receptor antagonist, clobenpropit (VUF9153) on spatial memory deficits induced by scopolamine was investigated in rats.	Scopolamine	114-125	histamine receptor H3	Rattus norvegicus	19-40
10995853-7	2000	However, scopolamine dose-dependently facilitated the striatal ECF dopamine induced by the DAT inhibitor GBR12909 at a dose of 0.5 mg/kg.	Scopolamine	9-20	solute carrier family 6 member 3	Homo sapiens	91-94
10991934-2	2000	We studied the effects of low doses of 8-OH-DPAT, a 5-HT(1A) receptor agonist, on the impairment of spatial learning caused by scopolamine injected into the CA1 region of the dorsal hippocampus of rats performing a two-platform spatial discrimination task.	Scopolamine	127-138	carbonic anhydrase 1	Rattus norvegicus	157-160
10991934-4	2000	Bilateral injections of 4 microg (in 1 microl) of scopolamine into the CA1 region of the dorsal hippocampus 10 min before each training session impaired choice accuracy with no effect on choice latency and errors of omission.	Scopolamine	50-61	carbonic anhydrase 1	Homo sapiens	71-74
10998544-12	2000	Furthermore, nocistatin counteracted the impairment of learning and memory induced by Noc/OFQ or scopolamine.	Scopolamine	97-108	prepronociceptin	Homo sapiens	13-23
10794821-1	2000	The effects of fmol doses of nociceptin/orphanin FQ on scopolamine-induced impairment of learning and/or memory were examined using spontaneous alternation of Y-maze and step-down type passive avoidance tasks.	Scopolamine	55-66	prepronociceptin	Mus musculus	40-51
10814969-9	2000	The maximum decrease in LPO levels of 42 per cent was obtained for the Se+E group.	Scopolamine	71-75	lactoperoxidase	Gallus gallus	24-27
10594314-5	1999	The inability of higher doses of the cholinesterase inhibitors to antagonise memory deficits induced by scopolamine may be related to excessive cholinergic stimulation in the central nervous system.	Scopolamine	104-115	butyrylcholinesterase	Rattus norvegicus	37-51
10780250-9	1999	Scopolamine, in CD-1 mice, dose-dependently disrupted habituation in an anterograde (0.1-1 mg/kg) and retrograde (1-10 mg/kg) procedure.	Scopolamine	0-11	CD1 antigen complex	Mus musculus	16-20
10578133-0	1999	S 15535, a benzodioxopiperazine acting as presynaptic agonist and postsynaptic 5-HT1A receptor antagonist, prevents the impairment of spatial learning caused by intrahippocampal scopolamine.	Scopolamine	178-189	5-hydroxytryptamine receptor 1A	Homo sapiens	79-94
10578133-2	1999	2 Scopolamine (4.0 microg microl-1), injected bilaterally into the CA1 region of the dorsal hippocampus 10 min before each training session, impaired choice accuracy with no effect on choice latency and errors of omission.	Scopolamine	2-13	carbonic anhydrase 1	Homo sapiens	67-70
11125734-0	1999	Effects of histamine H3 receptor agonists and antagonists on cognitive performance and scopolamine-induced amnesia.	Scopolamine	87-98	histamine receptor H3	Rattus norvegicus	11-32
10414867-5	1999	A pretreatment of the ganglion with atropine or scopolamine reduced the amplitude of the SC1-induced depolarizing wave, suggesting a possible cholinergic muscarinic target.	Scopolamine	48-59	new glue 1	Drosophila melanogaster	89-92
10414867-8	1999	Application of SC1 to oocytes expressing a cloned Drosophila muscarinic receptor (Dml) induced a biphasic response comprising: (1) a large fast Cl- current that was abolished by pretreatment with atropine and scopolamine and (2) a slow and small oscillating Cl- current corresponding to the response observed in control oocytes.	Scopolamine	209-220	new glue 1	Drosophila melanogaster	15-18
10414867-8	1999	Application of SC1 to oocytes expressing a cloned Drosophila muscarinic receptor (Dml) induced a biphasic response comprising: (1) a large fast Cl- current that was abolished by pretreatment with atropine and scopolamine and (2) a slow and small oscillating Cl- current corresponding to the response observed in control oocytes.	Scopolamine	209-220	muscarinic Acetylcholine Receptor, A-type	Drosophila melanogaster	61-80
10578133-5	1999	5 The results confirm a previous report (Carli et al., 1998) that stimulation of presynaptic 5-HT1A receptors in the dorsal raphe counteracts the deficit caused by intrahippocampal scopolamine, probably by facilitating the transfer of facilitatory information from the entorhinal cortex to the hippocampus.	Scopolamine	181-192	5-hydroxytryptamine receptor 1A	Homo sapiens	93-99
10460315-9	1999	The scopolamine induced EEG slowing was less prominent in apoE-deficient than in control mice, and the difference between the strains became slightly clearer during ageing.	Scopolamine	4-15	apolipoprotein E	Mus musculus	58-62
10485959-0	1999	The acetylcholinesterase inhibitor, ENA 713 (Exelon), attenuates the working memory impairment induced by scopolamine in an operant DNMTP task in rats.	Scopolamine	106-117	acetylcholinesterase	Rattus norvegicus	4-24
10460315-13	1999	CONCLUSIONS: The regulation of cortical EEG activity of apoE-deficient mice was somewhat altered during ageing and the response to scopolamine treatment was blunted.	Scopolamine	131-142	apolipoprotein E	Mus musculus	56-60
10375657-5	1999	The scopolamine-induced abolishment of rCBF response was restored by the administration of FK960 at relatively wide dosing range from 1 to 1000 microg/kg (i.v.	Scopolamine	4-15	CCAAT/enhancer binding protein zeta	Rattus norvegicus	39-43
10343183-8	1999	Our finding of decreased rCBF in the thalamus and increased rCBF in the occipital cortex may be attributable to effects of scopolamine per se rather than conditioning.	Scopolamine	123-134	CCAAT/enhancer binding protein zeta	Rattus norvegicus	25-29
10401555-7	1999	The present study was designed to investigate whether nociceptin/orphanin FQ and nocistatin could modulate impairment of learning and memory induced by scopolamine, a muscarinic cholinergic receptor antagonist, using spontaneous alternation of Y-maze and step-down type passive avoidance tasks in mice.	Scopolamine	152-163	prepronociceptin	Mus musculus	65-76
10343183-8	1999	Our finding of decreased rCBF in the thalamus and increased rCBF in the occipital cortex may be attributable to effects of scopolamine per se rather than conditioning.	Scopolamine	123-134	CCAAT/enhancer binding protein zeta	Rattus norvegicus	60-64
9770546-1	1998	When administered intracerebroventricularly to mice performing various learning tasks involving either short-term or long-term memory, secreted forms of the beta-amyloid precursor protein (APPs751 and APPs695) have potent memory-enhancing effects and block learning deficits induced by scopolamine.	Scopolamine	286-297	amyloid beta (A4) precursor protein	Mus musculus	157-187
10027508-8	1999	The agonist-induced increases in PI hydrolysis were fully blocked by the 5HT2A antagonist MDL100907 and the muscarinic antagonist scopolamine, indicating the mediation by 5HT2A receptors in frontal cortex and PI-coupled muscarinic receptors (ml, m3, and m5) in hippocampus, respectively.	Scopolamine	130-141	5-hydroxytryptamine receptor 2A	Rattus norvegicus	171-176
10452094-0	1999	Attenuation of scopolamine-induced deficits in navigational memory performance in rats by bis(7)-tacrine, a novel dimeric AChE inhibitor.	Scopolamine	15-26	acetylcholinesterase	Rattus norvegicus	122-126
9689457-4	1998	The rCBF response abolished by scopolamine was recovered by the administration of physostigmine, a cholinesterase inhibitor in a dose-dependent manner.	Scopolamine	31-42	butyrylcholinesterase	Homo sapiens	99-113
9819798-2	1998	Intracerebroventricular injections of SP (0.1 microgram), NKA (0.3 microgram) and senktide (3 ng) inhibited the scopolamine (1 mg/kg)-induced impairment of spontaneous alternation performance without influencing total arm entries, indicating the antiamnesic effects of tachykinins.	Scopolamine	112-123	tachykinin 1	Mus musculus	38-40
9819798-2	1998	Intracerebroventricular injections of SP (0.1 microgram), NKA (0.3 microgram) and senktide (3 ng) inhibited the scopolamine (1 mg/kg)-induced impairment of spontaneous alternation performance without influencing total arm entries, indicating the antiamnesic effects of tachykinins.	Scopolamine	112-123	tachykinin 1	Mus musculus	58-61
9819798-4	1998	However, the effects of SP on the scopolamine-induced impairment of spontaneous alternation performance were not influenced by pretreatment with the mu-opioid receptor antagonist, beta-funaltrexamine (5 micrograms), the delta-opioid receptor antagonist, naltrindole (4 ng), and the kappa-opioid receptor antagonist, nor-binaltorphimine (4 micrograms).	Scopolamine	34-45	tachykinin 1	Mus musculus	24-26
9712169-10	1998	These results suggest that Nle1-Ang IV acts to counteract the disruption of spatial learning induced by scopolamine.	Scopolamine	104-115	notchless homolog 1	Rattus norvegicus	27-31
9683012-1	1998	The involvement of dopamine receptors in the beneficial effects of intracerebroventricular injection of substance P, neurokinin A and senktide on the scopolamine-induced impairment of spontaneous alternation performance was investigated in mice.	Scopolamine	150-161	tachykinin 1	Mus musculus	104-115
9570817-12	1998	Pretreatment with the selective muscarinic receptor antagonist scopolamine blocked the convulsions and prevented increased Fos and GFAP staining in PC.	Scopolamine	63-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
9570817-12	1998	Pretreatment with the selective muscarinic receptor antagonist scopolamine blocked the convulsions and prevented increased Fos and GFAP staining in PC.	Scopolamine	63-74	glial fibrillary acidic protein	Rattus norvegicus	131-135
9683012-1	1998	The involvement of dopamine receptors in the beneficial effects of intracerebroventricular injection of substance P, neurokinin A and senktide on the scopolamine-induced impairment of spontaneous alternation performance was investigated in mice.	Scopolamine	150-161	tachykinin 1	Mus musculus	117-129
9683012-2	1998	Scopolamine (1 mg/kg) significantly impaired spontaneous alternation performance, while substance P (0.1 microg), neurokinin A (0.3 microg), senktide (0.003 microg) and S(-)-sulpiride (10 mg/kg), a dopamine D2 receptor antagonist, improved the scopolamine (1 mg/kg)-induced disturbance of spontaneous alternation performance.	Scopolamine	0-11	dopamine receptor D2	Mus musculus	198-218
9460750-1	1998	The sigma1 (sigma 1) receptor agonists exert potent anti-amnesic effects, as they apparently block the learning impairments either induced by the muscarinic receptor antagonist scopolamine, the N-methyl-D-aspartate receptor antagonist dizocilpine or inherently due to the age-related deficits in senescence-accelerated mice.	Scopolamine	177-188	sigma non-opioid intracellular receptor 1	Mus musculus	4-29
9602037-4	1998	Microinjection of the muscarinic receptor antagonist scopolamine into the unilateral RVLM inhibited the pressor response to L-glutamate injected ipsilaterally into the lateral PBN, whereas microinjection of the cholinesterase inhibitor physostigmine into the RVLM enhanced it.	Scopolamine	53-64	butyrylcholinesterase	Rattus norvegicus	211-225
9588325-2	1998	This short review considers some data concerning the effects of several cytokines, interleukin (IL)-1, IL-2, IL-6 and granulocyte-macrophage colony-stimulating factor on scopolamine-induced amnesia for a passive avoidance response, and on hippocampal neurotransmitter amino acid levels in mice.	Scopolamine	170-181	interleukin 1 complex	Mus musculus	83-101
9588325-2	1998	This short review considers some data concerning the effects of several cytokines, interleukin (IL)-1, IL-2, IL-6 and granulocyte-macrophage colony-stimulating factor on scopolamine-induced amnesia for a passive avoidance response, and on hippocampal neurotransmitter amino acid levels in mice.	Scopolamine	170-181	interleukin 2	Mus musculus	103-107
9641797-3	1998	This short review considers some data concerning the effects of several cytokines, interleukin (IL)-1, IL-2, IL-6 and granulocyte-macrophage colony-stimulating factor on scopolamine-induced amnesia for a passive avoidance response, and on hippocampal neurotransmitter amino acid levels in mice.	Scopolamine	170-181	interleukin 1 complex	Mus musculus	83-101
9641797-3	1998	This short review considers some data concerning the effects of several cytokines, interleukin (IL)-1, IL-2, IL-6 and granulocyte-macrophage colony-stimulating factor on scopolamine-induced amnesia for a passive avoidance response, and on hippocampal neurotransmitter amino acid levels in mice.	Scopolamine	170-181	interleukin 2	Mus musculus	103-107
9588325-2	1998	This short review considers some data concerning the effects of several cytokines, interleukin (IL)-1, IL-2, IL-6 and granulocyte-macrophage colony-stimulating factor on scopolamine-induced amnesia for a passive avoidance response, and on hippocampal neurotransmitter amino acid levels in mice.	Scopolamine	170-181	interleukin 6	Mus musculus	109-113
9641797-3	1998	This short review considers some data concerning the effects of several cytokines, interleukin (IL)-1, IL-2, IL-6 and granulocyte-macrophage colony-stimulating factor on scopolamine-induced amnesia for a passive avoidance response, and on hippocampal neurotransmitter amino acid levels in mice.	Scopolamine	170-181	interleukin 6	Mus musculus	109-113
9641797-3	1998	This short review considers some data concerning the effects of several cytokines, interleukin (IL)-1, IL-2, IL-6 and granulocyte-macrophage colony-stimulating factor on scopolamine-induced amnesia for a passive avoidance response, and on hippocampal neurotransmitter amino acid levels in mice.	Scopolamine	170-181	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	118-166
9588325-2	1998	This short review considers some data concerning the effects of several cytokines, interleukin (IL)-1, IL-2, IL-6 and granulocyte-macrophage colony-stimulating factor on scopolamine-induced amnesia for a passive avoidance response, and on hippocampal neurotransmitter amino acid levels in mice.	Scopolamine	170-181	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	118-166
9753130-0	1998	Stimulation of 5-HT1A receptors in the dorsal raphe reverses the impairment of spatial learning caused by intrahippocampal scopolamine in rats.	Scopolamine	123-134	5-hydroxytryptamine receptor 1A	Rattus norvegicus	15-21
9753130-1	1998	This study investigated the effect of stimulating 5-HT1A receptors in the dorsal raphe on the impairment of learning caused by 4 microg/microL scopolamine injected in the CA1 region of the dorsal hippocampus in rats performing a two-platform spatial discrimination task.	Scopolamine	143-154	carbonic anhydrase 1	Rattus norvegicus	171-174
9753130-1	1998	This study investigated the effect of stimulating 5-HT1A receptors in the dorsal raphe on the impairment of learning caused by 4 microg/microL scopolamine injected in the CA1 region of the dorsal hippocampus in rats performing a two-platform spatial discrimination task.	Scopolamine	143-154	5-hydroxytryptamine receptor 1A	Rattus norvegicus	50-56
9753130-4	1998	The results show that stimulation of presynaptic 5-HT1A receptors in the dorsal raphe reverses the deficit caused by intrahippocampal scopolamine, probably by facilitating the transfer of facilitatory information from the entorhinal cortex to the hippocampus.	Scopolamine	134-145	5-hydroxytryptamine receptor 1A	Rattus norvegicus	49-55
9475612-6	1997	In the model, scopolamine blocks strengthening of recurrent connections in region CA3 to form attractor states for new items (encoding impaired) but allows recurrent excitation to drive the network into previously stored attractor states (retrieval spared).	Scopolamine	14-25	carbonic anhydrase 3	Homo sapiens	82-85
9449436-1	1997	The muscarinic acetylcholine receptor antagonist scopolamine, but not the beta-adrenoceptor antagonist propranolol or atenolol, suppressed tetanus-induced long-term potentiation (LTP) of population spikes in the rat hippocampal CA1 region.	Scopolamine	49-60	carbonic anhydrase 1	Rattus norvegicus	228-231
9262175-2	1997	Concurrent infusion of the selective and potent 5-hydroxytryptamine3 (5-HT3) receptor antagonist Y-25130 (0.32 and 1.0 microg/side) significantly attenuated the increase in working memory errors induced by intrahippocampal 3.2 microg/side scopolamine.	Scopolamine	239-250	5-hydroxytryptamine receptor 3A	Rattus norvegicus	70-85
9427297-0	1997	Interleukin-6 attenuation of scopolamine-induced amnesia: plausible involvement of cholinergic neuronal survival.	Scopolamine	29-40	interleukin 6	Homo sapiens	0-13
9270059-9	1997	The posttraumatic reduction in scopolamine-evoked ACh release was completely reversed with NGF.	Scopolamine	31-42	nerve growth factor	Rattus norvegicus	91-94
9452205-0	1997	WAY 100635, a 5-HT1A receptor antagonist, prevents the impairment of spatial learning caused by intrahippocampal administration of scopolamine or 7-chloro-kynurenic acid.	Scopolamine	131-142	5-hydroxytryptamine receptor 1A	Homo sapiens	14-29
9282916-4	1997	We observed an increase in NGF protein levels in the cortex and hippocampus after cholinergic immunolesions and also after muscarinic receptor blockade by chronic intracerebroventricular scopolamine infusion in sham-treated rats after 2 weeks.	Scopolamine	187-198	nerve growth factor	Rattus norvegicus	27-30
9296567-0	1997	Regionally different effects of scopolamine on NMDA antagonist-induced heat shock protein HSP70.	Scopolamine	32-43	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	90-95
9296567-3	1997	Pretreatment with the muscarinic receptor antagonist scopolamine (0.1-1 mg/kg) blocked induction of HSP-70 in layer III of the retrosplenial cortex.	Scopolamine	53-64	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	100-106
9296567-4	1997	However, induction of HSP-70 in layer V was augmented by scopolamine.	Scopolamine	57-68	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	22-28
9203561-1	1997	The selective sigma1 receptor agonist 1-(3,4-dimethoxyphenethyl)-4-(3-phenyl propyl)piperazine dihydrochloride (SA4503) was reported to reverse the amnesia induced by the muscarinic receptor antagonist scopolamine at sub-mg/kg doses.	Scopolamine	202-213	sigma non-opioid intracellular receptor 1	Mus musculus	14-29
9218681-0	1997	Effects of ginsenosides on maze performance and brain choline acetyltransferase activity in scopolamine-treated young rats and aged rats.	Scopolamine	92-103	choline O-acetyltransferase	Rattus norvegicus	54-79
9218681-1	1997	In young adult rats with scopolamine-induced cognitive impairment, choline acetyltransferase activity was increased in the medial septum, but not in the diagonal band, caudate and hippocampus, 30 min after the injection of ginsenosides Rg1 or Re.	Scopolamine	25-36	choline O-acetyltransferase	Rattus norvegicus	67-92
9035256-2	1997	Scopolamine was administered IP 30 min before the training session.	Scopolamine	0-11	interferon gamma inducible protein 30	Mus musculus	29-34
9062678-1	1997	The effects of intracerebroventricular administration of dynorphin A(1-13) on scopolamine- and pirenzepine-induced amnesia were investigated in mice by observing the step-down-type passive avoidance response and spontaneous alternation performance.	Scopolamine	78-89	prodynorphin	Mus musculus	57-73
9062678-3	1997	Dynorphin A(1-13) (1 microgram) given 15 min before training and retention tests, but not immediately after training, significantly improved the scopolamine (1 mg/kg)-induced impairment of passive avoidance response, indicating the anti-amnesic effects of dynorphin A(1-13).	Scopolamine	145-156	prodynorphin	Mus musculus	0-16
9062678-6	1997	Dynorphin A(1-13) (3, 5.6 and/or 10 micrograms) significantly improved the scopolamine (1 mg/kg)- and pirenzepine (3 micrograms)-induced impairment of spontaneous alternation performance.	Scopolamine	75-86	prodynorphin	Mus musculus	0-16
9062679-1	1997	Previously, the ability of co-administered nefiracetam to reverse scopolamine-induced learning deficits has been attributed to the preservation of a transient increase in neural cell adhesion molecule (NCAM) polysialylation state during a late phase of memory consolidation (Doyle et al., J. Neurosci.	Scopolamine	66-77	neural cell adhesion molecule 1	Rattus norvegicus	171-200
9205824-11	1997	Compared with placebo or zamifenacin, pulse rate fell following hyoscine administration (9 beats min-1, P < 0.01).	Scopolamine	64-72	CD59 molecule (CD59 blood group)	Homo sapiens	97-102
9190877-3	1997	Intravenous administration of scopolamine (50 microg/kg) resulted in abolishment of the rCBF response to stimulation.	Scopolamine	30-41	CCAAT/enhancer binding protein zeta	Rattus norvegicus	88-92
9190877-4	1997	The rCBF response abolished by pretreatment with scopolamine was recovered by administration of physostigmine (1 or 10 microg/kg), E2020 (10 or 100 microg/kg) or tacrine (100 or 1000 microg/kg), in a dose-dependent manner.	Scopolamine	49-60	CCAAT/enhancer binding protein zeta	Rattus norvegicus	4-8
9190877-6	1997	These findings suggest that these compounds reversed the scopolamine-abolished rCBF response to somatosensory stimulation via enhancement of cholinergic neurotransmission, which was mainly induced by cholinesterase inhibition.	Scopolamine	57-68	CCAAT/enhancer binding protein zeta	Rattus norvegicus	79-83
9190877-6	1997	These findings suggest that these compounds reversed the scopolamine-abolished rCBF response to somatosensory stimulation via enhancement of cholinergic neurotransmission, which was mainly induced by cholinesterase inhibition.	Scopolamine	57-68	butyrylcholinesterase	Homo sapiens	200-214
9189894-4	1997	The increase in working memory errors induced by intrahippocampal administration of 0.32 microgram/side scopolamine to rats treated with 10 mg/kg propranolol was decreased by concurrent injection of the cholinesterase inhibitor physostigmine (3.2 micrograms/side).	Scopolamine	104-115	butyrylcholinesterase	Rattus norvegicus	203-217
9189931-0	1997	Interleukin-6 affects scopolamine-induced amnesia, but not brain amino acid levels in mice.	Scopolamine	22-33	interleukin 6	Mus musculus	0-13
9189931-2	1997	In this study, we evaluated the effects of mouse interleukin-6 (IL-6) on the classical behavioural test of scopolamine-induced amnesia for a passive avoidance response in the mouse.	Scopolamine	107-118	interleukin 6	Mus musculus	49-62
9189931-2	1997	In this study, we evaluated the effects of mouse interleukin-6 (IL-6) on the classical behavioural test of scopolamine-induced amnesia for a passive avoidance response in the mouse.	Scopolamine	107-118	interleukin 6	Mus musculus	64-68
9130285-0	1997	Cognitive dysfunctions induced by scopolamine are reduced by systemic or intrahippocampal mineralocorticoid receptor blockade.	Scopolamine	34-45	nuclear receptor subfamily 3, group C, member 2	Rattus norvegicus	90-116
9070622-3	1997	Intravenous administration of scopolamine at doses ranging from 1 to 500 microg/kg resulted in a dose-dependent reduction of the rCBF response.	Scopolamine	30-41	CCAAT/enhancer binding protein zeta	Rattus norvegicus	129-133
9070622-4	1997	The rCBF response abolished by scopolamine (50 microg/kg) was recovered by administration of physostigmine (10 microg/kg).	Scopolamine	31-42	CCAAT/enhancer binding protein zeta	Rattus norvegicus	4-8
9035256-6	1997	Physostigmine, an acetylcholinesterase (AChE) inhibitor, alleviated the scopolamine-induced memory impairment in all these drug administration schedules.	Scopolamine	72-83	acetylcholinesterase	Mus musculus	18-38
9035256-6	1997	Physostigmine, an acetylcholinesterase (AChE) inhibitor, alleviated the scopolamine-induced memory impairment in all these drug administration schedules.	Scopolamine	72-83	acetylcholinesterase	Mus musculus	40-44
9035256-4	1997	(+)-N-Allylnormetazocine ((+)-SKF-10,047), a prototype sigma 1 receptor agonist, showed an ameliorating effect on the scopolamine-induced memory impairment in these 3 administration schedules, and (-)-SKF-10,047, a stereoisomer with low affinity for the sigma 1 receptor subtype, failed to reduce this memory impairment in mice.	Scopolamine	118-129	sigma non-opioid intracellular receptor 1	Mus musculus	55-71
9035256-4	1997	(+)-N-Allylnormetazocine ((+)-SKF-10,047), a prototype sigma 1 receptor agonist, showed an ameliorating effect on the scopolamine-induced memory impairment in these 3 administration schedules, and (-)-SKF-10,047, a stereoisomer with low affinity for the sigma 1 receptor subtype, failed to reduce this memory impairment in mice.	Scopolamine	118-129	sigma non-opioid intracellular receptor 1	Mus musculus	254-270
9030400-1	1997	To study the role of hippocampal muscarinic receptors in spatial learning, various doses of scopolamine were injected bilaterally into the CA1 region of the dorsal hippocampus of rats trained in a two-platform spatial discrimination task.	Scopolamine	92-103	carbonic anhydrase 1	Rattus norvegicus	139-142
9116242-4	1996	The mPRF of intact, halothane-anesthetized cats was dialyzed with Ringer"s solution (control) or Ringer"s containing the muscarinic antagonist scopolamine, Scopolamine caused a dose-dependent increase in mPRF ACh release and a concomitant decrease in the number of halothane-induced cortical EEG spindles.	Scopolamine	143-154	Spi-C transcription factor (Spi-1/PU.1 related)	Mus musculus	204-208
9116242-4	1996	The mPRF of intact, halothane-anesthetized cats was dialyzed with Ringer"s solution (control) or Ringer"s containing the muscarinic antagonist scopolamine, Scopolamine caused a dose-dependent increase in mPRF ACh release and a concomitant decrease in the number of halothane-induced cortical EEG spindles.	Scopolamine	156-167	Spi-C transcription factor (Spi-1/PU.1 related)	Mus musculus	4-8
9116242-4	1996	The mPRF of intact, halothane-anesthetized cats was dialyzed with Ringer"s solution (control) or Ringer"s containing the muscarinic antagonist scopolamine, Scopolamine caused a dose-dependent increase in mPRF ACh release and a concomitant decrease in the number of halothane-induced cortical EEG spindles.	Scopolamine	156-167	Spi-C transcription factor (Spi-1/PU.1 related)	Mus musculus	204-208
8950017-3	1996	Angiotensin-converting enzyme (ACE) inhibitors, which block the formation of AII from AI, improve acquisition and/or retention of basal performance inhibited by the muscarinic receptor antagonist, scopolamine, in conditioned avoidance and habituation tasks.	Scopolamine	197-208	angiotensin I converting enzyme	Rattus norvegicus	0-29
8950017-3	1996	Angiotensin-converting enzyme (ACE) inhibitors, which block the formation of AII from AI, improve acquisition and/or retention of basal performance inhibited by the muscarinic receptor antagonist, scopolamine, in conditioned avoidance and habituation tasks.	Scopolamine	197-208	angiotensin I converting enzyme	Rattus norvegicus	31-34
8950017-3	1996	Angiotensin-converting enzyme (ACE) inhibitors, which block the formation of AII from AI, improve acquisition and/or retention of basal performance inhibited by the muscarinic receptor antagonist, scopolamine, in conditioned avoidance and habituation tasks.	Scopolamine	197-208	angiotensinogen	Rattus norvegicus	77-80
8923522-2	1996	Acute administration of the non-selective muscarinic antagonist, scopolamine (2.5, 5 and 10 mg/kg, s.c.), caused a dose-dependent increase in preprodynorphin and substance P, but not preproenkephalin, messenger RNA expression in the dorsal and ventral striatum as revealed by quantitative in situ hybridization.	Scopolamine	65-76	prodynorphin	Rattus norvegicus	142-157
8923522-4	1996	Pretreatment with scopolamine (2.5 mg/kg, s.c.) significantly augmented striatal induction of preprodynorphin and substance P messenger RNA induced by acute injection of amphetamine (1.25 and 2.5 mg/kg, i.p.	Scopolamine	18-29	prodynorphin	Rattus norvegicus	94-109
8905166-6	1996	Treatment with scopolamine, a muscarinic receptor antagonist, suppressed veratrine-induced CCK-LI and DA release, but did not change NMDA-evoked CCK-LI and DA release.	Scopolamine	15-26	cholecystokinin	Rattus norvegicus	91-94
8922677-11	1996	The effects of scopolamine and SKF 38393 on c-fos induction in striatum are qualitatively similar to those reported in rats DA-depleted as adults and suggest that, at this single-label level of analysis, the ability of D1 and muscarinic receptors to influence striatal activity does not contribute to the marked age-related differences in the behavioral effects of DA depletions.	Scopolamine	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
8905730-2	1996	The increase in working memory errors induced by intrahippocampal 3.2 micrograms/side scopolamine was reduced by concurrent injection of the cholinesterase inhibitor physostigmine (1.0 and 3.2 micrograms/side.	Scopolamine	86-97	butyrylcholinesterase	Rattus norvegicus	141-155
9642415-0	1996	[Effects of ding zhi pills on the scopolamine-induced impairment of passive avoidance in rats].	Scopolamine	34-45	ring finger protein 2	Homo sapiens	12-16
8877002-0	1996	Peripherally administered GM-CSF interferes with scopolamine-induced amnesia in mice: involvement of interleukin-1.	Scopolamine	49-60	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	26-32
8877002-1	1996	We studied the effects of granulocyte-macrophage colony stimulating factor (GM-CSF) on the classical behavioral test of scopolamine-induced amnesia for a passive avoidance response in the mouse.	Scopolamine	120-131	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	26-74
8877002-1	1996	We studied the effects of granulocyte-macrophage colony stimulating factor (GM-CSF) on the classical behavioral test of scopolamine-induced amnesia for a passive avoidance response in the mouse.	Scopolamine	120-131	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	76-82
7658452-3	1995	They inhibit acetylcholinesterase in vitro, and many are active in vivo in reversing a scopolamine-induced impairment of 24 h memory in a passive avoidance paradigm.	Scopolamine	87-98	acetylcholinesterase (Cartwright blood group)	Homo sapiens	13-33
8861055-0	1996	Scopolamine augments c-fos and zip/268 messenger RNA expression induced by the full D(1) dopamine receptor agonist SKF-82958 in the intact rat striatum.	Scopolamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
8861055-0	1996	Scopolamine augments c-fos and zip/268 messenger RNA expression induced by the full D(1) dopamine receptor agonist SKF-82958 in the intact rat striatum.	Scopolamine	0-11	sequestosome 1	Rattus norvegicus	31-34
8861055-5	1996	However, scopolamine attenuated basal, and SKF-82958-stimulated, expression of c-fos and zif/268 messenger RNAs in the cortex.	Scopolamine	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
8861055-5	1996	However, scopolamine attenuated basal, and SKF-82958-stimulated, expression of c-fos and zif/268 messenger RNAs in the cortex.	Scopolamine	9-20	early growth response 1	Rattus norvegicus	89-96
8861055-6	1996	Scopolamine also enabled SKF-38393 to induce locomotor stimulation and c-fos and zif/268 messenger RNA expression in the normosensitive striatum of the rat when SKF-38393 alone caused no such changes.	Scopolamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
8861055-6	1996	Scopolamine also enabled SKF-38393 to induce locomotor stimulation and c-fos and zif/268 messenger RNA expression in the normosensitive striatum of the rat when SKF-38393 alone caused no such changes.	Scopolamine	0-11	early growth response 1	Rattus norvegicus	81-88
8905797-0	1996	Neurokinin A and senktide attenuate scopolamine-induced impairment of spontaneous alternation performance in mice.	Scopolamine	36-47	tachykinin 2	Mus musculus	0-12
8905797-4	1996	However, neurokinin A (0.3 and 1 microgram) and senktide (0.003 and 0.03 microgram) inhibited the scopolamine (1 mg/kg)-induced impairment of spontaneous alternation performance without affecting the scopolamine (1 mg/kg)-induced increase in total arm entries.	Scopolamine	98-109	tachykinin 2	Mus musculus	9-21
8905797-6	1996	These findings suggest that neurokinin A inhibits the scopolamine-induced impairment of spontaneous alternation performance associated with working memory through the mediation of tachykinin NK-2 receptors, while senktide has some pharmacological action other than its effects on NK-3 receptors.	Scopolamine	54-65	tachykinin 2	Mus musculus	28-40
8905797-6	1996	These findings suggest that neurokinin A inhibits the scopolamine-induced impairment of spontaneous alternation performance associated with working memory through the mediation of tachykinin NK-2 receptors, while senktide has some pharmacological action other than its effects on NK-3 receptors.	Scopolamine	54-65	tachykinin 2	Mus musculus	191-195
8793085-9	1996	The muscarinic antagonist scopolamine did not alter c-fos expression in the odour-selective area but increased significantly Fos labelling in the other bulbar aspects.	Scopolamine	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
8801468-8	1996	Focal potentials in response to stimulation of the perforant path in CA1 were suppressed to an equal extent (by 43%) during sensory stimulation inducing natural theta rhythm, during the action of eserine, and with stimulation of the MS-DB In the BU group, these effects led to the complete suppression of focal potentials; scopolamine restored them.	Scopolamine	323-334	carbonic anhydrase 1	Oryctolagus cuniculus	69-72
9053585-2	1995	In a behavioral study, thioperamide (20 mg/kg) alone slightly ameliorated scopolamine-induced learning deficit, and pretreatment with zolantidine, a histamine H2-receptor antagonist, significantly enhanced the ameliorating effect of thioperamide.	Scopolamine	74-85	histamine receptor H2	Mus musculus	149-170
8535837-2	1995	A putative sigma 1 receptor agonist, (+)-SKF-10,047, elicited an increase of hippocampal extracellular acetylcholine level and anti-amnesic effect against scopolamine-induced memory dysfunctions in rats.	Scopolamine	155-166	sigma non-opioid intracellular receptor 1	Rattus norvegicus	11-27
8780042-2	1996	Its action on vasopressin has been proposed as the underlying mechanism accounting for the ability of inhibitors of prolyl oligopeptidase to reverse scopolamine-induced amnesia in rats.	Scopolamine	149-160	arginine vasopressin	Rattus norvegicus	14-25
8780042-2	1996	Its action on vasopressin has been proposed as the underlying mechanism accounting for the ability of inhibitors of prolyl oligopeptidase to reverse scopolamine-induced amnesia in rats.	Scopolamine	149-160	prolyl endopeptidase	Mus musculus	116-137
8789616-0	1995	Scopolamine-induced impairment as a potential predictor of Alzheimer"s disease in individuals with Apolipoprotein E type 4 alleles.	Scopolamine	0-11	apolipoprotein E	Homo sapiens	99-115
7498302-0	1995	(S)-WAY 100135, a 5-HT1A receptor antagonist, prevents the impairment of spatial learning caused by intrahippocampal scopolamine.	Scopolamine	117-128	5-hydroxytryptamine receptor 1A	Rattus norvegicus	18-24
7498302-1	1995	Scopolamine, 3.75 micrograms/microliters infused bilaterally into the CA1 region of the dorsal hippocampus 10 min before each training session, impaired choice accuracy but had no effect on choice latency or errors of omission in rats trained in a two-platform spatial discrimination task.	Scopolamine	0-11	carbonic anhydrase 1	Rattus norvegicus	70-73
7562510-6	1995	In addition, coadministration of JTP-4819 and substance P, arginine-vasopressin or thyrotropin-releasing hormone (at doses at which each drug alone did not prolong the retention time) improved the retention time of rats with scopolamine-induced amnesia.	Scopolamine	225-236	arginine vasopressin	Rattus norvegicus	68-79
7562510-6	1995	In addition, coadministration of JTP-4819 and substance P, arginine-vasopressin or thyrotropin-releasing hormone (at doses at which each drug alone did not prolong the retention time) improved the retention time of rats with scopolamine-induced amnesia.	Scopolamine	225-236	thyrotropin releasing hormone	Rattus norvegicus	83-112
7724828-5	1995	PACAP 1-27 and PACAP 1-38 relax taenia caeci dose-dependently in the presence of guanethidine and scopolamine.	Scopolamine	98-109	adenylate cyclase activating polypeptide 1	Sus scrofa	0-5
7617671-7	1995	The yawning induced by oxytocin, alpha-MSH, or RS-86 administered in combination with pindolol was inhibited by scopolamine (0.5 mg/kg, SC), a mucarinic receptor antagonist, without being affected by spiperone (0.5 mg/kg, SC), a dopamine D2 receptor antagonist.	Scopolamine	112-123	proopiomelanocortin	Rattus norvegicus	33-42
7637570-9	1995	Neurokinin B mRNA levels were increased by 50% in the shell of the accumbens after scopolamine.	Scopolamine	83-94	tachykinin precursor 3	Rattus norvegicus	0-12
7637876-5	1995	When co-administered with haloperidol (seven days, 1 mg/kg s.c.), the muscarinic antagonist scopolamine (1 mg/kg, s.c.) completely blocked both haloperidol-induced catalepsy and increases in glutamate decarboxylase messenger RNA levels in the globus pallidus.	Scopolamine	92-103	glutamate-ammonia ligase	Rattus norvegicus	191-214
7541697-0	1995	Substance P markedly ameliorates scopolamine-induced impairment of spontaneous alternation performance in the mouse.	Scopolamine	33-44	tachykinin 1	Mus musculus	0-11
7541697-1	1995	We investigated the effects of intracerebroventricular injection of substance P (SP) on the scopolamine (1 mg/kg)-induced impairment of spontaneous alternation performance in the mouse.	Scopolamine	92-103	tachykinin 1	Mus musculus	68-79
7541697-1	1995	We investigated the effects of intracerebroventricular injection of substance P (SP) on the scopolamine (1 mg/kg)-induced impairment of spontaneous alternation performance in the mouse.	Scopolamine	92-103	tachykinin 1	Mus musculus	81-83
7541697-4	1995	In contrast, SP (0.01-1 micrograms) significantly improved the scopolamine (1 mg/kg)-induced impairment of spontaneous alternation performance without influencing the scopolamine (1 mg/kg)-induced increase in total arm entries.	Scopolamine	63-74	tachykinin 1	Mus musculus	13-15
7541697-5	1995	The effects of SP (0.1 micrograms) on the scopolamine (1 mg/kg)-induced impairment of spontaneous alternation performance were almost completely reversed by pretreatment with WIN 62577 (1 mg/kg), a tachykinin NK-1 receptor antagonist.	Scopolamine	42-53	tachykinin 1	Mus musculus	15-17
7541697-6	1995	These results suggest that SP improves the scopolamine-induced impairment of spontaneous alternation performance through the mediation of tachykinin NK-1 receptors.	Scopolamine	43-54	tachykinin 1	Mus musculus	27-29
7768285-0	1995	Dynorphin A-(1-13) potently improves scopolamine-induced impairment of passive avoidance response in mice.	Scopolamine	37-48	prodynorphin	Mus musculus	0-17
7768285-1	1995	The effects of intracerebroventricular administration of dynorphin A-(1-13) on scopolamine-induced amnesia were investigated in mice by using a step-down type passive avoidance task.	Scopolamine	79-90	prodynorphin	Mus musculus	57-74
7768285-3	1995	Dynorphin A-(1-13)(1 microgram) given 15 min before training and retention tests but not immediately after training significantly improved the scopolamine (1 mg/kg)-induced shortening of step-down latency of the passive avoidance response, indicating antiamnesic effects of dynorphin A-(1-13) (1 microgram).	Scopolamine	143-154	prodynorphin	Mus musculus	0-17
7768285-3	1995	Dynorphin A-(1-13)(1 microgram) given 15 min before training and retention tests but not immediately after training significantly improved the scopolamine (1 mg/kg)-induced shortening of step-down latency of the passive avoidance response, indicating antiamnesic effects of dynorphin A-(1-13) (1 microgram).	Scopolamine	143-154	prodynorphin	Mus musculus	274-291
7724828-5	1995	PACAP 1-27 and PACAP 1-38 relax taenia caeci dose-dependently in the presence of guanethidine and scopolamine.	Scopolamine	98-109	adenylate cyclase activating polypeptide 1	Sus scrofa	15-20
7672026-4	1995	Scopolamine decreased rCBF in the region of the right thalamus, the precuneus and the right and left lateral premotor areas.	Scopolamine	0-11	CCAAT/enhancer binding protein zeta	Rattus norvegicus	22-26
7672026-5	1995	Scopolamine attenuated memory-task-induced increases of rCBF in the left and right prefrontal cortex and the right anterior cingulate region.	Scopolamine	0-11	CCAAT/enhancer binding protein zeta	Rattus norvegicus	56-60
7869754-9	1994	Results show that the optical density of GABA antibody labeling is reduced by monocular deprivation, that substance P mRNA hybridization labeling is increased by scopolamine, and that retinal terminals are densely labeled by antibodies to glutamate.	Scopolamine	162-173	tachykinin precursor 1	Homo sapiens	106-117
8584605-1	1995	The effects of ginsenosides Rg1, Rd and Rb1 on impaired performance induced in the rat by scopolamine were examined in a radial-arm maze.	Scopolamine	90-101	RB transcriptional corepressor 1	Rattus norvegicus	40-43
7886620-0	1994	Differential effect of MK 801 and scopolamine on c-fos expression induced by L-dopa in the striatum of 6-hydroxydopamine lesioned rats.	Scopolamine	34-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7534387-2	1994	Subsequent systemic administration of either the D2 dopamine agonist, quinpirole, or the muscarinic antagonist, scopolamine, results in the reduction of the lesion-induced elevation in striatal enkephalin messenger RNA.	Scopolamine	112-123	proenkephalin	Rattus norvegicus	194-204
7534387-4	1994	To dissociate these possibilities, we have compared the effects of systemic and central administration of quinpirole and scopolamine on striatal enkephalin and substance P messenger RNAs using in situ hybridization histochemistry.	Scopolamine	121-132	proenkephalin	Rattus norvegicus	145-155
7534387-5	1994	Systemic administration of both quinpirole and scopolamine blocked the elevation of striatal enkephalin messenger RNA normally observed in 6-hydroxydopamine-lesioned rats.	Scopolamine	47-58	proenkephalin	Rattus norvegicus	93-103
7534387-11	1994	In contrast, the effect of systemic scopolamine on striatal enkephalin and substance P messenger RNAs may not be mediated within the striatum.	Scopolamine	36-47	proenkephalin	Rattus norvegicus	60-70
7714714-2	1994	Physostigmine, in combination with hyoscine, inhibited plasma cholinesterase, and red blood cell and brain acetylcholinesterase, in a concentration-dependent manner, did not affect the normal growth rate of guinea-pigs, and produced no obvious signs of poisoning.	Scopolamine	35-43	acetylcholinesterase	Cavia porcellus	107-127
7714714-3	1994	A dose rate of 4.85 micrograms h-1 physostigmine and 1.94 micrograms h-1 hyoscine was required to inhibit red cell acetylcholinesterase by 30% and brain acetylcholinesterase by 5-15%, with an accompanying plasma hyoscine concentration of 700-850 pg mL-1.	Scopolamine	73-81	acetylcholinesterase	Cavia porcellus	115-135
7714714-3	1994	A dose rate of 4.85 micrograms h-1 physostigmine and 1.94 micrograms h-1 hyoscine was required to inhibit red cell acetylcholinesterase by 30% and brain acetylcholinesterase by 5-15%, with an accompanying plasma hyoscine concentration of 700-850 pg mL-1.	Scopolamine	73-81	acetylcholinesterase	Cavia porcellus	153-173
7714714-8	1994	Red cell acetylcholinesterase activity, 24 h after soman poisoning, was higher following continuous pretreatment with physostigmine and hyoscine than after acute treatment with atropine.	Scopolamine	136-144	acetylcholinesterase	Cavia porcellus	9-29
7886073-5	1994	NGF given on days 5 and 7 increased paddling and treading on day 8, and this effect was more pronounced in scopolamine injected pups.	Scopolamine	107-118	nerve growth factor	Mus musculus	0-3
7886073-7	1994	The differences in the effects of scopolamine at successive ages suggest that distinct portions of the cholinergic system mature at different rates and that sensitivity to NGF is age dependent.	Scopolamine	34-45	nerve growth factor	Mus musculus	172-175
7816881-5	1994	The cholinesterase inhibitors tacrine (THA) and, to a lesser extent, physostigmine (PHYSO) and amodiaquine (AMDQ), caused an upward shift in the frequency of the resting electrocortical activity, although scopolamine significantly slowed the activity below baseline levels.	Scopolamine	205-216	butyrylcholinesterase	Homo sapiens	4-18
7862942-0	1994	5-HT1A receptor agonists improve the performance of normal and scopolamine-impaired rats in an operant delayed matching to position task.	Scopolamine	63-74	5-hydroxytryptamine receptor 1A	Rattus norvegicus	0-6
8057528-11	1994	However, SUN 8399 possesses different behavioral characteristics from those of the other two 5-HT1A agonists in terms of interactions with methamphetamine and scopolamine.	Scopolamine	159-170	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	93-99
8084895-4	1994	In the concentrations used, primary evoked potentials did not change significantly whereas P300 latency increased maximally 20-40 min following scopolamine administration.	Scopolamine	144-155	E1A binding protein p300	Homo sapiens	91-95
8084895-6	1994	When ALC administration was preceded by scopolamine, both P300 latency and amplitude maximally increased in 25-45 min.	Scopolamine	40-51	E1A binding protein p300	Homo sapiens	58-62
7834577-4	1994	Systemically administered scopolamine greatly increased the PPT stimulation evoked cortical release of ACh when the cortical probe was perfused with the cholinesterase inhibitor neostigmine.	Scopolamine	26-37	butyrylcholinesterase	Rattus norvegicus	153-167
8064320-10	1994	Maximum tolerated doses of the anti-cholinesterase, physostigmine, rather than tending to normalize abnormalities in these patients, further reduced cerebral metabolism (p < 0.01) and increased metabolism in thalamus in a pattern inversely correlated (p < 0.001) with that produced by scopolamine.	Scopolamine	285-296	butyrylcholinesterase	Homo sapiens	36-50
7813641-1	1994	The effect of an intravenous dose of 0.5 mg of scopolamine on the functional brain activity of normal subjects performing auditory discrimination (CPT) was determined in two independent positron emission tomography studies with [18F] 2-fluoro-deoxyglucose.	Scopolamine	47-58	choline phosphotransferase 1	Homo sapiens	147-150
8208360-0	1994	Effects of vasoactive intestinal peptide (VIP) on scopolamine-induced amnesia in the rat.	Scopolamine	50-61	vasoactive intestinal peptide	Rattus norvegicus	11-40
8208360-0	1994	Effects of vasoactive intestinal peptide (VIP) on scopolamine-induced amnesia in the rat.	Scopolamine	50-61	vasoactive intestinal peptide	Rattus norvegicus	42-45
8208360-4	1994	injection of VIP inhibited the reduction in the number of initial correct responses in rats with scopolamine-induced amnesia.	Scopolamine	97-108	vasoactive intestinal peptide	Rattus norvegicus	13-16
8208360-6	1994	Thus, VIP appears to have an ameliorating effect on spatial cognitive deficits induced by scopolamine in the rat.	Scopolamine	90-101	vasoactive intestinal peptide	Rattus norvegicus	6-9
7813641-4	1994	Because the second study was performed on a high-resolution scanner with improved methodology, we re-examined scopolamine"s effects on those brain regions established as determinants of CPT.	Scopolamine	110-121	choline phosphotransferase 1	Homo sapiens	186-189
8003924-0	1993	Peripherally administered IL-1 alpha interferes with scopolamine-induced amnesia in mice.	Scopolamine	53-64	interleukin 1 alpha	Mus musculus	26-36
22298534-1	1994	Effects of repeated intracerebroventricular administration of the thyrotrophin-releasing hormone (TRH) analogue, RX77368 (3,3"-dimethyl-TRH, 2 mug, once daily), on a scopolamine-induced performance deficit in an eight-arm radial maze were evaluated in adult rats.	Scopolamine	166-177	thyrotropin releasing hormone	Rattus norvegicus	66-96
8139380-0	1994	Scopolamine effects on the pressor response to thyrotropin-releasing hormone in humans.	Scopolamine	0-11	thyrotropin releasing hormone	Homo sapiens	47-76
8139380-4	1994	Results indicate that the pressor effect of TRH is attenuated by scopolamine, indicating a role of the cholinergic system in this response in humans.	Scopolamine	65-76	thyrotropin releasing hormone	Homo sapiens	44-47
7903377-0	1993	DAU 6215, a novel 5-HT3-receptor antagonist, selectively antagonizes scopolamine-induced deficit in a passive-avoidance task, but not scopolamine-induced hypermotility in rats.	Scopolamine	69-80	5-hydroxytryptamine receptor 3A	Rattus norvegicus	18-32
7504301-3	1993	In the brain, M40 acts as a potent galanin-receptor antagonist: M40, in doses comparable to that of galanin, antagonizes the stimulatory effects of galanin on feeding, and it blocks the galaninergic inhibition of the scopolamine-induced acetylcholine release in the ventral hippocampus in vivo.	Scopolamine	217-228	probasin	Rattus norvegicus	14-17
7504301-3	1993	In the brain, M40 acts as a potent galanin-receptor antagonist: M40, in doses comparable to that of galanin, antagonizes the stimulatory effects of galanin on feeding, and it blocks the galaninergic inhibition of the scopolamine-induced acetylcholine release in the ventral hippocampus in vivo.	Scopolamine	217-228	probasin	Rattus norvegicus	64-67
8117420-7	1993	By contrast, in the DMTP test, although both the cholinesterase inhibitors and L-687,306 reversed the effects of scopolamine-induced deficit, L-689,660 and AF102B were without effects.	Scopolamine	113-124	butyrylcholinesterase	Rattus norvegicus	49-63
8117420-8	1993	These results suggest that cholinesterase inhibitors and low efficacy M1 selective muscarinic receptor agonists can reverse the effects of a scopolamine-induced deficit in animal tests of reference and working memory at doses that do not induce the side-effects usually associated with cholinomimetics.	Scopolamine	141-152	butyrylcholinesterase	Rattus norvegicus	27-41
7901037-0	1993	Dopaminergic involvement in the improving effects of dynorphin A-(1-13) on scopolamine-induced impairment of alternation performance.	Scopolamine	75-86	prodynorphin	Mus musculus	53-70
7901037-1	1993	The present study was designed to clarify whether dopamine systems are involved in the effect of dynorphin A-(1-13), an endogenous kappa-opioid receptor agonist, on the scopolamine-induced impairment of spontaneous alternation performance related to working memory in mice.	Scopolamine	169-180	prodynorphin	Mus musculus	97-114
7901037-6	1993	Furthermore, the improving effect of dynorphin A-(1-13) on the scopolamine-induced impairment of spontaneous alternation performance may be based upon the inhibition of dopaminergic activity through the mediation of kappa-opioid receptors.	Scopolamine	63-74	prodynorphin	Mus musculus	37-54
8281324-11	1993	Scopolamine, a muscarinic antagonist, induced Fos in both striosomal and matrix compartments in the striatum.	Scopolamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
8241462-0	1993	Interleukin-2 enhances scopolamine-induced amnesia and hyperactivity in the mouse.	Scopolamine	23-34	interleukin 2	Mus musculus	0-13
8241462-1	1993	We studied the effects of human recombinant interleukin-2 (IL-2) on scopolamine-induced amnesia for a passive avoidance response and on scopolamine-induced hyperactivity, in the mouse.	Scopolamine	68-79	interleukin 2	Homo sapiens	44-57
8241462-1	1993	We studied the effects of human recombinant interleukin-2 (IL-2) on scopolamine-induced amnesia for a passive avoidance response and on scopolamine-induced hyperactivity, in the mouse.	Scopolamine	68-79	interleukin 2	Homo sapiens	59-63
8241462-7	1993	Intraperitoneal injection of IL-2 significantly enhanced the scopolamine-induced hyperactivity, whereas the cytokine alone was ineffective in modifying locomotor activity.	Scopolamine	61-72	interleukin 2	Mus musculus	29-33
8405091-0	1993	Effects of sustained release formulation of thyrotropin-releasing hormone on learning impairments caused by scopolamine and AF64A in rodents.	Scopolamine	108-119	thyrotropin releasing hormone	Rattus norvegicus	44-73
8003924-1	1993	We studied the effects of human recombinant interleukin-1 alpha on scopolamine-induced amnesia for a passive avoidance response in the mouse.	Scopolamine	67-78	interleukin 1 alpha	Homo sapiens	44-63
8102969-0	1993	Dynorphin A-(1-13) markedly improves scopolamine-induced impairment of spontaneous alternation performance in mice.	Scopolamine	37-48	prodynorphin	Mus musculus	0-17
8102969-4	1993	In contrast, dynorphin A-(1-13) (3 and 10 micrograms) significantly improved the impairment of spontaneously alternation performance induced by scopolamine (1 mg/kg s.c.).	Scopolamine	144-155	prodynorphin	Mus musculus	13-30
8102969-5	1993	Simultaneously, the scopolamine-induced increase in total arm entries was markedly attenuated by dynorphin A-(1-13) (10 micrograms).	Scopolamine	20-31	prodynorphin	Mus musculus	97-114
8102969-6	1993	The effect of dynorphin A-(1-13) (3 micrograms) on the scopolamine-induced impairment of spontaneous alternation was almost completely reversed by pretreatment with nor-binaltorphimine (4 micrograms i.c.v.	Scopolamine	55-66	prodynorphin	Mus musculus	14-31
8102969-8	1993	These findings suggest that dynorphin A-(1-13) improves through the mediation of kappa-opioid receptors the scopolamine-induced impairment of spontaneous alternation performance associated with working memory.	Scopolamine	108-119	prodynorphin	Mus musculus	28-45
8098138-2	1993	Studies on the expression of the early gene c-fos as reflected by the immunohistochemical demonstration of the Fos protein, show that administration of scopolamine (5 mg/kg, i.p.)	Scopolamine	152-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
8332555-3	1993	The first phase of NPY-induced contraction of neonatal duodenum was concentration dependent and partially inhibited by preincubation with tetrodotoxin, a Na+ channel blocker, hyoscine, a muscarinic antagonist, suramin, a P2 purinoceptor antagonist, and indomethacin, an inhibitor for prostaglandin biosynthesis.	Scopolamine	175-183	neuropeptide Y	Rattus norvegicus	19-22
8405262-5	1993	Pentobarbital (an enhancer of gabaergic functions) and scopolamine (a muscarinic receptor antagonist) blocked the effects of MK-801 on BDNF mRNA levels in the retrosplenial cortex, but the nicotinic and dopaminergic receptor antagonists mecamylamine and haloperidol, respectively, were ineffective.	Scopolamine	55-66	brain-derived neurotrophic factor	Rattus norvegicus	135-139
8098138-2	1993	Studies on the expression of the early gene c-fos as reflected by the immunohistochemical demonstration of the Fos protein, show that administration of scopolamine (5 mg/kg, i.p.)	Scopolamine	152-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
7870985-6	1993	Furthermore, the ACE inhibitor Hoe 288 (10 nmol ICV) and the angiotensin AT1 receptor antagonist losartan (10 mg/kg SC) also significantly attenuated the scopolamine-induced deficit.	Scopolamine	154-165	angiotensin I converting enzyme	Rattus norvegicus	17-20
8095539-4	1993	The effect of TRH-SR treatment was blocked by intraperitoneal scopolamine (0.1 mg kg-1) and mecamylamine (2 mg kg-1) but not by scopolamine methyl bromide (0.1 mg kg-1).	Scopolamine	62-73	thyrotropin releasing hormone	Rattus norvegicus	14-17
8100705-4	1993	This prolongation of shortened latency by the thyrotropin-releasing hormone and its analogues in cycloheximide-treated mice was antagonized by scopolamine but not by haloperidol.	Scopolamine	143-154	thyrotropin releasing hormone	Mus musculus	46-75
8323711-1	1993	Performance of three rhesus monkeys on a test of one-trial stimulus-reward association, in which recall intervals ranged from 0.5 to 6.5 min, was evaluated during nondrug-control conditions and following administration of the muscarinic-receptor blocker scopolamine.	Scopolamine	254-265	cholinergic receptor muscarinic 5	Macaca mulatta	226-245
1393566-0	1992	Scopolamine attenuates haloperidol-induced c-fos expression in the striatum.	Scopolamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	43-48
1393566-3	1992	In order to gain insight into the neurochemical and neuroanatomical substrates of haloperidol-induced catalepsy we examined the effects of the muscarinic receptor antagonist scopolamine on haloperidol-induced Fos expression in the striatum, nucleus accumbens and lateral septal nucleus.	Scopolamine	174-185	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	209-212
1393566-4	1992	At a dose that reduced the cataleptic effect of haloperidol, scopolamine decreased the neuroleptic-induced Fos expression in the striatum and lateral septal nucleus but not the nucleus accumbens.	Scopolamine	61-72	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	107-110
1382167-2	1992	In a mouse habituation model, ACE inhibitors improved basal performance and antagonized scopolamine-induced deficits.	Scopolamine	88-99	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	30-33
1740713-5	1992	Comparisons with [11C]scopolamine in rats showed 2-6 times greater brain uptake of [11C] TRB.	Scopolamine	22-33	T cell receptor beta locus	Homo sapiens	89-92
1740713-6	1992	Highly specific and saturable binding of [11C]TRB in the striatum and cortex was demonstrated by greater than 85% blockade of uptake following QNB or scopolamine pretreatment.	Scopolamine	150-161	T cell receptor beta locus	Homo sapiens	46-49
1397060-10	1992	), expression of c-fos mRNA was observed in the hypothalamus and in brain areas involved in sensory processing; these effects were totally blocked by pretreatment with 2 mg/kg scopolamine.	Scopolamine	176-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
1397027-13	1992	The muscarinic receptor antagonist scopolamine antagonized the effect of O-Me-THPO and partially inhibited the effect of Lu 26-046.	Scopolamine	35-46	thrombopoietin like 1	Rattus norvegicus	78-82
1315917-6	1992	In contrast, chronic administration of eticlopride, scopolamine or the two combined decreased striatal preprotachykinin (PPT) mRNA to the same extent, suggesting that there was no direct interaction between D2 dopaminergic and cholinergic mechanisms in the regulation of striatal PPT mRNA.	Scopolamine	52-63	tachykinin, precursor 1	Rattus norvegicus	103-119
1315917-6	1992	In contrast, chronic administration of eticlopride, scopolamine or the two combined decreased striatal preprotachykinin (PPT) mRNA to the same extent, suggesting that there was no direct interaction between D2 dopaminergic and cholinergic mechanisms in the regulation of striatal PPT mRNA.	Scopolamine	52-63	tachykinin, precursor 1	Rattus norvegicus	121-124
1541364-4	1992	The increase in BDNF and NGF mRNA levels were completely prevented by pretreatment with systemic injections of either scopolamine or diazepam.	Scopolamine	118-129	brain-derived neurotrophic factor	Rattus norvegicus	16-20
1541364-4	1992	The increase in BDNF and NGF mRNA levels were completely prevented by pretreatment with systemic injections of either scopolamine or diazepam.	Scopolamine	118-129	nerve growth factor	Rattus norvegicus	25-28
1541364-8	1992	The increase in BDNF mRNA after cortex injections was attenuated by diazepam but not by scopolamine.	Scopolamine	88-99	brain-derived neurotrophic factor	Rattus norvegicus	16-20
1382167-4	1992	ACE inhibition also improved scopolamine-impaired performance of rats in a swim-maze model.	Scopolamine	29-40	angiotensin I converting enzyme	Rattus norvegicus	0-3
22291397-1	1992	Thyrotropin-releasing hormone (TRH), a neuromodulator and possibly a neurotransmitter in the central nervous system, was shown in a prior study of young normal volunteers to attenuate the memory impairment induced by the anticholinergic drug scopolamine.	Scopolamine	242-253	thyrotropin releasing hormone	Homo sapiens	31-34
1641127-1	1992	The effect of scopolamine and atropine upon the increase in extracellular 3,4-dihydroxyphenylacetic acid induced by central injection of neurotensin was examined in the nucleus accumbens and the striatum of anaesthetized rats using in vivo differential pulse voltammetry with carbon fibre electrodes.	Scopolamine	14-25	neurotensin	Rattus norvegicus	137-148
22291397-1	1992	Thyrotropin-releasing hormone (TRH), a neuromodulator and possibly a neurotransmitter in the central nervous system, was shown in a prior study of young normal volunteers to attenuate the memory impairment induced by the anticholinergic drug scopolamine.	Scopolamine	242-253	thyrotropin releasing hormone	Homo sapiens	0-29
1641127-7	1992	Pretreatment with scopolamine (1 mg/kg) 15 min before neurotensin injection blocked the increase in extracellular 3,4-dihydroxyphenylacetic acid in the striatum but not in the nucleus accumbens whilst scopolamine (3 mg/kg) partially attenuated the effect of neurotensin in the nucleus accumbens and blocked the increase in 3,4-dihydroxyphenylacetic acid in the striatum.	Scopolamine	18-29	neurotensin	Rattus norvegicus	54-65
1641127-7	1992	Pretreatment with scopolamine (1 mg/kg) 15 min before neurotensin injection blocked the increase in extracellular 3,4-dihydroxyphenylacetic acid in the striatum but not in the nucleus accumbens whilst scopolamine (3 mg/kg) partially attenuated the effect of neurotensin in the nucleus accumbens and blocked the increase in 3,4-dihydroxyphenylacetic acid in the striatum.	Scopolamine	18-29	neurotensin	Rattus norvegicus	258-269
1667338-3	1991	Only in the guinea-pig small intestine CGRP induced a contraction of the smooth muscle which was sensitive to scopolamine and tetrodotoxin.	Scopolamine	110-121	calcitonin related polypeptide alpha	Homo sapiens	39-43
1738791-2	1992	Tacrine or galanthamine, inhibitors of acetylcholinesterase, given in conjunction with scopolamine partially reversed the scopolamine-induced deficit in passive avoidance performance.	Scopolamine	122-133	acetylcholinesterase	Rattus norvegicus	39-59
1851454-0	1991	Chronic treatment with scopolamine and physostigmine changes nerve growth factor (NGF) receptor density and NGF content in rat brain.	Scopolamine	23-34	nerve growth factor receptor	Rattus norvegicus	61-95
1681981-5	1991	The enhancing effect of somatostatin on LTP in the mossy fiber CA3 system was inhibited either by a muscarinic antagonist, scopolamine (10(-6) M), or a beta-adrenoceptor antagonist, timolol (10(-6) M).	Scopolamine	123-134	carbonic anhydrase 3	Cavia porcellus	63-66
1871189-3	1991	Dialysate concentrations of ACh in all 3 brain structures and locomotor activity were increased after scopolamine and the onset of the lights out condition.	Scopolamine	102-113	acyl-CoA thioesterase 12	Rattus norvegicus	28-31
1851454-0	1991	Chronic treatment with scopolamine and physostigmine changes nerve growth factor (NGF) receptor density and NGF content in rat brain.	Scopolamine	23-34	nerve growth factor	Rattus norvegicus	82-85
1851454-8	1991	In contrast, scopolamine treatment failed to change NGF levels in the cholinergic neuronal target regions but it decreased NGF content in the septal area.	Scopolamine	13-24	nerve growth factor	Rattus norvegicus	123-126
2032020-2	1991	A C18 column was used to separate scopolamine from the additional alkaloids and other biological material present in the vegetal extract.	Scopolamine	34-45	Bardet-Biedl syndrome 9	Homo sapiens	2-5
1776749-0	1991	Cholinesterase inhibition in the scopolamine model of dementia.	Scopolamine	33-44	butyrylcholinesterase	Homo sapiens	0-14
2032020-3	1991	The C18 column was coupled through a six-port switching valve to two beta-cyclodextrin columns in series which were used to resolve the scopolamine enantiomers.	Scopolamine	136-147	Bardet-Biedl syndrome 9	Homo sapiens	4-7
2243341-1	1990	The effects of cholinesterase inhibitors, cholinergic agonists, dopaminergic agonists and dopaminergic antagonists on the hyperactivity produced by the muscarinic cholinergic antagonist scopolamine were evaluated in mice.	Scopolamine	186-197	butyrylcholinesterase	Mus musculus	15-29
22282560-1	1991	Two studies were undertaken to investigate the effects of acute (Study 1) or repeated (Study 2) administration of the angiotensin converting enzyme (ACE) inhibitor enalapril on the cognitive deficits produced by scopolamine administration in volunteers.	Scopolamine	212-223	angiotensin I converting enzyme	Homo sapiens	118-147
2263955-1	1990	The purpose of this study was to investigate the effects of microinjection of scopolamine, a M-cholinergic antagonist and picrotoxin, a GABA-ergic antagonist into the rat hippocampal CA3 area on the learning-dependent long-term potentiation (LDLTP) during the establishment, extinction and re-establishment of conditioned drinking response.	Scopolamine	78-89	carbonic anhydrase 3	Rattus norvegicus	183-186
20504702-2	1991	The lower dose combination (physostigmine 20 ?g/kg, hyoscine 10 ?g/kg, s.c.) inhibited brain regional acetylcholinesterase (AChE) by between 13.5 and 37.6% in all regions except the striatum, where there was no statistically significant inhibition.	Scopolamine	52-60	acetylcholinesterase	Cavia porcellus	102-122
20504702-2	1991	The lower dose combination (physostigmine 20 ?g/kg, hyoscine 10 ?g/kg, s.c.) inhibited brain regional acetylcholinesterase (AChE) by between 13.5 and 37.6% in all regions except the striatum, where there was no statistically significant inhibition.	Scopolamine	52-60	acetylcholinesterase	Cavia porcellus	124-128
2391775-6	1990	After Se-E treatment, plasma Lpx levels before the exercise were decreased from 1.24 +/- 0.09 nmol/ml to 0.86 +/- 0.03 nmol/ml, however, SOD, GSHpx, and catalase activities were not varied.	Scopolamine	6-10	catalase	Equus caballus	153-161
2263955-3	1990	The results were as follows: the synaptic efficacy and the development of LDLTP in hippocampal CA3 were depressed significantly by scopolamine, but the extinction of LDLTP was accelerated.	Scopolamine	131-142	carbonic anhydrase 3	Rattus norvegicus	95-98
2234546-4	1990	Scopolamine hyperactivity is enhanced around weaning by NGF pretreatment.	Scopolamine	0-11	nerve growth factor	Homo sapiens	56-59
1964494-2	1990	AT II and the cholinergic agonists, administered together potentiated their retention-improving effects, while scopolamine abolished the memory effect of AT II.	Scopolamine	111-122	angiotensinogen	Rattus norvegicus	154-159
2327054-2	1990	Short-term administration of the cholinomimetic arecoline or the anticholinergic scopolamine induced rat liver mitochondrial aldehyde dehydrogenase (L-ALDH) isoenzyme with the apparent high and low Km, respectively.	Scopolamine	81-92	aldehyde dehydrogenase 2 family member	Rattus norvegicus	111-147
33815562-8	2021	HemoHIM treatment attenuated the scopolamine-induced hyperactivation of acetylcholinesterase (AchE) activity.	Scopolamine	33-44	acetylcholinesterase	Mus musculus	72-92
33815562-8	2021	HemoHIM treatment attenuated the scopolamine-induced hyperactivation of acetylcholinesterase (AchE) activity.	Scopolamine	33-44	acetylcholinesterase	Mus musculus	94-98
33815562-9	2021	In addition, ChAT, mAchR, and CREB mRNA levels were increased in the hippocampus compared with the scopolamine group.	Scopolamine	99-110	cAMP responsive element binding protein 1	Mus musculus	30-34
33591165-8	2021	These data suggested that YVLLPSPK improved learning and memory in scopolamine-induced cognitive-impaired mice through a mechanism associated with PINK1-mediated mitophagy via the NRF2/KEAP1/HO-1 pathway.	Scopolamine	67-78	PTEN induced putative kinase 1	Mus musculus	147-152
33591165-8	2021	These data suggested that YVLLPSPK improved learning and memory in scopolamine-induced cognitive-impaired mice through a mechanism associated with PINK1-mediated mitophagy via the NRF2/KEAP1/HO-1 pathway.	Scopolamine	67-78	nuclear factor, erythroid derived 2, like 2	Mus musculus	180-184
33591165-8	2021	These data suggested that YVLLPSPK improved learning and memory in scopolamine-induced cognitive-impaired mice through a mechanism associated with PINK1-mediated mitophagy via the NRF2/KEAP1/HO-1 pathway.	Scopolamine	67-78	kelch-like ECH-associated protein 1	Mus musculus	185-190
33591165-8	2021	These data suggested that YVLLPSPK improved learning and memory in scopolamine-induced cognitive-impaired mice through a mechanism associated with PINK1-mediated mitophagy via the NRF2/KEAP1/HO-1 pathway.	Scopolamine	67-78	heme oxygenase 1	Mus musculus	191-195
2296571-1	1990	As travel by air and ship becomes increasingly popular, more and more travelers are using transdermal scopolamine to avoid motion sickness.	Scopolamine	102-113	inositol polyphosphate-5-phosphatase D	Homo sapiens	21-25
2104988-0	1990	TRH attenuates scopolamine-induced memory impairment in humans.	Scopolamine	15-26	thyrotropin releasing hormone	Homo sapiens	0-3
2104988-3	1990	Compared to placebo, TRH markedly attenuated scopolamine-induced impairment of some measures of memory, most notably on a selective reminding task.	Scopolamine	45-56	thyrotropin releasing hormone	Homo sapiens	21-24
31910792-5	2020	Therefore, this study aimed to assess whether cinnamaldehyde has the potency to prevent memory retrieval impairment and hippocampal protein kinase B (Akt) and MAPK (extracellular signal-regulated kinase (ERK)) alterations induced by scopolamine in mice.Methods: Adult male mice were pretreated with cinnamaldehyde (12.5, 25, 40 and 100 mg/kg/oral gavage) 10 days before training.	Scopolamine	233-244	mitogen-activated protein kinase 1	Mus musculus	165-202
31910792-9	2020	Furthermore, cinnamaldehyde prevented scopolamine induced dysregulations of hippocampal MAPK and Akt.Discussion: The results of the present study revealed that oral sub-chronic cinnamaldehyde administration has the capability to prevent memory retrieval deficit induced by cholinergic blockade and restores hippocampal MAPK and Akt dysregulations.	Scopolamine	38-49	thymoma viral proto-oncogene 1	Mus musculus	97-100
32795659-2	2020	Here we demonstrate the proof-of-concept of a minimally-invasive fUS imaging approach to detect the acute cholinergic modulatory effects of Scopolamine (ScoP) on functional brain connectivity in awake and behaving mice, through the intact skull.	Scopolamine	140-151	fused in sarcoma	Mus musculus	65-68
31910792-9	2020	Furthermore, cinnamaldehyde prevented scopolamine induced dysregulations of hippocampal MAPK and Akt.Discussion: The results of the present study revealed that oral sub-chronic cinnamaldehyde administration has the capability to prevent memory retrieval deficit induced by cholinergic blockade and restores hippocampal MAPK and Akt dysregulations.	Scopolamine	38-49	thymoma viral proto-oncogene 1	Mus musculus	328-331
32795659-2	2020	Here we demonstrate the proof-of-concept of a minimally-invasive fUS imaging approach to detect the acute cholinergic modulatory effects of Scopolamine (ScoP) on functional brain connectivity in awake and behaving mice, through the intact skull.	Scopolamine	153-157	fused in sarcoma	Mus musculus	65-68
34740600-14	2022	In ex vivo assay, MTDZ also protected against the alteration of AChE activity, reactive species (RS) levels, thiobarbituric acid reative species (TBARS) levels, catalase (CAT) activity in tissues, as well as in transaminase activities of plasma caused by SCO in mice.	Scopolamine	255-258	acetylcholinesterase	Mus musculus	64-68
34480999-0	2022	Amelioration of Scopolamine-induced Learning and Memory Impairment by the TRPV4 Inhibitor HC067047 in ICR Mice.	Scopolamine	16-27	transient receptor potential cation channel, subfamily V, member 4	Mus musculus	74-79
34480999-13	2022	The results demonstrated that HC067047 treatment decreased the protein levels of proapoptotic proteins such as Bax and caspase-3 in the hippocampus of SCP mice.	Scopolamine	151-154	BCL2-associated X protein	Mus musculus	111-114
34480999-13	2022	The results demonstrated that HC067047 treatment decreased the protein levels of proapoptotic proteins such as Bax and caspase-3 in the hippocampus of SCP mice.	Scopolamine	151-154	caspase 3	Mus musculus	119-128
34778972-13	2021	Viphyllin (100 mg/kg) was found to be neuroprotective by reducing the Scop-induced upregulation of p-JNK and p-p38 MAPK proteins, Bax/Bcl-2 ratio, and caspase activation in the brain.	Scopolamine	70-74	mitogen-activated protein kinase 8	Mus musculus	101-104
34244776-0	2021	Activation of 5-HT 1b/d receptor restores the cognitive function by reducing glutamate release, deposition of beta-amyloid and TLR-4 pathway in the brain of scopolamine-induced dementia in rat.	Scopolamine	157-168	5-hydroxytryptamine receptor 1B	Rattus norvegicus	14-21
34244776-0	2021	Activation of 5-HT 1b/d receptor restores the cognitive function by reducing glutamate release, deposition of beta-amyloid and TLR-4 pathway in the brain of scopolamine-induced dementia in rat.	Scopolamine	157-168	toll-like receptor 4	Rattus norvegicus	127-132
34244776-1	2021	OBJECTIVES: This study evaluates the effect of 5-HT 1b/d agonist on cognitive function in scopolamine (SPN)-induced dementia in the rat.	Scopolamine	90-101	5-hydroxytryptamine receptor 1B	Rattus norvegicus	47-54
34244776-1	2021	OBJECTIVES: This study evaluates the effect of 5-HT 1b/d agonist on cognitive function in scopolamine (SPN)-induced dementia in the rat.	Scopolamine	103-106	5-hydroxytryptamine receptor 1B	Rattus norvegicus	47-54
34669098-9	2021	Furthermore, scopolamine treatment altered the endogenous antioxidants and pro-inflammatory mediators, elevated acetylcholinesterase activity and promoted chromatolysis of the cortico-hippocampal neuron.	Scopolamine	13-24	acetylcholinesterase	Mus musculus	112-132
34850372-4	2022	mTORC1 activation is essential for the antidepressant effects of ketamine and scopolamine.	Scopolamine	78-89	CREB regulated transcription coactivator 1	Mus musculus	0-6
34850372-5	2022	Thus, we hypothesized that metformin may attenuate ketamine- or scopolamine-induced antidepressant efficacies by blocking their mTORC1 activation.	Scopolamine	64-75	CREB regulated transcription coactivator 1	Mus musculus	128-134
34943096-12	2021	Moreover, CPO significantly (p < 0.05) ameliorated the activities of antioxidant enzymes such as catalase, superoxide dismutase (SOD) and reduced malondialdehyde (MDA) equivalents by 22.48%, 45.41%, and 86.61%, respectively, compared to scopolamine.	Scopolamine	237-248	catalase	Rattus norvegicus	97-105
34943096-13	2021	Furthermore, CPO administration decreased scopolamine-induced elevated acetylcholinesterase levels in rats" hippocampi by 51.30%.	Scopolamine	42-53	acetylcholinesterase	Rattus norvegicus	71-91
34778972-0	2021	A standardized black pepper seed extract containing beta-caryophyllene improves cognitive function in scopolamine-induced amnesia model mice via regulation of brain-derived neurotrophic factor and MAPK proteins.	Scopolamine	102-113	brain derived neurotrophic factor	Mus musculus	159-192
34778972-13	2021	Viphyllin (100 mg/kg) was found to be neuroprotective by reducing the Scop-induced upregulation of p-JNK and p-p38 MAPK proteins, Bax/Bcl-2 ratio, and caspase activation in the brain.	Scopolamine	70-74	mitogen-activated protein kinase 14	Mus musculus	111-119
34778972-13	2021	Viphyllin (100 mg/kg) was found to be neuroprotective by reducing the Scop-induced upregulation of p-JNK and p-p38 MAPK proteins, Bax/Bcl-2 ratio, and caspase activation in the brain.	Scopolamine	70-74	BCL2-associated X protein	Mus musculus	130-133
34778972-13	2021	Viphyllin (100 mg/kg) was found to be neuroprotective by reducing the Scop-induced upregulation of p-JNK and p-p38 MAPK proteins, Bax/Bcl-2 ratio, and caspase activation in the brain.	Scopolamine	70-74	B cell leukemia/lymphoma 2	Mus musculus	134-139
34885665-7	2021	Additionally, Sco-induced brain oxidative stress and increasing of acetylcholinesterase (AChE) activity were attenuated by the administration of OEO.	Scopolamine	14-17	acetylcholinesterase	Danio rerio	67-87
34850372-10	2022	Notably, ketamine, scopolamine, and metformin all exerted significant antidepressant-like actions, as evidenced by increased AMPK phosphorylation and BDNF expression.	Scopolamine	19-30	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	125-129
34850372-10	2022	Notably, ketamine, scopolamine, and metformin all exerted significant antidepressant-like actions, as evidenced by increased AMPK phosphorylation and BDNF expression.	Scopolamine	19-30	brain-derived neurotrophic factor	Rattus norvegicus	150-154
34885665-7	2021	Additionally, Sco-induced brain oxidative stress and increasing of acetylcholinesterase (AChE) activity were attenuated by the administration of OEO.	Scopolamine	14-17	acetylcholinesterase	Danio rerio	89-93
34951183-0	2021	(Total flavonoids of Drynariae Rhizoma regulates ER-p38 MAPK signaling pathway to improve scopolamine-induced learning and memory impairments in model mice).	Scopolamine	90-101	mitogen-activated protein kinase 14	Mus musculus	52-60
34830164-12	2021	Both compounds elevated DDAH1 expression, and slight decreases in PMRT1 and PMRT5 in the cortex after scopolamine (acute) and MK-801 (chronic) administration were observed in the PFC, respectively.	Scopolamine	102-113	dimethylarginine dimethylaminohydrolase 1	Homo sapiens	24-29
34830164-14	2021	Chronic MK-801 and scopolamine administration affected S-nitrosylation of GLT-1 transport protein.	Scopolamine	19-30	solute carrier family 1 member 2	Homo sapiens	74-79
34607024-11	2021	Biological activity of CNO is usually attributed to metabolism of CNO to clozapine and we found that clozapine, and the muscarinic cholinergic antagonist, scopolamine, produced results similar to CNO, preferentially affecting males.	Scopolamine	155-166	biogenesis of lysosomal organelles complex 1 subunit 4	Homo sapiens	23-26
34951183-10	2021	It has been proved that the total flavonoids of Drynariae Rhizoma obviously alleviate scopolamine-induced learning and memory impairments in mice, which may be achieved by regulating the neuronal apoptotic system and oxidative stress via the ER-p38 mitogen-activated protein kinase(ER-p38 MAPK) signaling pathway.	Scopolamine	86-97	mitogen-activated protein kinase 14	Mus musculus	245-248
34259275-0	2021	Neuroprotective effects of NDEELNK from sea cucumber ovum against scopolamine-induced PC12 cell damage through enhancing energy metabolism and upregulation of the PKA/BDNF/NGF signaling pathway.	Scopolamine	66-77	brain-derived neurotrophic factor	Rattus norvegicus	167-171
34259275-5	2021	Our results demonstrated that NDEELNK supplementation alleviated scopolamine-induced PC12 cell damage by improving the cholinergic system, increasing energy metabolism and upregulating the expression of phosphorylated protein kinase A (p-PKA), brain-derived neurotrophic factor (BNDF) and nerve growth factor (NGF) signaling proteins in in vitro experiments.	Scopolamine	65-76	brain-derived neurotrophic factor	Rattus norvegicus	244-277
34259275-5	2021	Our results demonstrated that NDEELNK supplementation alleviated scopolamine-induced PC12 cell damage by improving the cholinergic system, increasing energy metabolism and upregulating the expression of phosphorylated protein kinase A (p-PKA), brain-derived neurotrophic factor (BNDF) and nerve growth factor (NGF) signaling proteins in in vitro experiments.	Scopolamine	65-76	brain-derived neurotrophic factor	Rattus norvegicus	279-283
34269783-0	2021	Pine nut antioxidant peptides ameliorate the memory impairment in a scopolamine-induced mouse model via SIRT3-induced synaptic plasticity.	Scopolamine	68-79	NUT midline carcinoma, family member 1	Mus musculus	5-8
34269783-0	2021	Pine nut antioxidant peptides ameliorate the memory impairment in a scopolamine-induced mouse model via SIRT3-induced synaptic plasticity.	Scopolamine	68-79	sirtuin 3	Mus musculus	104-109
34371027-7	2021	Overall DHAc reversed behavioral anomalies in the scopolamine treated mice via oxidative stress quenching, enhancing antioxidative enzyme activity, enhancing BDNF and synaptophysin mRNA levels and reducing expression of apoptotic protein Bax.	Scopolamine	50-61	brain derived neurotrophic factor	Mus musculus	158-162
34269783-1	2021	This study aimed to investigate the effects of a pine nut albumin hydrolysate (fraction <3 kDa) and of its short peptide derivative, Trp-Tyr-Pro-Gly-Lys (WYPGK), on synaptic plasticity and memory function in scopolamine-induced memory-impaired mice, as well as the potential underlying mechanism in PC12 cells.	Scopolamine	208-219	NUT midline carcinoma, family member 1	Mus musculus	54-57
34252414-0	2021	alpha-MSH ameliorates corneal surface dysfunction in scopolamine-induced dry eye rats and human corneal epithelial cells via enhancing EGFR expression.	Scopolamine	53-64	Stam binding protein	Rattus norvegicus	0-9
34252414-3	2021	In this study we topically applied alpha-melanocyte stimulating hormone (alpha-MSH) on the ocular surface of scopolamine-induced DE rats and found that it promoted tear secretion, reduced tear breakup time and fluorescein sodium staining and increased the number of conjunctival goblet cells.	Scopolamine	109-120	proopiomelanocortin	Rattus norvegicus	35-71
34252414-3	2021	In this study we topically applied alpha-melanocyte stimulating hormone (alpha-MSH) on the ocular surface of scopolamine-induced DE rats and found that it promoted tear secretion, reduced tear breakup time and fluorescein sodium staining and increased the number of conjunctival goblet cells.	Scopolamine	109-120	Stam binding protein	Rattus norvegicus	73-82
34371027-7	2021	Overall DHAc reversed behavioral anomalies in the scopolamine treated mice via oxidative stress quenching, enhancing antioxidative enzyme activity, enhancing BDNF and synaptophysin mRNA levels and reducing expression of apoptotic protein Bax.	Scopolamine	50-61	synaptophysin	Mus musculus	167-180
34371027-7	2021	Overall DHAc reversed behavioral anomalies in the scopolamine treated mice via oxidative stress quenching, enhancing antioxidative enzyme activity, enhancing BDNF and synaptophysin mRNA levels and reducing expression of apoptotic protein Bax.	Scopolamine	50-61	BCL2-associated X protein	Mus musculus	238-241
34183865-3	2021	Here we show that methyl-CpG-binding protein 2 (MeCP2) phosphorylation at Ser421 (pMeCP2) is essential for the sustained, but not the rapid, antidepressant effects of ketamine and scopolamine in mice.	Scopolamine	180-191	methyl CpG binding protein 2	Mus musculus	18-46
34347557-7	2021	PSD-95 and neurexin 1 and neuroligin concentrations were significantly reduced, whereas COX-2 and activated caspase-3 were enhanced in the hippocampus of scopolamine-injected subjects.	Scopolamine	154-165	discs large MAGUK scaffold protein 4	Rattus norvegicus	0-6
34347557-7	2021	PSD-95 and neurexin 1 and neuroligin concentrations were significantly reduced, whereas COX-2 and activated caspase-3 were enhanced in the hippocampus of scopolamine-injected subjects.	Scopolamine	154-165	neurexin 1	Rattus norvegicus	11-21
34347557-7	2021	PSD-95 and neurexin 1 and neuroligin concentrations were significantly reduced, whereas COX-2 and activated caspase-3 were enhanced in the hippocampus of scopolamine-injected subjects.	Scopolamine	154-165	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	88-93
34347557-7	2021	PSD-95 and neurexin 1 and neuroligin concentrations were significantly reduced, whereas COX-2 and activated caspase-3 were enhanced in the hippocampus of scopolamine-injected subjects.	Scopolamine	154-165	caspase 3	Rattus norvegicus	108-117
34183865-3	2021	Here we show that methyl-CpG-binding protein 2 (MeCP2) phosphorylation at Ser421 (pMeCP2) is essential for the sustained, but not the rapid, antidepressant effects of ketamine and scopolamine in mice.	Scopolamine	180-191	methyl CpG binding protein 2	Mus musculus	48-53
34183865-4	2021	Our results reveal that pMeCP2 is downstream of BDNF, a critical factor in ketamine and scopolamine antidepressant action.	Scopolamine	88-99	brain derived neurotrophic factor	Homo sapiens	48-52
34093254-0	2021	M2-AChR Mediates Rapid Antidepressant Effects of Scopolamine Through Activating the mTORC1-BDNF Signaling Pathway in the Medial Prefrontal Cortex.	Scopolamine	49-60	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	3-7
34371027-4	2021	In the molecular level these changes are monitored as reduced oxidative load followed by significantly lower lipid peroxidation and protein carbonylation, increased superoxide dismutase, catalase, acetylcholinesterase, caspase-3 activity and glutathione content followed by higher expression of anti apoptotic protein bcl-2 in mice brain as compared to scopolamine (1 mg/kg bw) treated mice.	Scopolamine	353-364	catalase	Mus musculus	187-195
34371027-4	2021	In the molecular level these changes are monitored as reduced oxidative load followed by significantly lower lipid peroxidation and protein carbonylation, increased superoxide dismutase, catalase, acetylcholinesterase, caspase-3 activity and glutathione content followed by higher expression of anti apoptotic protein bcl-2 in mice brain as compared to scopolamine (1 mg/kg bw) treated mice.	Scopolamine	353-364	acetylcholinesterase	Mus musculus	197-217
34371027-4	2021	In the molecular level these changes are monitored as reduced oxidative load followed by significantly lower lipid peroxidation and protein carbonylation, increased superoxide dismutase, catalase, acetylcholinesterase, caspase-3 activity and glutathione content followed by higher expression of anti apoptotic protein bcl-2 in mice brain as compared to scopolamine (1 mg/kg bw) treated mice.	Scopolamine	353-364	caspase 3	Mus musculus	219-228
34371027-4	2021	In the molecular level these changes are monitored as reduced oxidative load followed by significantly lower lipid peroxidation and protein carbonylation, increased superoxide dismutase, catalase, acetylcholinesterase, caspase-3 activity and glutathione content followed by higher expression of anti apoptotic protein bcl-2 in mice brain as compared to scopolamine (1 mg/kg bw) treated mice.	Scopolamine	353-364	B cell leukemia/lymphoma 2	Mus musculus	318-323
34371027-5	2021	Meanwhile real time PCR shows higher expression of brain derived neurotrophic factor (BDNF) and synaptophysin in DHAc pretreated scopolamine treated mice brain.	Scopolamine	129-140	brain derived neurotrophic factor	Mus musculus	51-84
34371027-5	2021	Meanwhile real time PCR shows higher expression of brain derived neurotrophic factor (BDNF) and synaptophysin in DHAc pretreated scopolamine treated mice brain.	Scopolamine	129-140	brain derived neurotrophic factor	Mus musculus	86-90
34371027-5	2021	Meanwhile real time PCR shows higher expression of brain derived neurotrophic factor (BDNF) and synaptophysin in DHAc pretreated scopolamine treated mice brain.	Scopolamine	129-140	synaptophysin	Mus musculus	96-109
34093254-0	2021	M2-AChR Mediates Rapid Antidepressant Effects of Scopolamine Through Activating the mTORC1-BDNF Signaling Pathway in the Medial Prefrontal Cortex.	Scopolamine	49-60	CREB regulated transcription coactivator 1	Mus musculus	84-90
34093254-0	2021	M2-AChR Mediates Rapid Antidepressant Effects of Scopolamine Through Activating the mTORC1-BDNF Signaling Pathway in the Medial Prefrontal Cortex.	Scopolamine	49-60	brain-derived neurotrophic factor	Rattus norvegicus	91-95
34093254-3	2021	Several studies implicate M2-AChR as a potential antidepressant target of scopolamine.	Scopolamine	74-85	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	29-33
34093254-4	2021	This study aimed to explore the role of M2-AChR in scopolamine"s antidepressant-like effects and determine the underlying mechanisms.	Scopolamine	51-62	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	43-47
34093254-8	2021	Results: Consistent with previous studies, mPFC was required for the antidepressant-like effects of scopolamine, and intracerebroventricular injection of MCT into rats could produce similar antidepressant-like effects.	Scopolamine	100-111	complement factor properdin	Mus musculus	43-47
34093254-9	2021	Use of AAV-shRNA to knock down M2-AChR in the mPFC resulted in the antidepressant-like effects of scopolamine being blunted.	Scopolamine	98-109	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	34-38
34093254-9	2021	Use of AAV-shRNA to knock down M2-AChR in the mPFC resulted in the antidepressant-like effects of scopolamine being blunted.	Scopolamine	98-109	complement factor properdin	Mus musculus	46-50
34093254-11	2021	Conclusion: Our results indicate that M2-AChR in the mPFC mediates the antidepressant-like effects of scopolamine by increasing the expression of BDNF and activating the mTORC1 signaling pathway.	Scopolamine	102-113	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	41-45
34093254-11	2021	Conclusion: Our results indicate that M2-AChR in the mPFC mediates the antidepressant-like effects of scopolamine by increasing the expression of BDNF and activating the mTORC1 signaling pathway.	Scopolamine	102-113	complement factor properdin	Mus musculus	53-57
34093254-11	2021	Conclusion: Our results indicate that M2-AChR in the mPFC mediates the antidepressant-like effects of scopolamine by increasing the expression of BDNF and activating the mTORC1 signaling pathway.	Scopolamine	102-113	brain-derived neurotrophic factor	Rattus norvegicus	146-150
34093254-11	2021	Conclusion: Our results indicate that M2-AChR in the mPFC mediates the antidepressant-like effects of scopolamine by increasing the expression of BDNF and activating the mTORC1 signaling pathway.	Scopolamine	102-113	CREB regulated transcription coactivator 1	Mus musculus	170-176
34672296-0	2021	Effects of scopolamine treatment and consequent convulsion development in c-fos expression in fed, fasted, and refed mice.	Scopolamine	11-22	FBJ osteosarcoma oncogene	Mus musculus	74-79
34066108-5	2021	In vivo behavioral experiments (Y-maze and Morris water maze test) confirmed that LOS-ME alleviated cognitive impairments induced by scopolamine and the amount of iNOS expression decreased in the hippocampus of the mouse brain.	Scopolamine	133-144	nitric oxide synthase 2, inducible	Mus musculus	163-167
34672296-13	2021	Scopolamine treatment in 1-24 h fasted animals increased c-fos expression, but decreased in 48 h fasted animals.	Scopolamine	0-11	FBJ osteosarcoma oncogene	Mus musculus	57-62
34672296-14	2021	Whereas convulsion development in scopolamine-treated 3, 6, 12 and 24 h refed animals suppressed c-fos expression.	Scopolamine	34-45	FBJ osteosarcoma oncogene	Mus musculus	97-102
34672296-15	2021	These results demonstrate that re-feeding and scopolamine treatment induces neuronal activity in the hypothalamus, while scopolamine induced convulsions after food intake suppressed the c-fos activity.	Scopolamine	121-132	FBJ osteosarcoma oncogene	Mus musculus	186-191
35475510-8	2022	Furthermore, increased cholinesterases, adenosine deaminase (ADA), ATP hydrolysis, monoamine oxidase (MAO), and arginase activities induced by scopolamine were significantly reduced in rats treated with SM and PN leaves extract.	Scopolamine	143-154	adenosine deaminase	Rattus norvegicus	40-59
35174445-2	2022	Our results confirmed that Sco administration induces significant memory impairment, worsens exploratory behaviour and habituation, increases acetylcholinesterase (AChE) activity, and induces pathological monoamine content changes in the prefrontal cortex and hippocampus.	Scopolamine	27-30	acetylcholinesterase	Rattus norvegicus	164-168
35563597-0	2022	Novel CFTR Activator Cact-3 Ameliorates Ocular Surface Dysfunctions in Scopolamine-Induced Dry Eye Mice.	Scopolamine	71-82	cystic fibrosis transmembrane conductance regulator	Mus musculus	6-10
35475510-8	2022	Furthermore, increased cholinesterases, adenosine deaminase (ADA), ATP hydrolysis, monoamine oxidase (MAO), and arginase activities induced by scopolamine were significantly reduced in rats treated with SM and PN leaves extract.	Scopolamine	143-154	adenosine deaminase	Rattus norvegicus	61-64
35475510-8	2022	Furthermore, increased cholinesterases, adenosine deaminase (ADA), ATP hydrolysis, monoamine oxidase (MAO), and arginase activities induced by scopolamine were significantly reduced in rats treated with SM and PN leaves extract.	Scopolamine	143-154	monoamine oxidase A	Rattus norvegicus	83-100
35475510-8	2022	Furthermore, increased cholinesterases, adenosine deaminase (ADA), ATP hydrolysis, monoamine oxidase (MAO), and arginase activities induced by scopolamine were significantly reduced in rats treated with SM and PN leaves extract.	Scopolamine	143-154	monoamine oxidase A	Rattus norvegicus	102-105
35546461-11	2022	PECB attenuated scopolamine-induced increase of tumor necrosis factor-alpha and interleukin (IL)-1beta concentrations in the hippocampus with reversed diminished IL-10 level toward normal in the brain.	Scopolamine	16-27	tumor necrosis factor	Rattus norvegicus	48-75
35448865-0	2022	Wasp Venom Ameliorates Scopolamine-Induced Learning and Memory Impairment in Mice.	Scopolamine	23-34	Wiskott-Aldrich syndrome	Mus musculus	0-4
35531724-0	2022	(Mechanism of Tibetan medicine Ershiwuwei Shanhu Pills on scopolamine-induced learning and memory impairment in mice based on Keap1/Nrf2/HO-1 signaling pathway).	Scopolamine	58-69	kelch-like ECH-associated protein 1	Mus musculus	126-131
35531724-0	2022	(Mechanism of Tibetan medicine Ershiwuwei Shanhu Pills on scopolamine-induced learning and memory impairment in mice based on Keap1/Nrf2/HO-1 signaling pathway).	Scopolamine	58-69	nuclear factor, erythroid derived 2, like 2	Mus musculus	132-136
35531724-0	2022	(Mechanism of Tibetan medicine Ershiwuwei Shanhu Pills on scopolamine-induced learning and memory impairment in mice based on Keap1/Nrf2/HO-1 signaling pathway).	Scopolamine	58-69	heme oxygenase 1	Mus musculus	137-141
35531724-1	2022	This study aims to investigate the mechanism of the Tibetan medicine Ershiwuwei Shanhu Pills(ESP) in improving scopolamine-induced learning and memory impairment in mice based on Keap1/Nrf2/HO-1 signaling pathway.	Scopolamine	111-122	kelch-like ECH-associated protein 1	Mus musculus	179-184
35531724-1	2022	This study aims to investigate the mechanism of the Tibetan medicine Ershiwuwei Shanhu Pills(ESP) in improving scopolamine-induced learning and memory impairment in mice based on Keap1/Nrf2/HO-1 signaling pathway.	Scopolamine	111-122	nuclear factor, erythroid derived 2, like 2	Mus musculus	185-189
35531724-1	2022	This study aims to investigate the mechanism of the Tibetan medicine Ershiwuwei Shanhu Pills(ESP) in improving scopolamine-induced learning and memory impairment in mice based on Keap1/Nrf2/HO-1 signaling pathway.	Scopolamine	111-122	heme oxygenase 1	Mus musculus	190-194
35531724-15	2022	In conclusion, ESP protected mice against the scopolamine-induced learning and memory impairment by regulating the Keap1/Nrf2/HO-1 signaling pathway.	Scopolamine	46-57	kelch-like ECH-associated protein 1	Mus musculus	115-120
35531724-15	2022	In conclusion, ESP protected mice against the scopolamine-induced learning and memory impairment by regulating the Keap1/Nrf2/HO-1 signaling pathway.	Scopolamine	46-57	nuclear factor, erythroid derived 2, like 2	Mus musculus	121-125
35546461-11	2022	PECB attenuated scopolamine-induced increase of tumor necrosis factor-alpha and interleukin (IL)-1beta concentrations in the hippocampus with reversed diminished IL-10 level toward normal in the brain.	Scopolamine	16-27	interleukin 1 alpha	Rattus norvegicus	80-102
35212831-13	2022	CP + SCOP induced a concentration-dependent increase in AChE inhibition and ACh depletion.	Scopolamine	5-9	acetylcholinesterase (Cartwright blood group)	Homo sapiens	56-60
34982353-8	2022	The reduction observed in mean concentrations of hippocampal synaptic proteins (including neurexin1, neuroligin, and postsynaptic density protein 95) in scopolamine-treated animals was attenuated by apelin-13 treatment.	Scopolamine	153-164	neurexin 1	Rattus norvegicus	90-99
34982353-8	2022	The reduction observed in mean concentrations of hippocampal synaptic proteins (including neurexin1, neuroligin, and postsynaptic density protein 95) in scopolamine-treated animals was attenuated by apelin-13 treatment.	Scopolamine	153-164	discs large MAGUK scaffold protein 4	Rattus norvegicus	117-148
35212831-0	2022	Novel insights on acetylcholinesterase inhibition by Convolvulus pluricaulis, scopolamine and their combination in zebrafish.	Scopolamine	78-89	acetylcholinesterase	Danio rerio	18-38
35237756-0	2022	Stephania japonica Ameliorates Scopolamine-Induced Memory Impairment in Mice through Inhibition of Acetylcholinesterase and Oxidative Stress.	Scopolamine	31-42	acetylcholinesterase	Mus musculus	99-119
35137748-13	2022	Furthermore, scopolamine treatment promoted oxidative stress and acetylcholinesterase activity.	Scopolamine	13-24	acetylcholinesterase	Rattus norvegicus	65-85
35178203-11	2022	IL-6 levels were higher in the scopolamine group than the curcumin group (P=0.017) and the control group (P=0.005).	Scopolamine	31-42	interleukin 6	Rattus norvegicus	0-4
35128865-8	2022	Compared with the model group, both EA and SCOP remarkably increased the sucrose preference (P<0.001), shortened the feeding latency (P<0.001), up-regulated the BDNF, mTORC1, p-mTORC1, PSD95, Synapsin I, and GluR1 expression in PFC(P<0.05,P<0.01,P<0.001), and elevated the total and immature spine dendritic densities (P<0.001,P<0.01).	Scopolamine	43-47	brain-derived neurotrophic factor	Rattus norvegicus	161-165
35128865-8	2022	Compared with the model group, both EA and SCOP remarkably increased the sucrose preference (P<0.001), shortened the feeding latency (P<0.001), up-regulated the BDNF, mTORC1, p-mTORC1, PSD95, Synapsin I, and GluR1 expression in PFC(P<0.05,P<0.01,P<0.001), and elevated the total and immature spine dendritic densities (P<0.001,P<0.01).	Scopolamine	43-47	CREB regulated transcription coactivator 1	Mus musculus	167-173
35128865-8	2022	Compared with the model group, both EA and SCOP remarkably increased the sucrose preference (P<0.001), shortened the feeding latency (P<0.001), up-regulated the BDNF, mTORC1, p-mTORC1, PSD95, Synapsin I, and GluR1 expression in PFC(P<0.05,P<0.01,P<0.001), and elevated the total and immature spine dendritic densities (P<0.001,P<0.01).	Scopolamine	43-47	CREB regulated transcription coactivator 1	Mus musculus	177-183
35128865-8	2022	Compared with the model group, both EA and SCOP remarkably increased the sucrose preference (P<0.001), shortened the feeding latency (P<0.001), up-regulated the BDNF, mTORC1, p-mTORC1, PSD95, Synapsin I, and GluR1 expression in PFC(P<0.05,P<0.01,P<0.001), and elevated the total and immature spine dendritic densities (P<0.001,P<0.01).	Scopolamine	43-47	discs large MAGUK scaffold protein 4	Rattus norvegicus	185-190
35128865-8	2022	Compared with the model group, both EA and SCOP remarkably increased the sucrose preference (P<0.001), shortened the feeding latency (P<0.001), up-regulated the BDNF, mTORC1, p-mTORC1, PSD95, Synapsin I, and GluR1 expression in PFC(P<0.05,P<0.01,P<0.001), and elevated the total and immature spine dendritic densities (P<0.001,P<0.01).	Scopolamine	43-47	synapsin I	Rattus norvegicus	192-202
35128865-8	2022	Compared with the model group, both EA and SCOP remarkably increased the sucrose preference (P<0.001), shortened the feeding latency (P<0.001), up-regulated the BDNF, mTORC1, p-mTORC1, PSD95, Synapsin I, and GluR1 expression in PFC(P<0.05,P<0.01,P<0.001), and elevated the total and immature spine dendritic densities (P<0.001,P<0.01).	Scopolamine	43-47	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	208-213
2706478-2	1989	A brief tetanus (200 Hz for 1 s) caused an increase in amplitude of the population spike recorded from the CA1 area (typically about 200% of control), which lasted for more than 2 h. LTP was suppressed by perfusion of the muscarinic antagonist scopolamine (10(-5) M) from 5 min before to 15 min after the tetanus.	Scopolamine	244-255	carbonic anhydrase 1	Rattus norvegicus	107-110
2611661-1	1989	Neuropeptide Y (NPY) is a 36 amino acid peptide which was shown to enhance memory retention, recall and prevent amnesia induced by either scopolamine or anisomycin.	Scopolamine	138-149	neuropeptide Y	Mus musculus	0-14
2611661-1	1989	Neuropeptide Y (NPY) is a 36 amino acid peptide which was shown to enhance memory retention, recall and prevent amnesia induced by either scopolamine or anisomycin.	Scopolamine	138-149	neuropeptide Y	Mus musculus	16-19
2478047-2	1989	IgE antibodies that reacted with morphine and codeine were detected in the serum of a subject who experienced a life-threatening anaphylactic reaction following the administration of Omnopon-Scopolamine (papaveretum-hyoscine).	Scopolamine	216-224	immunoglobulin heavy constant epsilon	Homo sapiens	0-3
2478047-7	1989	Hyoscine reacted weakly with IgE antibodies in the subject"s serum, but this was thought to be due to weak cross-reaction between this compound and morphine.	Scopolamine	0-8	immunoglobulin heavy constant epsilon	Homo sapiens	29-32
2757465-6	1989	In addition, the decrease in hippocampal ACh and choline content following an injection of scopolamine was lessened by aniracetam 100 mg/kg, p.o.	Scopolamine	91-102	acyl-CoA thioesterase 12	Rattus norvegicus	41-44
2929375-8	1989	Scopolamine abolished the VIP-induced secretion.	Scopolamine	0-11	VIP peptides	Cavia porcellus	26-29
2710412-3	1989	Scopolamine at concentration of 10 microM had no effect on LTP in CA1 but significantly suppressed LTP in CA3.	Scopolamine	0-11	carbonic anhydrase 3	Cavia porcellus	106-109
2570433-2	1989	These impairments can be reversed by appropriate agents such as the cholinesterase inhibitor physostigmine in the case of scopolamine or the benzodiazepine antagonist Ro 15-1788 in the case of lorazepam.	Scopolamine	122-133	butyrylcholinesterase	Homo sapiens	68-82
3417793-4	1988	Global CBF was significantly reduced 25 min after scopolamine.	Scopolamine	50-61	CCAAT enhancer binding protein zeta	Homo sapiens	7-10
3339943-7	1988	B10 mice were more sensitive than NZB or NZBWF mice to both the disruptive effects of scopolamine and the facilitory effects of physostigmine on swim maze learning.	Scopolamine	86-97	granzyme C	Mus musculus	0-3
2901077-1	1988	Transdermal scopolamine (Transderm-Scop) is being increasingly used for effective prophylaxis of motion sickness.	Scopolamine	12-23	PH domain and leucine rich repeat protein phosphatase 1	Homo sapiens	35-39
20501200-2	1988	The acute treatment with the anticholinergic drugs atropine and scopolamine increased neurotensin concentrations in the striatum and, in the former case, also in the nucleus accumbens.	Scopolamine	64-75	neurotensin	Rattus norvegicus	86-97
3253717-2	1988	For what concerns the effects on locomotor activity, it was demonstrated that three histamine H1 receptor antagonists, chlorpheniramine, diphenhydramine and tripelennamine enhance morphine-, but not amphetamine and scopolamine-induced hyperactivity in mice.	Scopolamine	215-226	histamine receptor H1	Mus musculus	84-105
3691642-3	1987	administration of the cholinomimetics oxotremorine and arecoline and the cholinesterase blocker physostigmine evoked theta wave activity in the hippocampus, which was blocked by scopolamine.	Scopolamine	178-189	butyrylcholinesterase	Rattus norvegicus	73-87
3690274-7	1987	NPY was also found to alleviate the amnesia caused by anisomycin, a protein synthesis inhibitor, and scopolamine, an anticholinergic.	Scopolamine	101-112	neuropeptide Y	Homo sapiens	0-3
2888127-8	1987	On the other hand, a specific CCK antagonist, proglumide, significantly inhibited pancreatic enzyme secretion induced by oleate in the presence of scopolamine.	Scopolamine	147-158	cholecystokinin	Rattus norvegicus	30-33
3588515-3	1987	In the presence of scopolamine (0.3 microM), however, there was a large enhancement (87.0%) of potassium evoked release during soman inhibited (100%) AChE-activity.	Scopolamine	19-30	acetylcholinesterase	Rattus norvegicus	150-154
3579494-3	1987	The patients with DAT showed significant behavioral and cognitive but not physiologic changes at a lower scopolamine dose (0.25 mg) than did the normal elderly controls.	Scopolamine	105-116	solute carrier family 6 member 3	Homo sapiens	18-21
3579494-4	1987	Cognitive tests of new learning and semantic knowledge revealed significant impairments at the 0.25-mg scopolamine dose in the patients with DAT, while the responses of the control population were essentially unchanged.	Scopolamine	103-114	solute carrier family 6 member 3	Homo sapiens	141-144
3950635-1	1986	The anticholinergic drug hyoscine hydrobromide produced a slowing of the P2 and N3 components of the flash visual evoked potential (VEP) in young normals but did not affect the pattern reversal VEP.	Scopolamine	25-46	peripheral myelin protein 2	Homo sapiens	73-82
3101313-0	1986	[Effect of thyrotropin-releasing hormone (TRH) and its analog DN-1417 on scopolamine-induced impairment of short-term memory in rats].	Scopolamine	73-84	thyrotropin releasing hormone	Rattus norvegicus	11-40
3101313-0	1986	[Effect of thyrotropin-releasing hormone (TRH) and its analog DN-1417 on scopolamine-induced impairment of short-term memory in rats].	Scopolamine	73-84	thyrotropin releasing hormone	Rattus norvegicus	42-45
3742245-0	1986	Pretreatment of young mice with nerve growth factor enhances scopolamine-induced hyperactivity.	Scopolamine	61-72	nerve growth factor	Mus musculus	32-51
3728677-3	1986	The VIP-induced contractions seem to be related to three components, the scopolamine-sensitive, the scopolamine-insensitive, the tetrodotoxin-sensitive, and the tetrodotoxin-insensitive contractions.	Scopolamine	73-84	VIP peptides	Cavia porcellus	4-7
3728677-3	1986	The VIP-induced contractions seem to be related to three components, the scopolamine-sensitive, the scopolamine-insensitive, the tetrodotoxin-sensitive, and the tetrodotoxin-insensitive contractions.	Scopolamine	100-111	VIP peptides	Cavia porcellus	4-7
3018822-6	1986	Scopolamine significantly attenuated the physostigmine-associated increase in plasma concentrations of cortisol, growth hormone, prolactin, ACTH, and dopamine compared to methscopolamine, and a close-to-significant attenuation of epinephrine as well.	Scopolamine	0-11	growth hormone 1	Homo sapiens	113-127
3018822-6	1986	Scopolamine significantly attenuated the physostigmine-associated increase in plasma concentrations of cortisol, growth hormone, prolactin, ACTH, and dopamine compared to methscopolamine, and a close-to-significant attenuation of epinephrine as well.	Scopolamine	0-11	proopiomelanocortin	Homo sapiens	140-144
6685825-3	1983	Scopolamine also delayed the onset of frequency potentiation in CA1, but only at high dose (10 mg/kg).	Scopolamine	0-11	carbonic anhydrase 1	Rattus norvegicus	64-67
3935977-0	1985	Comparative effects of scopolamine and atropine in preventing cholinesterase inhibitor induced lethality.	Scopolamine	23-34	butyrylcholinesterase	Homo sapiens	62-76
2408907-0	1985	Block of the hyoscine-resistant opiate withdrawal contracture of ileum by a new substance P antagonist [D-Arg1,D-Phe5,D- Trp7,9,Leu 11]substance P.	Scopolamine	13-21	arginase 1	Homo sapiens	106-110
2408907-0	1985	Block of the hyoscine-resistant opiate withdrawal contracture of ileum by a new substance P antagonist [D-Arg1,D-Phe5,D- Trp7,9,Leu 11]substance P.	Scopolamine	13-21	transient receptor potential cation channel subfamily C member 7	Homo sapiens	121-125
6144364-3	1984	Pretreatment with scopolamine prevented the losses in GAD without affecting those in TH.	Scopolamine	18-29	glutamate-ammonia ligase	Rattus norvegicus	54-57
2994873-6	1985	Scopolamine reversed the inhibitory effects of the muscarinic agents on basal and stimulated ACTH secretion and cyclic AMP formation.	Scopolamine	0-11	pro-opiomelanocortin-alpha	Mus musculus	93-97
2987726-1	1985	The grooming behavior induced by intracerebroventricular administration of ACTH was specifically antagonized by the muscarinic receptor antagonists, atropine and scopolamine.	Scopolamine	162-173	proopiomelanocortin	Homo sapiens	75-79
3924793-10	1985	However, atropine and scopolamine potentiated the circling inducing action of TRH or DN-1417, in contrast with suppression of the licking behavior.	Scopolamine	22-33	thyrotropin releasing hormone	Mus musculus	78-81
6534036-8	1984	Scopolamine, 1 mg/kg ip, significantly suppressed the lever press at FR 1 sessions, and the latency time until the first lever press was also prolonged significantly in these sessions.	Scopolamine	0-11	aldo-keto reductase family 1, member B8	Mus musculus	69-73
13893256-0	1962	Coma due to a combination of barbiturates, scopolamine and dihydroergotamine.	Scopolamine	43-54	COMA	Homo sapiens	0-4
6129770-6	1982	CAR and UER inhibition induced by cis(Z)-flupentixol and haloperidol was attenuated by scopolamine, but was only weakly influenced by methysergide and prazosin.	Scopolamine	87-98	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	0-3
119692-5	1979	The DA releasing effect of TRH was completely blocked by cholinergic blockers (scopolamine, hexamethonium and hemicholinium), Ca2+ chelator(EGTA), Ca2+ antagonist(CoCl2) and Ca2+ influx blocker(D-600) or by the removal of Ca2+ from the medium.	Scopolamine	79-90	thyrotropin releasing hormone	Rattus norvegicus	27-30
1252961-1	1976	The direct application of crystalline dopamine, D-amphetamine or scopolamine in microgram quantities to the ventral anterior region of the corpus striatum (VAS) of rats increased their responding for food on a modified DRL-30 sec schedule of reinforcement.	Scopolamine	65-76	arginine vasopressin	Rattus norvegicus	156-159
6104604-4	1980	The contractile response to TRH of the small intestine was abolished and replaced by a relaxation in the presence of hyoscine.	Scopolamine	117-125	thyrotropin releasing hormone	Cavia porcellus	28-31
6104604-6	1980	The taenial response to TRH was partially inhibited by either hyoscine or methysergide and markedly diminished by the two together.	Scopolamine	62-70	thyrotropin releasing hormone	Cavia porcellus	24-27
154749-6	1979	In the scopolamine group there was an unexpected fall in factors X and V and also in plasminogen and alpha 1-antitrypsin.	Scopolamine	7-18	serpin family A member 1	Homo sapiens	101-120
921393-0	1977	The effects of ATP-receptor blocking agents on the response to the guinea-pig isolated bladder preparation to hyoscine-resistant nerve stimulation.	Scopolamine	110-118	P2X purinoceptor 2	Cavia porcellus	15-27
11829024-12	1977	Scopolamine/Dexedrine caused consistent elevations in urinary cortisol and epinephrine and a transient elevation in ADH.	Scopolamine	0-11	arginine vasopressin	Homo sapiens	116-119
33755857-9	2021	Scopolamine induced memory deficits, increased acetylcholinesterase activity and oxidative damage, and decreased Na+/K+-ATPase activity in cerebral cortex and hippocampus.	Scopolamine	0-11	acetylcholinesterase	Rattus norvegicus	47-67
33755857-11	2021	Scopolamine also induced an increase in acetylcholinesterase activity in lymphocytes and whereas butyrylcholinesterase in serum and treatment with DS12 prevented these changes.	Scopolamine	0-11	acetylcholinesterase	Rattus norvegicus	40-60
33721210-12	2021	Scopolamine enhanced the AChE activity and oxidative stress in the brain of mice which resulted in memory impairment.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	25-29
33352242-6	2021	RESULTS: Scopolamine-induced rats with co-treatment of EGb 761 and donepezil had significantly improved cognitive function in the Morris water maze test with increased brain levels of superoxide dismutase and decreased brain levels of acetylcholinesterase and malondialdehyde than that with treatment of only EGb 761 or donepezil.	Scopolamine	9-20	acetylcholinesterase	Rattus norvegicus	235-255
34024109-3	2021	The optimal compound 27g possessed excellent dual AChE/GSK-3 inhibition both in terms of potency and equilibrium (AChE: IC50 = 51.1 nM; GSK-3beta: IC50 = 89.3 nM) and displayed significant amelioration on cognitive deficits in scopolamine-induced amnesia mice and efficient reduction against phosphorylation of tau protein on Ser-199 and Ser-396 sites in glyceraldehyde (GA)-stimulated differentiated SH-SY5Y cells.	Scopolamine	227-238	glycogen synthase kinase 3 beta	Mus musculus	55-60
33545198-2	2021	Previous studies demonstrated that Rb1 protected against scopolamine-induced amnesia and exhibited memory-enhancing effects in the SAMP8 mouse model.	Scopolamine	57-68	RB transcriptional corepressor 1	Mus musculus	35-38
33863952-8	2021	Scopolamine treatment showed significant increase in the level of anxiety and impairments in memory and cognitive function associated with increased level of pro-inflammatory cytokines and NLRP3 inflammasome components.	Scopolamine	0-11	NLR family, pyrin domain containing 3	Mus musculus	189-194
33649977-11	2021	The results demonstrated that vit D has protective effects on scopolamine-associated learning and memory impairment by improving BDNF levels and attenuating NO and brain tissue oxidative damage.	Scopolamine	62-73	vitrin	Rattus norvegicus	30-33
33437162-0	2021	Oral administration of hydrolyzed red ginseng extract improves learning and memory capability of scopolamine-treated C57BL/6J mice via upregulation of Nrf2-mediated antioxidant mechanism.	Scopolamine	97-108	nuclear factor, erythroid derived 2, like 2	Mus musculus	151-155
33620666-8	2021	Pre-treatment with the scopolamine hydrobromide showed significant upregulation of different TLRs like TLR3, TLR7, and TLR8, interleukins like IL-4, and IL-10, as well as IFNs and their regulatory factors.	Scopolamine	23-47	toll like receptor 3	Homo sapiens	103-107
33620666-8	2021	Pre-treatment with the scopolamine hydrobromide showed significant upregulation of different TLRs like TLR3, TLR7, and TLR8, interleukins like IL-4, and IL-10, as well as IFNs and their regulatory factors.	Scopolamine	23-47	toll like receptor 7	Homo sapiens	109-113
33620666-8	2021	Pre-treatment with the scopolamine hydrobromide showed significant upregulation of different TLRs like TLR3, TLR7, and TLR8, interleukins like IL-4, and IL-10, as well as IFNs and their regulatory factors.	Scopolamine	23-47	toll like receptor 8	Homo sapiens	119-123
33620666-8	2021	Pre-treatment with the scopolamine hydrobromide showed significant upregulation of different TLRs like TLR3, TLR7, and TLR8, interleukins like IL-4, and IL-10, as well as IFNs and their regulatory factors.	Scopolamine	23-47	interleukin 4	Homo sapiens	143-147
33620666-8	2021	Pre-treatment with the scopolamine hydrobromide showed significant upregulation of different TLRs like TLR3, TLR7, and TLR8, interleukins like IL-4, and IL-10, as well as IFNs and their regulatory factors.	Scopolamine	23-47	interleukin 10	Homo sapiens	153-158
33620666-10	2021	These results indicate that scopolamine hydrobromide contributes much to launch antiviral effects by remoulding the TLR and IFN signaling pathways that are involved in sensing and initiating the much-needed anti-JEV responses.	Scopolamine	28-52	tlr	None	116-119
33171279-4	2021	More than one-third of the cholinergic cells expressed CB1R, so we speculated that RVD and VD might have ability to inhibit the memory-impairing effect of scopolamine.	Scopolamine	155-166	cannabinoid receptor 1 (brain)	Mus musculus	55-59
33441928-0	2021	A combination of CMC and alpha-MSH inhibited ROS activated NLRP3 inflammasome in hyperosmolarity stressed HCECs and scopolamine-induced dry eye rats.	Scopolamine	116-127	Stam binding protein	Rattus norvegicus	25-34
33441928-0	2021	A combination of CMC and alpha-MSH inhibited ROS activated NLRP3 inflammasome in hyperosmolarity stressed HCECs and scopolamine-induced dry eye rats.	Scopolamine	116-127	NLR family, pyrin domain containing 3	Rattus norvegicus	59-64
33363155-0	2020	A Novel PDE4D Inhibitor BPN14770 Reverses Scopolamine-Induced Cognitive Deficits via cAMP/SIRT1/Akt/Bcl-2 Pathway.	Scopolamine	42-53	phosphodiesterase 4D, cAMP specific	Mus musculus	8-13
32754961-0	2021	Protective effect of ginsenoside Rh2 on scopolamine-induced memory deficits through regulation of cholinergic transmission, oxidative stress and the ERK-CREB-BDNF signaling pathway.	Scopolamine	40-51	mitogen-activated protein kinase 1	Mus musculus	149-152
32754961-0	2021	Protective effect of ginsenoside Rh2 on scopolamine-induced memory deficits through regulation of cholinergic transmission, oxidative stress and the ERK-CREB-BDNF signaling pathway.	Scopolamine	40-51	cAMP responsive element binding protein 1	Mus musculus	153-157
32754961-0	2021	Protective effect of ginsenoside Rh2 on scopolamine-induced memory deficits through regulation of cholinergic transmission, oxidative stress and the ERK-CREB-BDNF signaling pathway.	Scopolamine	40-51	brain derived neurotrophic factor	Mus musculus	158-162
33363155-0	2020	A Novel PDE4D Inhibitor BPN14770 Reverses Scopolamine-Induced Cognitive Deficits via cAMP/SIRT1/Akt/Bcl-2 Pathway.	Scopolamine	42-53	sirtuin 1	Mus musculus	90-95
33363155-0	2020	A Novel PDE4D Inhibitor BPN14770 Reverses Scopolamine-Induced Cognitive Deficits via cAMP/SIRT1/Akt/Bcl-2 Pathway.	Scopolamine	42-53	thymoma viral proto-oncogene 1	Mus musculus	96-99
33363155-0	2020	A Novel PDE4D Inhibitor BPN14770 Reverses Scopolamine-Induced Cognitive Deficits via cAMP/SIRT1/Akt/Bcl-2 Pathway.	Scopolamine	42-53	B cell leukemia/lymphoma 2	Mus musculus	100-105
33363155-4	2020	Relatively low doses of BPN14770 were effective at reversing scopolamine-induced memory and cognitive deficits in humanized PDE4D mice.	Scopolamine	61-72	phosphodiesterase 4D, cAMP specific	Mus musculus	124-129
33170051-10	2020	The cognitive-enhancing activity of AHR against scopolamine-induced memory impairments was investigated using Y-maze, the novel object recognition test (NORT) and the Morris water maze (MWM) test.	Scopolamine	48-59	aryl-hydrocarbon receptor	Mus musculus	36-39
33170051-14	2020	In in vivo test, AHR (15 mg/kg) significantly increased in spontaneous alternation performance in the Y-maze test (p < 0.01), it significantly increased the time spent exploring the novel object (p < 0.05) comparison with scopolamine-treated group.	Scopolamine	222-233	aryl-hydrocarbon receptor	Mus musculus	17-20
33324798-10	2020	Scopolamine-mediated changes in AChE, malondialdehyde, reduced glutathione, glutathione peroxidase, superoxide dismutase, and catalase were improved after the treatment with oleoresins.	Scopolamine	0-11	acetylcholinesterase	Rattus norvegicus	32-36
32653763-5	2020	The LOQs for atropine and scopolamine were around 0.4 and 1.2 microg/kg in cereal products, and in tea and herbal infusions, respectively.	Scopolamine	26-37	TARBP2 subunit of RISC loading complex	Homo sapiens	4-8
33183243-0	2020	Electroacupuncture reduces scopolamine-induced amnesia via mediating the miR-210/SIN3A and miR-183/SIN3A signaling pathway.	Scopolamine	27-38	microRNA 210	Rattus norvegicus	73-80
33183243-0	2020	Electroacupuncture reduces scopolamine-induced amnesia via mediating the miR-210/SIN3A and miR-183/SIN3A signaling pathway.	Scopolamine	27-38	SIN3 transcription regulator family member A	Rattus norvegicus	81-86
33183243-0	2020	Electroacupuncture reduces scopolamine-induced amnesia via mediating the miR-210/SIN3A and miR-183/SIN3A signaling pathway.	Scopolamine	27-38	microRNA 183	Rattus norvegicus	91-98
33183243-0	2020	Electroacupuncture reduces scopolamine-induced amnesia via mediating the miR-210/SIN3A and miR-183/SIN3A signaling pathway.	Scopolamine	27-38	SIN3 transcription regulator family member A	Rattus norvegicus	99-104
33183243-1	2020	BACKGROUND: The expression of SIN3A is closely correlated with electroacupuncture (EA) treatment efficacy of scopolamine-induced amnesia (SIA), but its underlying mechanisms remain to be further explored.	Scopolamine	109-120	SIN3 transcription regulator family member A	Rattus norvegicus	30-35
33183243-12	2020	CONCLUSION: In summary, the findings of this study demonstrated that scopolamine-induced amnesia was associated with downregulated expression of miR-210/miR-183 and upregulated expression of SIN3A.	Scopolamine	69-80	microRNA 210	Rattus norvegicus	145-152
33183243-12	2020	CONCLUSION: In summary, the findings of this study demonstrated that scopolamine-induced amnesia was associated with downregulated expression of miR-210/miR-183 and upregulated expression of SIN3A.	Scopolamine	69-80	microRNA 183	Rattus norvegicus	153-160
33183243-12	2020	CONCLUSION: In summary, the findings of this study demonstrated that scopolamine-induced amnesia was associated with downregulated expression of miR-210/miR-183 and upregulated expression of SIN3A.	Scopolamine	69-80	SIN3 transcription regulator family member A	Rattus norvegicus	191-196
33183243-13	2020	Furthermore, treatment with EA alleviated scopolamine-induced amnesia in rats and was associated with upregulated expression of miR-210/miR-183 and downregulated expression of SIN3A.	Scopolamine	42-53	microRNA 210	Rattus norvegicus	128-135
33183243-13	2020	Furthermore, treatment with EA alleviated scopolamine-induced amnesia in rats and was associated with upregulated expression of miR-210/miR-183 and downregulated expression of SIN3A.	Scopolamine	42-53	microRNA 183	Rattus norvegicus	136-143
33054164-8	2020	Interestingly, our molecular docking analysis revealed that atropine and scopolamine interact with the His288 residue of NS3 protein, a crucial residue for RNA unwinding and ATPase activity that was further confirmed by degradation of NS3 protein.	Scopolamine	73-84	KRAS proto-oncogene, GTPase	Homo sapiens	121-124
33054164-8	2020	Interestingly, our molecular docking analysis revealed that atropine and scopolamine interact with the His288 residue of NS3 protein, a crucial residue for RNA unwinding and ATPase activity that was further confirmed by degradation of NS3 protein.	Scopolamine	73-84	KRAS proto-oncogene, GTPase	Homo sapiens	235-238
32874571-10	2020	Correspondingly, APT significantly increased ACh and ChAT levels in the hippocampus and prefrontal cortex of scopolamine-induced mice.	Scopolamine	109-120	choline acetyltransferase	Mus musculus	53-57
33158153-8	2020	TEO ameliorated Sco-induced increasing of AChE activity, amnesia, anxiety, and reduced the brain antioxidant capacity.	Scopolamine	16-19	acetylcholinesterase	Danio rerio	42-46
33054666-9	2022	An increase in NTPdase, ADA, MAO, and ACE activities were observed in the brain of rats treated with SCOP.	Scopolamine	101-105	monoamine oxidase A	Rattus norvegicus	29-32
33137907-0	2020	Tert-butyl-(4-hydroxy-3-((3-(2-methylpiperidin-yl)propyl)carbamoyl)phenyl)carbamate Has Moderated Protective Activity in Astrocytes Stimulated with Amyloid Beta 1-42 and in a Scopolamine Model.	Scopolamine	175-186	telomerase reverse transcriptase	Rattus norvegicus	0-4
33070149-6	2021	In contrast, stimulation of Gad1, Sst, or Pvalb interneurons in mPFC abolished the effects of scopolamine and prevented scopolamine induction of synaptic plasticity.	Scopolamine	94-105	somatostatin	Mus musculus	34-37
33070149-6	2021	In contrast, stimulation of Gad1, Sst, or Pvalb interneurons in mPFC abolished the effects of scopolamine and prevented scopolamine induction of synaptic plasticity.	Scopolamine	94-105	parvalbumin	Mus musculus	42-47
33070149-6	2021	In contrast, stimulation of Gad1, Sst, or Pvalb interneurons in mPFC abolished the effects of scopolamine and prevented scopolamine induction of synaptic plasticity.	Scopolamine	120-131	somatostatin	Mus musculus	34-37
33070149-6	2021	In contrast, stimulation of Gad1, Sst, or Pvalb interneurons in mPFC abolished the effects of scopolamine and prevented scopolamine induction of synaptic plasticity.	Scopolamine	120-131	parvalbumin	Mus musculus	42-47
33054666-9	2022	An increase in NTPdase, ADA, MAO, and ACE activities were observed in the brain of rats treated with SCOP.	Scopolamine	101-105	angiotensin I converting enzyme	Rattus norvegicus	38-41
32516489-4	2020	We measured these RT parameters under vehicle treatment and systemic administration of the muscarinic receptor antagonist scopolamine.	Scopolamine	122-133	cholinergic receptor muscarinic 5	Macaca mulatta	91-110
32990646-10	2020	Scopolamine-induced nitrosative/oxidative stress and increased acetylcholinesterase activity in the prefrontal cortex and hippocampus were significantly attenuated by the pretreatment of mice with rutin.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	63-83
32133639-7	2020	Moreover, we determined that the effects of maslinic acid on scopolamine-induced memory impairment in the passive avoidance test were abolished by a specific TrkB receptor antagonist (ANA-12).	Scopolamine	61-72	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	158-162
32776896-7	2020	The extract markedly reduced brain AChE, MDA, and nitrite contents in mice injected with scopolamine (p<0.05).	Scopolamine	89-100	acetylcholinesterase	Mus musculus	35-39
32679768-0	2020	Enteromorpha prolifera Extract Improves Memory in Scopolamine-Treated Mice via Downregulating Amyloid-beta Expression and Upregulating BDNF/TrkB Pathway.	Scopolamine	50-61	brain derived neurotrophic factor	Mus musculus	135-139
32679768-0	2020	Enteromorpha prolifera Extract Improves Memory in Scopolamine-Treated Mice via Downregulating Amyloid-beta Expression and Upregulating BDNF/TrkB Pathway.	Scopolamine	50-61	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	140-144
32638218-4	2020	Scopolamine has been linked to increases in both Abeta production and oxidative stress in rat and mice brains.	Scopolamine	0-11	amyloid beta precursor protein	Rattus norvegicus	49-54
32219881-11	2020	Increased acetyl-cholinesterase activity and oxidative stress, as shown by decreased antioxidant substrates (glutathione and catalase) and elevated malondialdehyde contents in mice with scopolamine amnesia were also attenuated by DRLC.	Scopolamine	186-197	catalase	Mus musculus	125-133
32454411-0	2020	Fat-1 expression enhance hippocampal memory in scopolamine-induced amnesia.	Scopolamine	47-58	FAT atypical cadherin 1	Mus musculus	0-5
32454411-3	2020	We performed Y-maze and passive avoidance tests to evaluate the memory function of fat-1 mice treated with scopolamine.	Scopolamine	107-118	FAT atypical cadherin 1	Mus musculus	83-88
32454411-5	2020	The effects of scopolamine on hippocampal neurogenesis were confirmed by increases in the number of Ki-67- and DCX-positive cells in the fat-1 mice.	Scopolamine	15-26	antigen identified by monoclonal antibody Ki 67	Mus musculus	100-105
32454411-5	2020	The effects of scopolamine on hippocampal neurogenesis were confirmed by increases in the number of Ki-67- and DCX-positive cells in the fat-1 mice.	Scopolamine	15-26	doublecortin	Mus musculus	111-114
32454411-5	2020	The effects of scopolamine on hippocampal neurogenesis were confirmed by increases in the number of Ki-67- and DCX-positive cells in the fat-1 mice.	Scopolamine	15-26	FAT atypical cadherin 1	Mus musculus	137-142
32454411-7	2020	These findings suggest that higher endogenous omega-3 PUFA prevented granular cell loss, increased BDNF signaling, and decreased apoptosis signaling in scopolamine-treated fat-1 mice.	Scopolamine	152-163	FAT atypical cadherin 1	Mus musculus	172-177
32375073-8	2020	Analog 7a could effectively reverse the increased levels of AChE and BChE in scopolamine-treated animals and exhibited potent ex-vivo antioxidant properties.	Scopolamine	77-88	acetylcholinesterase	Mus musculus	60-64
32375073-8	2020	Analog 7a could effectively reverse the increased levels of AChE and BChE in scopolamine-treated animals and exhibited potent ex-vivo antioxidant properties.	Scopolamine	77-88	butyrylcholinesterase	Mus musculus	69-73
32573587-9	2020	The Morris water maze experiment showed that scopolamine-induced AD-like dementia in rats treated with PC/SHP-2-Bn/SHP-2-16 nanoparticles was significantly reduced.	Scopolamine	45-56	protein tyrosine phosphatase, non-receptor type 11	Rattus norvegicus	106-111
32573587-9	2020	The Morris water maze experiment showed that scopolamine-induced AD-like dementia in rats treated with PC/SHP-2-Bn/SHP-2-16 nanoparticles was significantly reduced.	Scopolamine	45-56	protein tyrosine phosphatase, non-receptor type 11	Rattus norvegicus	115-120
32543989-11	2022	In scopolamine-treated rats, AChE, BChE, MAO and NTPdases activities, and antioxidant status were upturned in rats pretreated with BLAE.	Scopolamine	3-14	butyrylcholinesterase	Rattus norvegicus	35-39
32543989-11	2022	In scopolamine-treated rats, AChE, BChE, MAO and NTPdases activities, and antioxidant status were upturned in rats pretreated with BLAE.	Scopolamine	3-14	monoamine oxidase A	Rattus norvegicus	41-44
32217627-3	2020	Damage to long-term memory by prevention of this process, with the use of mAChR antagonist scopolamine prior to novel taste learning, can be rescued by local QR2 inhibition, demonstrating that QR2 acts downstream of local muscarinic activation.	Scopolamine	91-102	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	193-196
32026225-8	2020	The AERI at higher dose also counteracted the scopolamine-induced decrease in acetylcholine levels, increase in AChE activity, and decrease in antioxidant enzymes activities.	Scopolamine	46-57	acetylcholinesterase	Rattus norvegicus	112-116
31821013-6	2020	Compound 1 protected against increasing in lipid peroxidation levels and AChE activity caused by SCO in the cerebral cortex and hippocampus of mice.	Scopolamine	97-100	acetylcholinesterase	Mus musculus	73-77
32035879-0	2020	Dracocephalum moldavica attenuates scopolamine-induced cognitive impairment through activation of hippocampal ERK-CREB signaling in mice.	Scopolamine	35-46	mitogen-activated protein kinase 1	Mus musculus	110-113
32035879-0	2020	Dracocephalum moldavica attenuates scopolamine-induced cognitive impairment through activation of hippocampal ERK-CREB signaling in mice.	Scopolamine	35-46	cAMP responsive element binding protein 1	Mus musculus	114-118
32048104-10	2020	Moreover, SCO increased AChE and CAT activities, decreased Na+/K+-ATPase activity and increased TBARS levels in the cerebral structures of mice.	Scopolamine	10-13	acetylcholinesterase	Mus musculus	24-28
32174034-0	2020	GAPT regulates cholinergic dysfunction and oxidative stress in the brains of learning and memory impairment mice induced by scopolamine.	Scopolamine	124-135	Grb2-binding adaptor, transmembrane	Mus musculus	0-4
32174034-8	2020	RESULTS: After one-half or 1 month of intragastric administration, GAPT can ameliorate scopolamine-induced behavioral changes in learning and memory impaired mice.	Scopolamine	87-98	Grb2-binding adaptor, transmembrane	Mus musculus	67-71
32174034-11	2020	CONCLUSIONS: GAPT can improve the learning and memory ability of scopolamine-induced mice, and its mechanism may be related to protecting cholinergic neurons and reducing oxidative stress injury.	Scopolamine	65-76	Grb2-binding adaptor, transmembrane	Mus musculus	13-17
32131034-8	2020	TM-4 presented precognitive effect on scopolamine-induced memory impairment.	Scopolamine	38-49	tropomyosin 4	Rattus norvegicus	0-4
32048104-10	2020	Moreover, SCO increased AChE and CAT activities, decreased Na+/K+-ATPase activity and increased TBARS levels in the cerebral structures of mice.	Scopolamine	10-13	catalase	Mus musculus	33-36
31960226-8	2020	Similarly scopolamine up-regulated HDAC2 and HDAC5 by 3.12 fold and 3.64-fold, respectively.	Scopolamine	10-21	histone deacetylase 5	Mus musculus	45-50
31933104-6	2020	SAK3 inhibited scopolamine-induced cellular apoptosis (morphologically and by determination of pro- and anti-apoptotic factor levels), increase in ROS levels, decrease in choline acetyltransferase level, phosphorylation of NF-kappaB, activation of Akt, JNK and p38 intracellular signaling pathways, and elevation of proinflammatory cytokines IL-1beta and IL-6, but not enhanced level of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1).	Scopolamine	15-26	nuclear factor kappa B subunit 1	Homo sapiens	223-232
31960226-2	2020	The focus of the work was to elucidate the modulation of the chromatin modifying enzymes: DNMT1, DNMT3a, DNMT3b, HDAC2, HDAC5 and CPB in scopolamine induced amnesic mice after treatment with bacoside rich extract of Bacopa monniera (BA) and BA encapsulated in lactoferrin conjugated PEG-PLA-PCL-OH based polymersomes (BAN).	Scopolamine	137-148	DNA methyltransferase (cytosine-5) 1	Mus musculus	90-95
31960226-2	2020	The focus of the work was to elucidate the modulation of the chromatin modifying enzymes: DNMT1, DNMT3a, DNMT3b, HDAC2, HDAC5 and CPB in scopolamine induced amnesic mice after treatment with bacoside rich extract of Bacopa monniera (BA) and BA encapsulated in lactoferrin conjugated PEG-PLA-PCL-OH based polymersomes (BAN).	Scopolamine	137-148	DNA methyltransferase 3A	Mus musculus	97-103
31960226-2	2020	The focus of the work was to elucidate the modulation of the chromatin modifying enzymes: DNMT1, DNMT3a, DNMT3b, HDAC2, HDAC5 and CPB in scopolamine induced amnesic mice after treatment with bacoside rich extract of Bacopa monniera (BA) and BA encapsulated in lactoferrin conjugated PEG-PLA-PCL-OH based polymersomes (BAN).	Scopolamine	137-148	DNA methyltransferase 3B	Mus musculus	105-111
31960226-2	2020	The focus of the work was to elucidate the modulation of the chromatin modifying enzymes: DNMT1, DNMT3a, DNMT3b, HDAC2, HDAC5 and CPB in scopolamine induced amnesic mice after treatment with bacoside rich extract of Bacopa monniera (BA) and BA encapsulated in lactoferrin conjugated PEG-PLA-PCL-OH based polymersomes (BAN).	Scopolamine	137-148	histone deacetylase 2	Mus musculus	113-118
31960226-2	2020	The focus of the work was to elucidate the modulation of the chromatin modifying enzymes: DNMT1, DNMT3a, DNMT3b, HDAC2, HDAC5 and CPB in scopolamine induced amnesic mice after treatment with bacoside rich extract of Bacopa monniera (BA) and BA encapsulated in lactoferrin conjugated PEG-PLA-PCL-OH based polymersomes (BAN).	Scopolamine	137-148	histone deacetylase 5	Mus musculus	120-125
31960226-5	2020	Scopolamine treatment showed up-regulation of DNMT1 expression in qRT-PCR by 3.14-fold as compared to the control, which was considerably decreased by 1.5-fold after treatment with BA and remarkably decreased 0.11-fold by BAN treatment.	Scopolamine	0-11	DNA methyltransferase (cytosine-5) 1	Mus musculus	46-51
31960226-6	2020	Scopolamine treatment up-regulated the expression of DNMT3a by 1.6-fold while for DNMT3b by 3.13-fold.	Scopolamine	0-11	DNA methyltransferase 3A	Mus musculus	53-59
31960226-6	2020	Scopolamine treatment up-regulated the expression of DNMT3a by 1.6-fold while for DNMT3b by 3.13-fold.	Scopolamine	0-11	DNA methyltransferase 3B	Mus musculus	82-88
31960226-8	2020	Similarly scopolamine up-regulated HDAC2 and HDAC5 by 3.12 fold and 3.64-fold, respectively.	Scopolamine	10-21	histone deacetylase 2	Mus musculus	35-40
32183056-4	2020	Further in vivo experiments showed that scopolamine induced neuronal injury, characterized by downregulated glutathione (GSH), glutathione S-transferase (GST), catalase, and upregulated lipid peroxidation (LPO).	Scopolamine	40-51	glutathione S-transferase kappa 1	Homo sapiens	127-152
32183056-4	2020	Further in vivo experiments showed that scopolamine induced neuronal injury, characterized by downregulated glutathione (GSH), glutathione S-transferase (GST), catalase, and upregulated lipid peroxidation (LPO).	Scopolamine	40-51	glutathione S-transferase kappa 1	Homo sapiens	154-157
32183056-5	2020	Moreover, scopolamine increased the expression of inflammatory mediators such as cyclooxygenase2 (COX2), nuclear factor kappa B (NF-kB), tumor necrosis factor (TNF-alpha), further associated with cognitive impairment.	Scopolamine	10-21	prostaglandin-endoperoxide synthase 2	Homo sapiens	81-96
32183056-5	2020	Moreover, scopolamine increased the expression of inflammatory mediators such as cyclooxygenase2 (COX2), nuclear factor kappa B (NF-kB), tumor necrosis factor (TNF-alpha), further associated with cognitive impairment.	Scopolamine	10-21	prostaglandin-endoperoxide synthase 2	Homo sapiens	98-102
32183056-5	2020	Moreover, scopolamine increased the expression of inflammatory mediators such as cyclooxygenase2 (COX2), nuclear factor kappa B (NF-kB), tumor necrosis factor (TNF-alpha), further associated with cognitive impairment.	Scopolamine	10-21	tumor necrosis factor	Homo sapiens	137-158
32183056-5	2020	Moreover, scopolamine increased the expression of inflammatory mediators such as cyclooxygenase2 (COX2), nuclear factor kappa B (NF-kB), tumor necrosis factor (TNF-alpha), further associated with cognitive impairment.	Scopolamine	10-21	tumor necrosis factor	Homo sapiens	160-169
31933104-6	2020	SAK3 inhibited scopolamine-induced cellular apoptosis (morphologically and by determination of pro- and anti-apoptotic factor levels), increase in ROS levels, decrease in choline acetyltransferase level, phosphorylation of NF-kappaB, activation of Akt, JNK and p38 intracellular signaling pathways, and elevation of proinflammatory cytokines IL-1beta and IL-6, but not enhanced level of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1).	Scopolamine	15-26	mitogen-activated protein kinase 14	Homo sapiens	261-264
31933104-6	2020	SAK3 inhibited scopolamine-induced cellular apoptosis (morphologically and by determination of pro- and anti-apoptotic factor levels), increase in ROS levels, decrease in choline acetyltransferase level, phosphorylation of NF-kappaB, activation of Akt, JNK and p38 intracellular signaling pathways, and elevation of proinflammatory cytokines IL-1beta and IL-6, but not enhanced level of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1).	Scopolamine	15-26	interleukin 1 beta	Homo sapiens	342-350
31933104-6	2020	SAK3 inhibited scopolamine-induced cellular apoptosis (morphologically and by determination of pro- and anti-apoptotic factor levels), increase in ROS levels, decrease in choline acetyltransferase level, phosphorylation of NF-kappaB, activation of Akt, JNK and p38 intracellular signaling pathways, and elevation of proinflammatory cytokines IL-1beta and IL-6, but not enhanced level of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1).	Scopolamine	15-26	interleukin 6	Homo sapiens	355-359
31933104-6	2020	SAK3 inhibited scopolamine-induced cellular apoptosis (morphologically and by determination of pro- and anti-apoptotic factor levels), increase in ROS levels, decrease in choline acetyltransferase level, phosphorylation of NF-kappaB, activation of Akt, JNK and p38 intracellular signaling pathways, and elevation of proinflammatory cytokines IL-1beta and IL-6, but not enhanced level of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1).	Scopolamine	15-26	beta-secretase 1	Homo sapiens	387-440
31933104-6	2020	SAK3 inhibited scopolamine-induced cellular apoptosis (morphologically and by determination of pro- and anti-apoptotic factor levels), increase in ROS levels, decrease in choline acetyltransferase level, phosphorylation of NF-kappaB, activation of Akt, JNK and p38 intracellular signaling pathways, and elevation of proinflammatory cytokines IL-1beta and IL-6, but not enhanced level of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1).	Scopolamine	15-26	beta-secretase 1	Homo sapiens	442-447
31644927-6	2020	Systemic administration of SCOP for seven days caused memory impairment which manifested as decreased time spent in platform quadrant in Morris water maze test, decreased retention latencies in passive avoidance test, and increased acetylcholinesterase (AChE) activity, Abeta, and free iron deposition.	Scopolamine	27-31	acetylcholinesterase	Rattus norvegicus	232-252
32001261-7	2020	Scopolamine induced amnesia and cholinergic dysfunction by increasing the acetylcholinesterase (AChE) activity and content, decreasing the muscarinic M1 receptor levels in the prefrontal cortex and hippocampus of mice.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	74-94
32001261-7	2020	Scopolamine induced amnesia and cholinergic dysfunction by increasing the acetylcholinesterase (AChE) activity and content, decreasing the muscarinic M1 receptor levels in the prefrontal cortex and hippocampus of mice.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	96-100
32001261-11	2020	FDPI 10 mg/kg reversed the increase in the AChE activity and content, oxidative stress parameters, and modulated Nrf2/HO-1 signaling in the prefrontal cortex of scopolamine-exposed mice.	Scopolamine	161-172	nuclear factor, erythroid derived 2, like 2	Mus musculus	113-117
32001261-11	2020	FDPI 10 mg/kg reversed the increase in the AChE activity and content, oxidative stress parameters, and modulated Nrf2/HO-1 signaling in the prefrontal cortex of scopolamine-exposed mice.	Scopolamine	161-172	heme oxygenase 1	Mus musculus	118-122
31768942-6	2020	In addition, after scopolamine administration, the Abeta and superoxide anion levels were increased, and NADPH oxidase 2 (NOX2), nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor kappa B (NFkB) genes were overexpressed.	Scopolamine	19-30	cytochrome b-245 beta chain	Homo sapiens	105-120
31768942-6	2020	In addition, after scopolamine administration, the Abeta and superoxide anion levels were increased, and NADPH oxidase 2 (NOX2), nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor kappa B (NFkB) genes were overexpressed.	Scopolamine	19-30	cytochrome b-245 beta chain	Homo sapiens	122-126
31876680-4	2020	The results indicated impairment of memory consolidation by posttraining intra-CA3 microinjection of scopolamine (1 and 2 microg/mouse).	Scopolamine	101-112	carbonic anhydrase 3	Mus musculus	79-82
31644927-6	2020	Systemic administration of SCOP for seven days caused memory impairment which manifested as decreased time spent in platform quadrant in Morris water maze test, decreased retention latencies in passive avoidance test, and increased acetylcholinesterase (AChE) activity, Abeta, and free iron deposition.	Scopolamine	27-31	acetylcholinesterase	Rattus norvegicus	254-258
31885818-9	2019	Moreover, the increased MDA level and low total antioxidant capacity in SCOP-treated mouse brains are reversed by FA-97, with the increased expression of HO-1, NQO-1, and nuclear Nrf2.	Scopolamine	72-76	heme oxygenase 1	Mus musculus	154-158
31876680-6	2020	Posttraining application of cannabinoid CB2 receptor antagonist, AM630 (1, 10 and 100 microg/mouse; intra-CA3) alone had no significant influence on memory performance, but its coinjection with significant dose of scopolamine (1 microg/mouse) decreased memory consolidation.	Scopolamine	214-225	cannabinoid receptor 2 (macrophage)	Mus musculus	40-43
31876680-8	2020	Posttraining coadministration of diverse doses of GP1a (1, 10 and 100 microg/mouse; intra-CA3) with an effective dose of scopolamine (1 microg/mouse) meaningfully increased deficiency of memory consolidation produced by GP1a (100 microg/mouse).	Scopolamine	121-132	carbonic anhydrase 3	Mus musculus	90-93
31936010-1	2020	Background: We performed this prospective double-blind randomized controlled trial to identify the effect of a preoperative prophylactic transdermal scopolamine (TDS) patch on postoperative nausea and vomiting (PONV) after retromastoid craniectomy with microvascular decompression (RMC-MVD).	Scopolamine	149-160	mevalonate diphosphate decarboxylase	Homo sapiens	286-289
31670201-0	2020	A novel chalcone derivative as Nrf2 activator attenuates learning and memory impairment in a scopolamine-induced mouse model.	Scopolamine	93-104	nuclear factor, erythroid derived 2, like 2	Mus musculus	31-35
31936730-8	2020	In addition, a reduced brain AChE activity following the administration of REO in scopolamine-treated fish was observed.	Scopolamine	82-93	acetylcholinesterase	Danio rerio	29-33
31918396-7	2020	Finally, MT-6 was evaluated against scopolamine induced dementia model of mice and this compound actively improved memory deficit and cognition impairment in scopolamine treated mice.	Scopolamine	36-47	protease, serine 33	Mus musculus	9-13
31918396-7	2020	Finally, MT-6 was evaluated against scopolamine induced dementia model of mice and this compound actively improved memory deficit and cognition impairment in scopolamine treated mice.	Scopolamine	158-169	protease, serine 33	Mus musculus	9-13
31885818-9	2019	Moreover, the increased MDA level and low total antioxidant capacity in SCOP-treated mouse brains are reversed by FA-97, with the increased expression of HO-1, NQO-1, and nuclear Nrf2.	Scopolamine	72-76	NAD(P)H dehydrogenase, quinone 1	Mus musculus	160-165
31885818-9	2019	Moreover, the increased MDA level and low total antioxidant capacity in SCOP-treated mouse brains are reversed by FA-97, with the increased expression of HO-1, NQO-1, and nuclear Nrf2.	Scopolamine	72-76	nuclear factor, erythroid derived 2, like 2	Mus musculus	179-183
31278934-3	2019	FRP pretreatment suppressed scopolamine-induced cognitive impairment in passive-avoidance test and significantly upregulated levels of brain-derived neurotrophic factor (BDNF) and induced the phosphorylation of cAMP response element binding (CREB) protein and extracellular signal-regulated kinase (ERK) in the hippocampus of scopolamine-treated mice.	Scopolamine	326-337	cAMP responsive element binding protein 1	Mus musculus	211-240
31623364-5	2019	Moreover, similar protective effects were observed on the secretion of BDNF in SP+GEGR treated mice.	Scopolamine	79-81	brain derived neurotrophic factor	Mus musculus	71-75
31623364-6	2019	The expression of TrkB receptor, and phosphorylation of PI3K on the TrkB receptor signaling pathway were dramatically protected in the SP-induced model after GEGR treatment, whereas the expression of p75NTR receptor, the phosphorylation of JNK, and expression of Bax/Bcl-2 on the p75NTR receptor signaling pathway was significantly protected in the same group.	Scopolamine	135-137	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	18-22
31623364-6	2019	The expression of TrkB receptor, and phosphorylation of PI3K on the TrkB receptor signaling pathway were dramatically protected in the SP-induced model after GEGR treatment, whereas the expression of p75NTR receptor, the phosphorylation of JNK, and expression of Bax/Bcl-2 on the p75NTR receptor signaling pathway was significantly protected in the same group.	Scopolamine	135-137	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	68-72
31623364-6	2019	The expression of TrkB receptor, and phosphorylation of PI3K on the TrkB receptor signaling pathway were dramatically protected in the SP-induced model after GEGR treatment, whereas the expression of p75NTR receptor, the phosphorylation of JNK, and expression of Bax/Bcl-2 on the p75NTR receptor signaling pathway was significantly protected in the same group.	Scopolamine	135-137	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	200-206
31623364-6	2019	The expression of TrkB receptor, and phosphorylation of PI3K on the TrkB receptor signaling pathway were dramatically protected in the SP-induced model after GEGR treatment, whereas the expression of p75NTR receptor, the phosphorylation of JNK, and expression of Bax/Bcl-2 on the p75NTR receptor signaling pathway was significantly protected in the same group.	Scopolamine	135-137	BCL2-associated X protein	Mus musculus	263-266
31623364-6	2019	The expression of TrkB receptor, and phosphorylation of PI3K on the TrkB receptor signaling pathway were dramatically protected in the SP-induced model after GEGR treatment, whereas the expression of p75NTR receptor, the phosphorylation of JNK, and expression of Bax/Bcl-2 on the p75NTR receptor signaling pathway was significantly protected in the same group.	Scopolamine	135-137	B cell leukemia/lymphoma 2	Mus musculus	267-272
31623364-6	2019	The expression of TrkB receptor, and phosphorylation of PI3K on the TrkB receptor signaling pathway were dramatically protected in the SP-induced model after GEGR treatment, whereas the expression of p75NTR receptor, the phosphorylation of JNK, and expression of Bax/Bcl-2 on the p75NTR receptor signaling pathway was significantly protected in the same group.	Scopolamine	135-137	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	280-286
31623364-8	2019	Taken together, these results indicate that the anti-oxidant activity of GEGR contributes to improving the neuronal cell function and survival during cognitive impairment in the SP-induced model through regulation of BDNF secretion and their receptor signaling pathway.	Scopolamine	178-180	brain derived neurotrophic factor	Mus musculus	217-221
31772634-5	2019	Additionally, GBE prevented SCP-induced reductions in acetylcholine by decreasing acetylcholinesterase activity and upregulating choline acetyltransferase mRNA levels in the hippocampus.	Scopolamine	28-31	choline acetyltransferase	Mus musculus	129-154
31772634-6	2019	GBE mitigated SCP-mediated mRNA decreases in brain-derived neurotrophic factor levels and its associated signaling molecules.	Scopolamine	14-17	brain derived neurotrophic factor	Mus musculus	45-78
31278934-3	2019	FRP pretreatment suppressed scopolamine-induced cognitive impairment in passive-avoidance test and significantly upregulated levels of brain-derived neurotrophic factor (BDNF) and induced the phosphorylation of cAMP response element binding (CREB) protein and extracellular signal-regulated kinase (ERK) in the hippocampus of scopolamine-treated mice.	Scopolamine	28-39	frizzled-related protein	Mus musculus	0-3
31278934-3	2019	FRP pretreatment suppressed scopolamine-induced cognitive impairment in passive-avoidance test and significantly upregulated levels of brain-derived neurotrophic factor (BDNF) and induced the phosphorylation of cAMP response element binding (CREB) protein and extracellular signal-regulated kinase (ERK) in the hippocampus of scopolamine-treated mice.	Scopolamine	28-39	cAMP responsive element binding protein 1	Mus musculus	211-240
31278934-3	2019	FRP pretreatment suppressed scopolamine-induced cognitive impairment in passive-avoidance test and significantly upregulated levels of brain-derived neurotrophic factor (BDNF) and induced the phosphorylation of cAMP response element binding (CREB) protein and extracellular signal-regulated kinase (ERK) in the hippocampus of scopolamine-treated mice.	Scopolamine	326-337	frizzled-related protein	Mus musculus	0-3
31278934-4	2019	Additionally, scopolamine-treated mice showed significantly decreased acetylcholine levels and increased acetylcholine-esterase activity in the hippocampus as compared with controls; however, these changes were suppressed by FRP pretreatment.	Scopolamine	14-25	frizzled-related protein	Mus musculus	225-228
31894062-0	2019	Nootropic effects of synthetic flavonoid derivatives on scopolamine induced memory impairment in mice via cholinesterase inhibition and antioxidant system.	Scopolamine	56-67	butyrylcholinesterase	Mus musculus	106-120
31400468-6	2019	The relative expression increase of miR-1 and miR-10 in the PFC and the hippocampus was shown in memory loss induced by scopolamine administration or 30-min stress.	Scopolamine	120-131	microRNA 1	Rattus norvegicus	36-41
31400468-7	2019	The PFC level of miR-10 and also hippocampal level of miR-1 and miR-10 were significantly up-regulated, while amygdala miR-1 and miR-26 were down-regulated in scopolamine-induced memory loss under stress.	Scopolamine	159-170	microRNA 1	Rattus norvegicus	17-22
31894062-5	2019	Scopolamine elevated significantly the AChE level, decreased the contents of ACh, SOD and CAT in the brain in amnesic model.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	39-43
31894062-5	2019	Scopolamine elevated significantly the AChE level, decreased the contents of ACh, SOD and CAT in the brain in amnesic model.	Scopolamine	0-11	catalase	Mus musculus	90-93
30949953-10	2019	Scopolamine-induced alteration of oxidant-antioxidant balance, acetylcholinesterase activity and neurogenesis in the hippocampus and prefrontal cortex were attenuated by HPT treatment.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	63-83
31176239-0	2019	Design and development of 1,3,4-oxadiazole derivatives as potential inhibitors of acetylcholinesterase to ameliorate scopolamine-induced cognitive dysfunctions.	Scopolamine	117-128	acetylcholinesterase (Cartwright blood group)	Homo sapiens	82-102
31754658-0	2019	Curcumin Downregulates GSK3 and Cdk5 in Scopolamine-Induced Alzheimer"s Disease Rats Abrogating Abeta40/42 and Tau Hyperphosphorylation.	Scopolamine	40-51	cyclin-dependent kinase 5	Rattus norvegicus	32-36
31350730-0	2019	Isoorientin improves scopolamine-induced cognitive impairments by restoring the cholinergic system, antioxidant defense, and p-CREB/BDNF signaling in the hippocampus and frontal cortex.	Scopolamine	21-32	cAMP responsive element binding protein 1	Mus musculus	127-131
31350730-0	2019	Isoorientin improves scopolamine-induced cognitive impairments by restoring the cholinergic system, antioxidant defense, and p-CREB/BDNF signaling in the hippocampus and frontal cortex.	Scopolamine	21-32	brain derived neurotrophic factor	Mus musculus	132-136
31350730-8	2019	Moreover, Western blot results indicated that ISO reversed the decreases in expression of phosphorylated cAMP response element binding (CREB) and brain-derived neurotrophic factor (BDNF) in the hippocampus and frontal cortex of scopolamine-treated mice.	Scopolamine	228-239	cAMP responsive element binding protein 1	Mus musculus	105-134
31350730-8	2019	Moreover, Western blot results indicated that ISO reversed the decreases in expression of phosphorylated cAMP response element binding (CREB) and brain-derived neurotrophic factor (BDNF) in the hippocampus and frontal cortex of scopolamine-treated mice.	Scopolamine	228-239	cAMP responsive element binding protein 1	Mus musculus	136-140
31350730-8	2019	Moreover, Western blot results indicated that ISO reversed the decreases in expression of phosphorylated cAMP response element binding (CREB) and brain-derived neurotrophic factor (BDNF) in the hippocampus and frontal cortex of scopolamine-treated mice.	Scopolamine	228-239	brain derived neurotrophic factor	Mus musculus	146-179
31350730-8	2019	Moreover, Western blot results indicated that ISO reversed the decreases in expression of phosphorylated cAMP response element binding (CREB) and brain-derived neurotrophic factor (BDNF) in the hippocampus and frontal cortex of scopolamine-treated mice.	Scopolamine	228-239	brain derived neurotrophic factor	Mus musculus	181-185
31350730-9	2019	Thus, our results provide initial evidence that ISO ameliorates scopolamine-induced memory and cognitive impairments partly by restoring the cholinergic system, antioxidant defense, and p-CREB/BDNF signaling pathway, thereby exhibiting memory-enhancing activities.	Scopolamine	64-75	cAMP responsive element binding protein 1	Mus musculus	188-192
31350730-9	2019	Thus, our results provide initial evidence that ISO ameliorates scopolamine-induced memory and cognitive impairments partly by restoring the cholinergic system, antioxidant defense, and p-CREB/BDNF signaling pathway, thereby exhibiting memory-enhancing activities.	Scopolamine	64-75	brain derived neurotrophic factor	Mus musculus	193-197
30992239-9	2019	Patients who were given scopolamine had lower Visual Analog Scale pain scores on postoperative days (POD) 0 through 2 (P &lt; .01), were able to walk further distances on POD 0 through 3 (P &lt; .001), and received fewer morphine equivalents on POD 1 and 2 (P &lt; .001).	Scopolamine	24-35	coronin 7	Homo sapiens	245-256
29916145-0	2019	Vdac1 Downregulation Causes Mitochondrial Disintegration Leading to Hippocampal Neurodegeneration in Scopolamine-Induced Amnesic Mice.	Scopolamine	101-112	voltage-dependent anion channel 1	Mus musculus	0-5
30919246-0	2019	Soursop fruit extract mitigates scopolamine-induced amnesia and oxidative stress via activating cholinergic and Nrf2/HO-1 pathways.	Scopolamine	32-43	NFE2 like bZIP transcription factor 2	Rattus norvegicus	112-116
30919246-0	2019	Soursop fruit extract mitigates scopolamine-induced amnesia and oxidative stress via activating cholinergic and Nrf2/HO-1 pathways.	Scopolamine	32-43	heme oxygenase 1	Rattus norvegicus	117-121
30737653-10	2019	Additionally, eugenol attenuated scopolamine-induced hippocampal cholinergic dysfunction (decrease in acetylcholine level, increase in acetylcholinesterase activity, and decrease in density and affinity of M1 and total muscarinic receptor), glutamate neurotoxicity (increase in levels of glutamate, calcium, calcium-dependent calpain-2, and brain-derived neurotropic factor), and mitochondrial dysfunction (decrease in formazan produced, membrane potential, and oxidative stress) in rats.	Scopolamine	33-44	acetylcholinesterase	Rattus norvegicus	135-155
30772273-8	2019	IRN reduced malondialdehyde and nitrite generation induced by scopolamine through increase in glutathione (GSH) level, superoxide dismutase (SOD) and catalase (CAT) activities in the prefrontal cortex and hippocampus.	Scopolamine	62-73	catalase	Mus musculus	150-158
30772273-8	2019	IRN reduced malondialdehyde and nitrite generation induced by scopolamine through increase in glutathione (GSH) level, superoxide dismutase (SOD) and catalase (CAT) activities in the prefrontal cortex and hippocampus.	Scopolamine	62-73	catalase	Mus musculus	160-163
30478761-2	2019	Based on the potential neuroprotective effects of melatonin, we here explored the possible underlying mechanisms of the protective effect of melatonin against scopolamine-induced oxidative stress-mediated c-Jun N-terminal kinase (JNK) activation, which ultimately results in synaptic dysfunction, neuroinflammation, and neurodegeneration.	Scopolamine	159-170	mitogen-activated protein kinase 8	Mus musculus	205-228
30478761-2	2019	Based on the potential neuroprotective effects of melatonin, we here explored the possible underlying mechanisms of the protective effect of melatonin against scopolamine-induced oxidative stress-mediated c-Jun N-terminal kinase (JNK) activation, which ultimately results in synaptic dysfunction, neuroinflammation, and neurodegeneration.	Scopolamine	159-170	mitogen-activated protein kinase 8	Mus musculus	230-233
30478761-3	2019	According to our findings, scopolamine administration resulted in LPO and ROS generation and decreased the protein levels of antioxidant proteins such as Nrf2 and HO-1; however, melatonin co-treatment mitigated the generation of oxidant factors while improving antioxidant protein levels.	Scopolamine	27-38	lactoperoxidase	Mus musculus	66-69
30478761-3	2019	According to our findings, scopolamine administration resulted in LPO and ROS generation and decreased the protein levels of antioxidant proteins such as Nrf2 and HO-1; however, melatonin co-treatment mitigated the generation of oxidant factors while improving antioxidant protein levels.	Scopolamine	27-38	nuclear factor, erythroid derived 2, like 2	Mus musculus	154-158
30478761-3	2019	According to our findings, scopolamine administration resulted in LPO and ROS generation and decreased the protein levels of antioxidant proteins such as Nrf2 and HO-1; however, melatonin co-treatment mitigated the generation of oxidant factors while improving antioxidant protein levels.	Scopolamine	27-38	heme oxygenase 1	Mus musculus	163-167
30478761-6	2019	We also found that scopolamine promoted neuronal loss by inducing Bax, Pro-Caspase-3, and Caspase-3 and reducing the levels of the antiapoptotic protein Bcl-2.	Scopolamine	19-30	BCL2-associated X protein	Mus musculus	66-69
30478761-6	2019	We also found that scopolamine promoted neuronal loss by inducing Bax, Pro-Caspase-3, and Caspase-3 and reducing the levels of the antiapoptotic protein Bcl-2.	Scopolamine	19-30	caspase 3	Mus musculus	75-84
30478761-6	2019	We also found that scopolamine promoted neuronal loss by inducing Bax, Pro-Caspase-3, and Caspase-3 and reducing the levels of the antiapoptotic protein Bcl-2.	Scopolamine	19-30	B cell leukemia/lymphoma 2	Mus musculus	153-158
31003156-7	2019	RESULTS: Pre-test scopolamine infusion in hippocampal CA1 and medial entorhinal cortex significantly reduced overall exploration of objects (p<0.001).	Scopolamine	18-29	carbonic anhydrase 1	Mus musculus	54-57
30763608-7	2019	The parasympatholytic compound scopolamine had the strongest relaxing effect (EC50 = 0.05 muM) followed by atropine (EC50 = 0.07 muM).	Scopolamine	31-42	latexin	Homo sapiens	90-93
30763608-7	2019	The parasympatholytic compound scopolamine had the strongest relaxing effect (EC50 = 0.05 muM) followed by atropine (EC50 = 0.07 muM).	Scopolamine	31-42	latexin	Homo sapiens	129-132
31141948-0	2019	Elaeagnus glabra f. oxyphylla Attenuates Scopolamine-Induced Learning and Memory Impairments in Mice by Improving Cholinergic Transmission via Activation of CREB/NGF Signaling.	Scopolamine	41-52	cAMP responsive element binding protein 1	Mus musculus	157-161
31141948-0	2019	Elaeagnus glabra f. oxyphylla Attenuates Scopolamine-Induced Learning and Memory Impairments in Mice by Improving Cholinergic Transmission via Activation of CREB/NGF Signaling.	Scopolamine	41-52	nerve growth factor	Mus musculus	162-165
31141948-9	2019	EGFO treatment also attenuated neural apoptosis in scopolamine-treated mice by decreasing the expression of apoptosis-related proteins such as Bax, Bcl2, cleaved caspase-3, and TUNEL staining.	Scopolamine	51-62	BCL2-associated X protein	Mus musculus	143-146
31141948-9	2019	EGFO treatment also attenuated neural apoptosis in scopolamine-treated mice by decreasing the expression of apoptosis-related proteins such as Bax, Bcl2, cleaved caspase-3, and TUNEL staining.	Scopolamine	51-62	B cell leukemia/lymphoma 2	Mus musculus	148-152
31141948-9	2019	EGFO treatment also attenuated neural apoptosis in scopolamine-treated mice by decreasing the expression of apoptosis-related proteins such as Bax, Bcl2, cleaved caspase-3, and TUNEL staining.	Scopolamine	51-62	caspase 3	Mus musculus	162-171
31001094-2	2019	We previously demonstrated that single or short-term administration of iso-alpha-acids, hop-derived bitter acids in beer, improves the spatial memory of scopolamine-induced amnesia model mice in the Y-maze and enhances novel object recognition in normal mice via activation of the vagus nerve and hippocampal dopaminergic system.	Scopolamine	153-164	HOP homeobox	Mus musculus	88-91
31049133-11	2019	Interestingly, sulforaphane-enriched broccoli sprouts improved the scopolamine-induced memory impairment in mice through Nrf2 activation, inhibiting neuronal apoptosis particularly through inhibition of caspase-3 activation which could lead to the neuroprotection against neurodegenerative disorders.	Scopolamine	67-78	nuclear factor, erythroid derived 2, like 2	Mus musculus	121-125
29916145-1	2019	Our previous report on hippocampal proteome analysis suggested the involvement of voltage-dependent anion channel (Vdac) 1 in scopolamine-induced amnesia.	Scopolamine	126-137	voltage-dependent anion channel 1	Mus musculus	82-122
29916145-6	2019	The expression of Vdac1 and total ATP level was decreased in the hippocampus of scopolamine-induced amnesic mice.	Scopolamine	80-91	voltage-dependent anion channel 1	Mus musculus	18-23
29916145-11	2019	Taken together, our study shows that downregulation of Vdac1 causes neurodegeneration through mitochondrial disintegration in the hippocampus of scopolamine-induced amnesic mice.	Scopolamine	145-156	voltage-dependent anion channel 1	Mus musculus	55-60
30598686-7	2018	Therefore, it can be concluded that the fermented extract exerts memory-improving effects in the hippocampus of scopolamine-treated mice through an initial increase in ERK signaling and a sequential induction of the expression of p-CREB and BDNF, and these effects are related to the antioxidant activities of beta-carotene and other components.	Scopolamine	112-123	mitogen-activated protein kinase 1	Mus musculus	168-171
30033800-0	2019	Schisanhenol improves learning and memory in scopolamine-treated mice by reducing acetylcholinesterase activity and attenuating oxidative damage through SIRT1-PGC-1alpha-Tau signaling pathway.	Scopolamine	45-56	acetylcholinesterase	Mus musculus	82-102
30033800-0	2019	Schisanhenol improves learning and memory in scopolamine-treated mice by reducing acetylcholinesterase activity and attenuating oxidative damage through SIRT1-PGC-1alpha-Tau signaling pathway.	Scopolamine	45-56	sirtuin 1	Mus musculus	153-158
30033800-0	2019	Schisanhenol improves learning and memory in scopolamine-treated mice by reducing acetylcholinesterase activity and attenuating oxidative damage through SIRT1-PGC-1alpha-Tau signaling pathway.	Scopolamine	45-56	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	159-169
30529315-0	2019	BDNF mediates the protective effects of scopolamine in reserpine-induced depression-like behaviors via up-regulation of 5-HTT and TPH1.	Scopolamine	40-51	brain derived neurotrophic factor	Mus musculus	0-4
30529315-0	2019	BDNF mediates the protective effects of scopolamine in reserpine-induced depression-like behaviors via up-regulation of 5-HTT and TPH1.	Scopolamine	40-51	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	120-125
30529315-0	2019	BDNF mediates the protective effects of scopolamine in reserpine-induced depression-like behaviors via up-regulation of 5-HTT and TPH1.	Scopolamine	40-51	tryptophan hydroxylase 1	Mus musculus	130-134
30529315-9	2019	In addition, the reserpine-induced decreases in serotonin transporter (5-HTT), brain-derived neurotrophic factor (BDNF) and tryptophan hydroxylase 1 (TPH1) in mouse hippocampus and prefrontal cortex (PFC) were significantly reversed by scopolamine.	Scopolamine	236-247	tryptophan hydroxylase 1	Mus musculus	150-154
30529315-10	2019	Our study provides evidence that scopolamine rapidly attenuates reserpine-induced depression in mice partially by regulating 5-HTT, BDNF and TPH1 in the hippocampus and PFC of mice.	Scopolamine	33-44	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	125-130
30529315-10	2019	Our study provides evidence that scopolamine rapidly attenuates reserpine-induced depression in mice partially by regulating 5-HTT, BDNF and TPH1 in the hippocampus and PFC of mice.	Scopolamine	33-44	brain derived neurotrophic factor	Mus musculus	132-136
30529315-10	2019	Our study provides evidence that scopolamine rapidly attenuates reserpine-induced depression in mice partially by regulating 5-HTT, BDNF and TPH1 in the hippocampus and PFC of mice.	Scopolamine	33-44	tryptophan hydroxylase 1	Mus musculus	141-145
30321530-13	2018	The results showed that curcumin treatment at 50 and 100 mg/kg doses prevented scopolamine-induced memory retrieval deficit and restored Akt and GSK dephosphorylation caused by scopolamine.	Scopolamine	177-188	thymoma viral proto-oncogene 1	Mus musculus	137-140
30321530-14	2018	Overall, these findings showed that pre-test scopolamine administration disrupts memory retrieval along with the diminished Akt and GSK-3beta phosphorylation in hippocampus while curcumin administration prevented those changes.	Scopolamine	45-56	thymoma viral proto-oncogene 1	Mus musculus	124-127
30321530-14	2018	Overall, these findings showed that pre-test scopolamine administration disrupts memory retrieval along with the diminished Akt and GSK-3beta phosphorylation in hippocampus while curcumin administration prevented those changes.	Scopolamine	45-56	glycogen synthase kinase 3 beta	Mus musculus	132-141
30372840-12	2018	The concentrations of TNF-alpha in hippocampus of the DM and donepezil groups was significantly lower than the Veh + scopolamine group (p &lt; 0.01).	Scopolamine	117-128	tumor necrosis factor	Rattus norvegicus	22-31
30033800-10	2019	CONCLUSIONS: Our findings indicated that Schisanhenol can attenuate scopolamine-induced learning impairment and enhance cognitive function, the mechanism via improve the cholinergic system and antioxidant ability, activate SIRT1-PGC1alpha signaling, inhibit the phosphorylation of Tau, and would be an effective candidate against cognitive disorders, such as Alzheimer"s disease.	Scopolamine	68-79	sirtuin 1	Mus musculus	223-228
30406376-0	2019	Neuroprotective effects of matrine on scopolamine-induced amnesia via inhibition of AChE/BuChE and oxidative stress.	Scopolamine	38-49	acetylcholinesterase	Mus musculus	84-88
30406376-0	2019	Neuroprotective effects of matrine on scopolamine-induced amnesia via inhibition of AChE/BuChE and oxidative stress.	Scopolamine	38-49	butyrylcholinesterase	Mus musculus	89-94
30598686-7	2018	Therefore, it can be concluded that the fermented extract exerts memory-improving effects in the hippocampus of scopolamine-treated mice through an initial increase in ERK signaling and a sequential induction of the expression of p-CREB and BDNF, and these effects are related to the antioxidant activities of beta-carotene and other components.	Scopolamine	112-123	cAMP responsive element binding protein 1	Mus musculus	232-236
30598686-7	2018	Therefore, it can be concluded that the fermented extract exerts memory-improving effects in the hippocampus of scopolamine-treated mice through an initial increase in ERK signaling and a sequential induction of the expression of p-CREB and BDNF, and these effects are related to the antioxidant activities of beta-carotene and other components.	Scopolamine	112-123	brain derived neurotrophic factor	Mus musculus	241-245
30111074-0	2018	Lactobacillus johnsonii CJLJ103 Attenuates Scopolamine-Induced Memory Impairment in Mice by Increasing BDNF Expression and Inhibiting NF-kappaB Activation.	Scopolamine	43-54	brain derived neurotrophic factor	Mus musculus	103-107
30369882-0	2018	Genistein Ameliorates Scopolamine-Induced Amnesia in Mice Through the Regulation of the Cholinergic Neurotransmission, Antioxidant System and the ERK/CREB/BDNF Signaling.	Scopolamine	22-33	mitogen-activated protein kinase 1	Mus musculus	146-149
30369882-0	2018	Genistein Ameliorates Scopolamine-Induced Amnesia in Mice Through the Regulation of the Cholinergic Neurotransmission, Antioxidant System and the ERK/CREB/BDNF Signaling.	Scopolamine	22-33	cAMP responsive element binding protein 1	Mus musculus	150-154
30369882-0	2018	Genistein Ameliorates Scopolamine-Induced Amnesia in Mice Through the Regulation of the Cholinergic Neurotransmission, Antioxidant System and the ERK/CREB/BDNF Signaling.	Scopolamine	22-33	brain derived neurotrophic factor	Mus musculus	155-159
30111074-0	2018	Lactobacillus johnsonii CJLJ103 Attenuates Scopolamine-Induced Memory Impairment in Mice by Increasing BDNF Expression and Inhibiting NF-kappaB Activation.	Scopolamine	43-54	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	134-143
30111074-3	2018	Furthermore, LJ treatment increased scopolamine-suppressed BDNF expression and CREB phosphorylation in the hippocampi of the brain, as well as suppressed TNF-alpha expression and NF-kappaB activation.	Scopolamine	36-47	brain derived neurotrophic factor	Mus musculus	59-63
30111074-3	2018	Furthermore, LJ treatment increased scopolamine-suppressed BDNF expression and CREB phosphorylation in the hippocampi of the brain, as well as suppressed TNF-alpha expression and NF-kappaB activation.	Scopolamine	36-47	cAMP responsive element binding protein 1	Mus musculus	79-83
30224763-2	2018	The present study demonstrates enhanced scopolamine production from transgenic hairy root clones of Duboisia leichhardtii wherein the expression of quinolinate phosphoribosyl transferase (QPT) gene was silenced using the QPT-RNAi construct under the control of CaMV 35 S promoter.	Scopolamine	40-51	quinolinate phosphoribosyltransferase	Homo sapiens	148-186
30224763-8	2018	The transgenic hairy roots cultures established with RNAi mediated silencing of quinolinate phosphoribosyl transferase gene provides an alternative approach to increase the yield of scopolamine in fulfilling the demand of this secondary metabolite.	Scopolamine	182-193	quinolinate phosphoribosyltransferase	Homo sapiens	80-118
29669266-4	2018	When animals received scopolamine or MK-801 treatment prior to conditioning sessions we observed significantly fewer TH-labeled (i.e., DA) cells in the VTA that expressed c-fos and significantly less conditioned approach responding during the CS-only test.	Scopolamine	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
29847860-2	2018	This study investigated the effects of a PDE5 inhibitor on scopolamine-induced cognitive dysfunction, using memory-related behavioural tests and biochemical assays.	Scopolamine	59-70	phosphodiesterase 5A, cGMP-specific	Mus musculus	41-45
29847860-3	2018	EXPERIMENTAL APPROACH: In mice were pretreated with PDE5 inhibitor, amnesia was induced by scopolamine.	Scopolamine	91-102	phosphodiesterase 5A, cGMP-specific	Mus musculus	52-56
29847860-8	2018	Moreover, KJH-1002 increased cGMP levels in the cortex and the scopolamine-reduced expression of phosphorylated CREB, Levels of ERK 1/2, Akt and brain-derived neurotrophic factor in the cortex and hippocampus were restored by KJH-1002 treatment.	Scopolamine	63-74	cAMP responsive element binding protein 1	Mus musculus	112-116
29847860-8	2018	Moreover, KJH-1002 increased cGMP levels in the cortex and the scopolamine-reduced expression of phosphorylated CREB, Levels of ERK 1/2, Akt and brain-derived neurotrophic factor in the cortex and hippocampus were restored by KJH-1002 treatment.	Scopolamine	63-74	mitogen-activated protein kinase 3	Mus musculus	128-135
29847860-8	2018	Moreover, KJH-1002 increased cGMP levels in the cortex and the scopolamine-reduced expression of phosphorylated CREB, Levels of ERK 1/2, Akt and brain-derived neurotrophic factor in the cortex and hippocampus were restored by KJH-1002 treatment.	Scopolamine	63-74	thymoma viral proto-oncogene 1	Mus musculus	137-140
29847860-8	2018	Moreover, KJH-1002 increased cGMP levels in the cortex and the scopolamine-reduced expression of phosphorylated CREB, Levels of ERK 1/2, Akt and brain-derived neurotrophic factor in the cortex and hippocampus were restored by KJH-1002 treatment.	Scopolamine	63-74	brain derived neurotrophic factor	Mus musculus	145-178
29729289-5	2018	In the present study, the expression of fibrillary acidic protein (GFAP) was detected to evaluate the activation of astrocyte after single injection of ketamine and scopolamine in respective efficient doses.	Scopolamine	165-176	glial fibrillary acidic protein	Homo sapiens	67-71
29616790-0	2018	Novel Tadalafil Derivatives Ameliorates Scopolamine-Induced Cognitive Impairment in Mice via Inhibition of Acetylcholinesterase (AChE) and Phosphodiesterase 5 (PDE5).	Scopolamine	40-51	acetylcholinesterase	Mus musculus	107-127
29616790-0	2018	Novel Tadalafil Derivatives Ameliorates Scopolamine-Induced Cognitive Impairment in Mice via Inhibition of Acetylcholinesterase (AChE) and Phosphodiesterase 5 (PDE5).	Scopolamine	40-51	acetylcholinesterase	Mus musculus	129-133
29616790-0	2018	Novel Tadalafil Derivatives Ameliorates Scopolamine-Induced Cognitive Impairment in Mice via Inhibition of Acetylcholinesterase (AChE) and Phosphodiesterase 5 (PDE5).	Scopolamine	40-51	phosphodiesterase 5A, cGMP-specific	Mus musculus	139-158
29616790-0	2018	Novel Tadalafil Derivatives Ameliorates Scopolamine-Induced Cognitive Impairment in Mice via Inhibition of Acetylcholinesterase (AChE) and Phosphodiesterase 5 (PDE5).	Scopolamine	40-51	phosphodiesterase 5A, cGMP-specific	Mus musculus	160-164
30166095-12	2018	Also, the scopolamine-induced alteration of the acetylcholinesterase activity and the oxidant-antioxidant balance in the rat hippocampus was recovered by the treatment with the extract.	Scopolamine	10-21	acetylcholinesterase	Rattus norvegicus	48-68
30166095-13	2018	Finally, we demonstrated that the extract restored the scopolamine-decreased BDNF expression and increased IL1beta expression in the rat hippocampus.	Scopolamine	55-66	brain-derived neurotrophic factor	Rattus norvegicus	77-81
30166095-13	2018	Finally, we demonstrated that the extract restored the scopolamine-decreased BDNF expression and increased IL1beta expression in the rat hippocampus.	Scopolamine	55-66	interleukin 1 beta	Rattus norvegicus	107-114
29740317-6	2018	Additionally, the protein expressions of phosphorylated Akt, ERK1/2, and CREB in the hippocampus were significantly decreased by scopolamine, but these decreases were reversed by MSE treatment.	Scopolamine	129-140	thymoma viral proto-oncogene 1	Mus musculus	56-59
29378112-0	2018	Scopolamine-Induced Memory Impairment Is Alleviated by Xanthotoxin: Role of Acetylcholinesterase and Oxidative Stress Processes.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	76-96
29494759-0	2018	Transcriptional co-repressor SIN3A silencing rescues decline in memory consolidation during scopolamine-induced amnesia.	Scopolamine	92-103	transcriptional regulator, SIN3A (yeast)	Mus musculus	0-34
29494759-2	2018	Earlier we demonstrated that scopolamine-induced decrease in memory consolidation is correlated with enhanced expression of hippocampal DNA methyltransferase 1 (DNMT1) and histone deacetylase 2 (HDAC2) in mice.	Scopolamine	29-40	DNA methyltransferase (cytosine-5) 1	Mus musculus	136-159
29494759-2	2018	Earlier we demonstrated that scopolamine-induced decrease in memory consolidation is correlated with enhanced expression of hippocampal DNA methyltransferase 1 (DNMT1) and histone deacetylase 2 (HDAC2) in mice.	Scopolamine	29-40	DNA methyltransferase (cytosine-5) 1	Mus musculus	161-166
29494759-2	2018	Earlier we demonstrated that scopolamine-induced decrease in memory consolidation is correlated with enhanced expression of hippocampal DNA methyltransferase 1 (DNMT1) and histone deacetylase 2 (HDAC2) in mice.	Scopolamine	29-40	histone deacetylase 2	Mus musculus	172-193
29494759-2	2018	Earlier we demonstrated that scopolamine-induced decrease in memory consolidation is correlated with enhanced expression of hippocampal DNA methyltransferase 1 (DNMT1) and histone deacetylase 2 (HDAC2) in mice.	Scopolamine	29-40	histone deacetylase 2	Mus musculus	195-200
29494759-6	2018	This study examines the role of co-repressor SIN3A in scopolamine-induced amnesia through epigenetic changes in the hippocampus.	Scopolamine	54-65	transcriptional regulator, SIN3A (yeast)	Mus musculus	45-50
29494759-7	2018	Scopolamine treatment remarkably enhanced hippocampal SIN3A expression in mice.	Scopolamine	0-11	transcriptional regulator, SIN3A (yeast)	Mus musculus	54-59
29494759-10	2018	Furthermore, it increased acetylation of H3K9 and H3K14 at neuronal IEGs (Arc, Egr1, Homer1 and Narp) promoter, prevented scopolamine-induced down-regulation of IEGs and improved consolidation of memory during novel object recognition task.	Scopolamine	122-133	early growth response 1	Mus musculus	79-83
29494759-10	2018	Furthermore, it increased acetylation of H3K9 and H3K14 at neuronal IEGs (Arc, Egr1, Homer1 and Narp) promoter, prevented scopolamine-induced down-regulation of IEGs and improved consolidation of memory during novel object recognition task.	Scopolamine	122-133	homer scaffolding protein 1	Mus musculus	85-91
29494759-10	2018	Furthermore, it increased acetylation of H3K9 and H3K14 at neuronal IEGs (Arc, Egr1, Homer1 and Narp) promoter, prevented scopolamine-induced down-regulation of IEGs and improved consolidation of memory during novel object recognition task.	Scopolamine	122-133	neuronal pentraxin 2	Mus musculus	96-100
29740317-6	2018	Additionally, the protein expressions of phosphorylated Akt, ERK1/2, and CREB in the hippocampus were significantly decreased by scopolamine, but these decreases were reversed by MSE treatment.	Scopolamine	129-140	mitogen-activated protein kinase 3	Mus musculus	61-67
29740317-6	2018	Additionally, the protein expressions of phosphorylated Akt, ERK1/2, and CREB in the hippocampus were significantly decreased by scopolamine, but these decreases were reversed by MSE treatment.	Scopolamine	129-140	cAMP responsive element binding protein 1	Mus musculus	73-77
29476728-7	2018	Two and 4 weeks of scopolamine treatment, the density of MBP immunoreactive myelinated nerve fibers was significantly decreased in the dentate gyrus; however, scopolamine and melatonin cotreatment significantly increased the scopolamine-induced reduction of MBP expression in the dentate gyrus.	Scopolamine	19-30	myelin basic protein	Mus musculus	57-60
29755345-0	2018	Analogous beta-Carboline Alkaloids Harmaline and Harmine Ameliorate Scopolamine-Induced Cognition Dysfunction by Attenuating Acetylcholinesterase Activity, Oxidative Stress, and Inflammation in Mice.	Scopolamine	68-79	acetylcholinesterase	Mus musculus	125-145
29476728-7	2018	Two and 4 weeks of scopolamine treatment, the density of MBP immunoreactive myelinated nerve fibers was significantly decreased in the dentate gyrus; however, scopolamine and melatonin cotreatment significantly increased the scopolamine-induced reduction of MBP expression in the dentate gyrus.	Scopolamine	19-30	myelin basic protein	Mus musculus	258-261
29476728-0	2018	Melatonin attenuates scopolamine-induced cognitive impairment via protecting against demyelination through BDNF-TrkB signaling in the mouse dentate gyrus.	Scopolamine	21-32	brain derived neurotrophic factor	Mus musculus	107-111
29476728-7	2018	Two and 4 weeks of scopolamine treatment, the density of MBP immunoreactive myelinated nerve fibers was significantly decreased in the dentate gyrus; however, scopolamine and melatonin cotreatment significantly increased the scopolamine-induced reduction of MBP expression in the dentate gyrus.	Scopolamine	159-170	myelin basic protein	Mus musculus	258-261
29476728-0	2018	Melatonin attenuates scopolamine-induced cognitive impairment via protecting against demyelination through BDNF-TrkB signaling in the mouse dentate gyrus.	Scopolamine	21-32	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	112-116
29476728-7	2018	Two and 4 weeks of scopolamine treatment, the density of MBP immunoreactive myelinated nerve fibers was significantly decreased in the dentate gyrus; however, scopolamine and melatonin cotreatment significantly increased the scopolamine-induced reduction of MBP expression in the dentate gyrus.	Scopolamine	159-170	myelin basic protein	Mus musculus	258-261
29476728-3	2018	In this study, using a mouse model of scopolamine-induced amnesia, we assessed spatial and short-term memory functions for 4 weeks, investigated the expression of myelin-basic protein (MBP) in the dentate gyrus, and examined whether melatonin and scopolamine cotreatment could keep cognitive function and MBP expression.	Scopolamine	38-49	myelin basic protein	Mus musculus	163-183
29476728-8	2018	Furthermore, the cotreatment of scopolamine and melatonin significantly increased the scopolamine-induced decrease of BDNF and TrKB immunoreactivity in the dentate gyrus.	Scopolamine	32-43	brain derived neurotrophic factor	Mus musculus	118-122
29476728-8	2018	Furthermore, the cotreatment of scopolamine and melatonin significantly increased the scopolamine-induced decrease of BDNF and TrKB immunoreactivity in the dentate gyrus.	Scopolamine	32-43	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	127-131
29476728-8	2018	Furthermore, the cotreatment of scopolamine and melatonin significantly increased the scopolamine-induced decrease of BDNF and TrKB immunoreactivity in the dentate gyrus.	Scopolamine	86-97	brain derived neurotrophic factor	Mus musculus	118-122
29476728-8	2018	Furthermore, the cotreatment of scopolamine and melatonin significantly increased the scopolamine-induced decrease of BDNF and TrKB immunoreactivity in the dentate gyrus.	Scopolamine	86-97	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	127-131
29476728-9	2018	Taken together, our results indicate that melatonin treatment exerts anti-amnesic effect and restores the scopolamine-induced reduction of MBP expression through increasing BDNF and TrkB expressions in the mouse dentate gyrus.	Scopolamine	106-117	myelin basic protein	Mus musculus	139-142
29476728-9	2018	Taken together, our results indicate that melatonin treatment exerts anti-amnesic effect and restores the scopolamine-induced reduction of MBP expression through increasing BDNF and TrkB expressions in the mouse dentate gyrus.	Scopolamine	106-117	brain derived neurotrophic factor	Mus musculus	173-177
29476728-9	2018	Taken together, our results indicate that melatonin treatment exerts anti-amnesic effect and restores the scopolamine-induced reduction of MBP expression through increasing BDNF and TrkB expressions in the mouse dentate gyrus.	Scopolamine	106-117	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	182-186
29532369-6	2018	This scopolamine-induced increase in SFK phosphorylation occurred in the two subdivisions of the striatum (caudate putamen and nucleus accumbens) and was time-dependent and reversible.	Scopolamine	5-16	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	37-40
29532369-8	2018	Coadministration of subthreshold doses of scopolamine and a dopamine D1 receptor agonist SKF81297 enhanced striatal SFK phosphorylation.	Scopolamine	42-53	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	116-119
29532369-9	2018	Between Fyn and Src proteins immunoprecipitated from striatal tissue, scopolamine selectively increased phosphorylation of Fyn.	Scopolamine	70-81	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	8-11
29532369-9	2018	Between Fyn and Src proteins immunoprecipitated from striatal tissue, scopolamine selectively increased phosphorylation of Fyn.	Scopolamine	70-81	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	16-19
29532369-9	2018	Between Fyn and Src proteins immunoprecipitated from striatal tissue, scopolamine selectively increased phosphorylation of Fyn.	Scopolamine	70-81	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	123-126
29532369-10	2018	The increase in Fyn phosphorylation was accompanied by an increase in Fyn kinase activity in response to scopolamine.	Scopolamine	105-116	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	16-19
29532369-10	2018	The increase in Fyn phosphorylation was accompanied by an increase in Fyn kinase activity in response to scopolamine.	Scopolamine	105-116	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	70-73
29584649-2	2018	Ethanol Extract of Oldenlandia diffusa Herba Attenuates Scopolamine-Induced Cognitive Impairments in Mice via Activation of BDNF, P-CREB and Inhibition of Acetylcholinesterase.	Scopolamine	56-67	brain derived neurotrophic factor	Mus musculus	124-128
29584649-2	2018	Ethanol Extract of Oldenlandia diffusa Herba Attenuates Scopolamine-Induced Cognitive Impairments in Mice via Activation of BDNF, P-CREB and Inhibition of Acetylcholinesterase.	Scopolamine	56-67	acetylcholinesterase	Mus musculus	155-175
29983948-9	2018	Similarly, elevations in activities of AChE, BChE, and MAO induced by scopolamine were significantly reversed in rats pretreated with dietary inclusions of AE and BN.	Scopolamine	70-81	acetylcholinesterase	Rattus norvegicus	39-43
29334662-10	2018	RESULTS: Administration of 2 mg/kg of scopolamine brought about a decrease in spatial and non-spatial memory indeces, increase in acetylcholinesterase and butyrylcholinesterase activities, as well as increased MDA content compared to the control.	Scopolamine	38-49	acetylcholinesterase	Rattus norvegicus	130-150
29983948-9	2018	Similarly, elevations in activities of AChE, BChE, and MAO induced by scopolamine were significantly reversed in rats pretreated with dietary inclusions of AE and BN.	Scopolamine	70-81	monoamine oxidase A	Rattus norvegicus	55-58
29274366-0	2018	Vesicular glutamate transporter 1 (VGLUT1)-mediated glutamate release and membrane GluA1 activation is involved in the rapid antidepressant-like effects of scopolamine in mice.	Scopolamine	156-167	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 7	Mus musculus	0-33
29274366-0	2018	Vesicular glutamate transporter 1 (VGLUT1)-mediated glutamate release and membrane GluA1 activation is involved in the rapid antidepressant-like effects of scopolamine in mice.	Scopolamine	156-167	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 7	Mus musculus	35-41
29274366-0	2018	Vesicular glutamate transporter 1 (VGLUT1)-mediated glutamate release and membrane GluA1 activation is involved in the rapid antidepressant-like effects of scopolamine in mice.	Scopolamine	156-167	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	83-88
29274366-7	2018	Remarkably, VGLUT1 knockdown alleviated the rapid antidepressant-like actions of scopolamine and the effects of scopolamine on membrane GluA1-mediated BDNF, VGF and BICC1 changes.	Scopolamine	81-92	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 7	Mus musculus	12-18
29274366-7	2018	Remarkably, VGLUT1 knockdown alleviated the rapid antidepressant-like actions of scopolamine and the effects of scopolamine on membrane GluA1-mediated BDNF, VGF and BICC1 changes.	Scopolamine	112-123	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 7	Mus musculus	12-18
29274366-7	2018	Remarkably, VGLUT1 knockdown alleviated the rapid antidepressant-like actions of scopolamine and the effects of scopolamine on membrane GluA1-mediated BDNF, VGF and BICC1 changes.	Scopolamine	112-123	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	136-141
29274366-7	2018	Remarkably, VGLUT1 knockdown alleviated the rapid antidepressant-like actions of scopolamine and the effects of scopolamine on membrane GluA1-mediated BDNF, VGF and BICC1 changes.	Scopolamine	112-123	brain derived neurotrophic factor	Mus musculus	151-155
29274366-7	2018	Remarkably, VGLUT1 knockdown alleviated the rapid antidepressant-like actions of scopolamine and the effects of scopolamine on membrane GluA1-mediated BDNF, VGF and BICC1 changes.	Scopolamine	112-123	VGF nerve growth factor inducible	Mus musculus	157-160
29274366-7	2018	Remarkably, VGLUT1 knockdown alleviated the rapid antidepressant-like actions of scopolamine and the effects of scopolamine on membrane GluA1-mediated BDNF, VGF and BICC1 changes.	Scopolamine	112-123	BicC family RNA binding protein 1	Mus musculus	165-170
29274366-8	2018	Altogether, our findings suggest that VGLUT1-mediated glutamate release and membrane GluA1 activation may play a critical role in the rapid-acting antidepressant-like effects of scopolamine in mice.	Scopolamine	178-189	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 7	Mus musculus	38-44
29274366-8	2018	Altogether, our findings suggest that VGLUT1-mediated glutamate release and membrane GluA1 activation may play a critical role in the rapid-acting antidepressant-like effects of scopolamine in mice.	Scopolamine	178-189	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	85-90
28929917-1	2018	AIM: The present study was designed to investigate the effect of mercurius solubilis (merc sol) on scopolamine induced memory deficits and motor coordination in mice.	Scopolamine	99-110	hnRNP-associated with lethal yellow	Mus musculus	65-69
28929917-12	2018	Administration of merc sol 30 X to mice significantly reduced scopolamine induced memory deficits and motor incoordination in all the performance tasks.	Scopolamine	62-73	hnRNP-associated with lethal yellow	Mus musculus	18-22
28929917-15	2018	CONCLUSION: Merc sol has antiamnesic effect in scopolamine induced deficits and motor coordination in mice.	Scopolamine	47-58	hnRNP-associated with lethal yellow	Mus musculus	12-16
29328430-2	2018	In the present study, the impact of vanillin on scopolamine-induced alterations in cognition and the expression of DNA binding protein inhibitor ID-1 (ID1), one of the inhibitors of DNA binding/differentiation proteins that regulate gene transcription, in the mouse hippocampus.	Scopolamine	48-59	inhibitor of DNA binding 1, HLH protein	Mus musculus	115-149
29328430-2	2018	In the present study, the impact of vanillin on scopolamine-induced alterations in cognition and the expression of DNA binding protein inhibitor ID-1 (ID1), one of the inhibitors of DNA binding/differentiation proteins that regulate gene transcription, in the mouse hippocampus.	Scopolamine	48-59	inhibitor of DNA binding 1, HLH protein	Mus musculus	151-154
29328430-0	2018	Vanillin improves scopolamine-induced memory impairment through restoration of ID1 expression in the mouse hippocampus.	Scopolamine	18-29	inhibitor of DNA binding 1, HLH protein	Mus musculus	79-82
29328430-6	2018	ID1-immunoreactive cells were revealed in the hippocampus of vehicle-treated mice, and were hardly detected 4 weeks following treatment with scopolamine.	Scopolamine	141-152	inhibitor of DNA binding 1, HLH protein	Mus musculus	0-3
29328430-7	2018	However, treatment with vanillin in scopolamine-treated mice markedly restored ID1-immunoreactive cells and expression 4 weeks subsequent to treatment.	Scopolamine	36-47	inhibitor of DNA binding 1, HLH protein	Mus musculus	79-82
29174736-10	2018	CONCLUSION: Our findings revealed that PKA pathway is necessary for scopolamine-induced synaptic plasticity and mTOR pathway activation, and indicated that a potential M2-PKA mechanism underlies scopolamine"s antidepressant effects.	Scopolamine	195-206	mechanistic target of rapamycin kinase	Rattus norvegicus	112-116
29260493-6	2018	Ki67 (a marker for cell proliferation)- and doublecortin (a marker for neuroblast differentiation)-positive cells were significantly decreased in the dentate gyrus 2 and 4 weeks after scopolamine treatment, however, cotreatment of scopolamine and melatonin significantly increased Ki67- and doublecortin-positive cells compared with scopolamine-treated group.	Scopolamine	184-195	antigen identified by monoclonal antibody Ki 67	Mus musculus	0-4
29260493-6	2018	Ki67 (a marker for cell proliferation)- and doublecortin (a marker for neuroblast differentiation)-positive cells were significantly decreased in the dentate gyrus 2 and 4 weeks after scopolamine treatment, however, cotreatment of scopolamine and melatonin significantly increased Ki67- and doublecortin-positive cells compared with scopolamine-treated group.	Scopolamine	231-242	antigen identified by monoclonal antibody Ki 67	Mus musculus	0-4
29260493-6	2018	Ki67 (a marker for cell proliferation)- and doublecortin (a marker for neuroblast differentiation)-positive cells were significantly decreased in the dentate gyrus 2 and 4 weeks after scopolamine treatment, however, cotreatment of scopolamine and melatonin significantly increased Ki67- and doublecortin-positive cells compared with scopolamine-treated group.	Scopolamine	231-242	antigen identified by monoclonal antibody Ki 67	Mus musculus	281-285
29260493-6	2018	Ki67 (a marker for cell proliferation)- and doublecortin (a marker for neuroblast differentiation)-positive cells were significantly decreased in the dentate gyrus 2 and 4 weeks after scopolamine treatment, however, cotreatment of scopolamine and melatonin significantly increased Ki67- and doublecortin-positive cells compared with scopolamine-treated group.	Scopolamine	231-242	antigen identified by monoclonal antibody Ki 67	Mus musculus	0-4
29260493-6	2018	Ki67 (a marker for cell proliferation)- and doublecortin (a marker for neuroblast differentiation)-positive cells were significantly decreased in the dentate gyrus 2 and 4 weeks after scopolamine treatment, however, cotreatment of scopolamine and melatonin significantly increased Ki67- and doublecortin-positive cells compared with scopolamine-treated group.	Scopolamine	231-242	antigen identified by monoclonal antibody Ki 67	Mus musculus	281-285
29670659-9	2018	Gagam-Palmultang has beneficial effects against scopolamine-induced memory impairments, which are exerted via modulation of the cholinergic system as well as the PI3K and ERK/CREB/BDNF signaling pathway.	Scopolamine	48-59	mitogen-activated protein kinase 1	Mus musculus	171-174
29670659-9	2018	Gagam-Palmultang has beneficial effects against scopolamine-induced memory impairments, which are exerted via modulation of the cholinergic system as well as the PI3K and ERK/CREB/BDNF signaling pathway.	Scopolamine	48-59	cAMP responsive element binding protein 1	Mus musculus	175-179
29670659-9	2018	Gagam-Palmultang has beneficial effects against scopolamine-induced memory impairments, which are exerted via modulation of the cholinergic system as well as the PI3K and ERK/CREB/BDNF signaling pathway.	Scopolamine	48-59	brain derived neurotrophic factor	Mus musculus	180-184
29394903-4	2018	Such a beneficial effect of Abeta40 on glutamate neurotransmission in human patients is absolutely necessary to reproduce clinical data on the ADAS-Cog in minimal cognitive impairment (MCI) patients with and without amyloid load, the effect of APOE genotype effect on the slope of the cognitive trajectory over time in placebo AD patients and higher sensitivity to cholinergic manipulation with scopolamine associated with higher Abeta in MCI subjects.	Scopolamine	395-406	amyloid beta precursor protein	Homo sapiens	28-33
29020410-11	2018	We further found that the rapid-acting antidepressant-like effects and the upregulation on brain-derived neurotrophic factor and VGF produced by a low dose of scopolamine (0.025 mg/kg) were completely blocked by verapamil.	Scopolamine	159-170	brain derived neurotrophic factor	Mus musculus	91-124
29020410-11	2018	We further found that the rapid-acting antidepressant-like effects and the upregulation on brain-derived neurotrophic factor and VGF produced by a low dose of scopolamine (0.025 mg/kg) were completely blocked by verapamil.	Scopolamine	159-170	VGF nerve growth factor inducible	Mus musculus	129-132
29020410-12	2018	Conclusions: These results indicate that L-type voltage-dependent calcium channels are likely involved in the behavioral changes in response to various doses of scopolamine through the regulation of brain-derived neurotrophic factor and VGF levels.	Scopolamine	161-172	brain derived neurotrophic factor	Mus musculus	199-232
29020410-12	2018	Conclusions: These results indicate that L-type voltage-dependent calcium channels are likely involved in the behavioral changes in response to various doses of scopolamine through the regulation of brain-derived neurotrophic factor and VGF levels.	Scopolamine	161-172	VGF nerve growth factor inducible	Mus musculus	237-240
29126931-9	2018	In addition, allylguaiacol significantly increased the expression of TrkA and B in the hippocampus from scopolamine-treated mice.	Scopolamine	104-115	neurotrophic tyrosine kinase, receptor, type 1	Mus musculus	69-73
29174736-0	2018	Protein kinase A mediates scopolamine-induced mTOR activation and an antidepressant response.	Scopolamine	26-37	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	0-16
29174736-0	2018	Protein kinase A mediates scopolamine-induced mTOR activation and an antidepressant response.	Scopolamine	26-37	mechanistic target of rapamycin kinase	Rattus norvegicus	46-50
29174736-2	2018	Animal experiments have proven that scopolamine induces mTOR pathway activation in an AMPAR dependent manner.	Scopolamine	36-47	mechanistic target of rapamycin kinase	Rattus norvegicus	56-60
29174736-2	2018	Animal experiments have proven that scopolamine induces mTOR pathway activation in an AMPAR dependent manner.	Scopolamine	36-47	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	86-91
29174736-3	2018	The present study aimed to determine the role of PKA in scopolamine-induced potentiation of AMPAR, as well as in mTOR pathway activation and rapid antidepressant effects.	Scopolamine	56-67	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	92-97
29174736-5	2018	RESULTS: Scopolamine (1muM) rapidly increased AMPAR-fEPSP amplitudes and membrane GluA1 expression in CA1 region of hippocampal slices, both of which were abolished by H89.	Scopolamine	9-20	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	82-87
29174736-5	2018	RESULTS: Scopolamine (1muM) rapidly increased AMPAR-fEPSP amplitudes and membrane GluA1 expression in CA1 region of hippocampal slices, both of which were abolished by H89.	Scopolamine	9-20	carbonic anhydrase 1	Rattus norvegicus	102-105
29174736-11	2018	Such findings suggest that GluA1 ser845 phosphorylation may be a trigger event for scopolamine"s actions, and that PKA may represent a novel target for the treatment of depressive symptoms.	Scopolamine	83-94	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	27-32
29370115-0	2018	Ethanol Extract of Oldenlandia diffusa Herba Attenuates Scopolamine-Induced Cognitive Impairments in Mice via Activation of BDNF, P-CREB and Inhibition of Acetylcholinesterase.	Scopolamine	56-67	brain derived neurotrophic factor	Mus musculus	124-128
29174736-6	2018	Moreover, scopolamine promoted AMPAR phosphorylation on GluA1 ser845, a PKA site involved in GluA1 membrane insertion.	Scopolamine	10-21	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	31-36
29174736-6	2018	Moreover, scopolamine promoted AMPAR phosphorylation on GluA1 ser845, a PKA site involved in GluA1 membrane insertion.	Scopolamine	10-21	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	56-61
29174736-6	2018	Moreover, scopolamine promoted AMPAR phosphorylation on GluA1 ser845, a PKA site involved in GluA1 membrane insertion.	Scopolamine	10-21	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	93-98
29370115-0	2018	Ethanol Extract of Oldenlandia diffusa Herba Attenuates Scopolamine-Induced Cognitive Impairments in Mice via Activation of BDNF, P-CREB and Inhibition of Acetylcholinesterase.	Scopolamine	56-67	cAMP responsive element binding protein 1	Mus musculus	132-136
29370115-0	2018	Ethanol Extract of Oldenlandia diffusa Herba Attenuates Scopolamine-Induced Cognitive Impairments in Mice via Activation of BDNF, P-CREB and Inhibition of Acetylcholinesterase.	Scopolamine	56-67	acetylcholinesterase	Mus musculus	155-175
29942435-10	2018	Increase in acetylcholinesterase activity and lipid peroxidation in both groups was observed 30 minutes after scopolamine administration.	Scopolamine	110-121	acetylcholinesterase	Rattus norvegicus	12-32
29225190-0	2018	Scopolamine-induced passive avoidance memory retrieval deficit is accompanied with hippocampal MMP2, MMP-9 and MAPKs alteration.	Scopolamine	0-11	matrix metallopeptidase 2	Mus musculus	95-99
29225190-0	2018	Scopolamine-induced passive avoidance memory retrieval deficit is accompanied with hippocampal MMP2, MMP-9 and MAPKs alteration.	Scopolamine	0-11	matrix metallopeptidase 9	Mus musculus	101-106
29225190-11	2018	This scopolamine treatment resulted in hippocampal MMP-2 and MMP-9 decline while increased MAPKs in the hippocampus.	Scopolamine	5-16	matrix metallopeptidase 2	Mus musculus	51-56
29225190-11	2018	This scopolamine treatment resulted in hippocampal MMP-2 and MMP-9 decline while increased MAPKs in the hippocampus.	Scopolamine	5-16	matrix metallopeptidase 9	Mus musculus	61-66
29337893-7	2018	Overall, glyceollins showed neuroprotection against glutamate-induced damage, and attenuated scopolamine-induced memory deficits in an Nrf2-dependent manner.	Scopolamine	93-104	nuclear factor, erythroid derived 2, like 2	Mus musculus	135-139
29491219-7	2018	Collectively, this study shows that SKF83959 has beneficial effects in the scopolamine model of dementia by modulation of hippocampal BDNF signaling, implying a novel and potential therapeutic agent for treating dementia in AD.	Scopolamine	75-86	brain derived neurotrophic factor	Homo sapiens	134-138
28751069-0	2018	Activity-Dependent Brain-Derived Neurotrophic Factor Release Is Required for the Rapid Antidepressant Actions of Scopolamine.	Scopolamine	113-124	brain derived neurotrophic factor	Mus musculus	19-52
28751069-4	2018	Here we tested the hypothesis that activity-dependent BDNF release within the mPFC is necessary for the antidepressant actions of scopolamine.	Scopolamine	130-141	brain derived neurotrophic factor	Mus musculus	54-58
28751069-7	2018	Further in vivo and in vitro experiments were performed to delineate BDNF-dependent mechanisms underlying the effects of scopolamine.	Scopolamine	121-132	brain derived neurotrophic factor	Mus musculus	69-73
28751069-8	2018	RESULTS: We found that BDNF Met/Met mice have attenuated responses to scopolamine and that anti-BDNF antibody infusions into the mPFC prevented the antidepressant-like behavioral effects of scopolamine.	Scopolamine	70-81	brain derived neurotrophic factor	Mus musculus	23-27
28751069-8	2018	RESULTS: We found that BDNF Met/Met mice have attenuated responses to scopolamine and that anti-BDNF antibody infusions into the mPFC prevented the antidepressant-like behavioral effects of scopolamine.	Scopolamine	190-201	brain derived neurotrophic factor	Mus musculus	96-100
28751069-9	2018	In vitro experiments show that scopolamine rapidly stimulates BDNF release and tropomyosin receptor kinase B-extracellular signal-regulated kinase signaling.	Scopolamine	31-42	brain derived neurotrophic factor	Mus musculus	62-66
28751069-12	2018	CONCLUSIONS: The results identify an essential role for activity-dependent BDNF release in the rapid antidepressant effects of scopolamine.	Scopolamine	127-138	brain derived neurotrophic factor	Mus musculus	75-79
28751069-13	2018	Attenuation of responses in BDNF Met mice indicates that patients with the Met allele may be less responsive to scopolamine.	Scopolamine	112-123	brain derived neurotrophic factor	Mus musculus	28-32
29136783-9	2018	The formulation also counteracted scopolamine-induced decreases in acetylcholine levels, increases in AChE activity, and decreases in activities of the antioxidant enzymes.	Scopolamine	34-45	acetylcholinesterase	Rattus norvegicus	102-106
29491219-5	2018	Moreover, SKF83959 treatment significantly antagonized the down-regulating effects of scopolamine on brain-derived neurotrophic factor (BDNF) signaling cascade in the hippocampus, but not cortex.	Scopolamine	86-97	brain derived neurotrophic factor	Homo sapiens	101-134
29491219-5	2018	Moreover, SKF83959 treatment significantly antagonized the down-regulating effects of scopolamine on brain-derived neurotrophic factor (BDNF) signaling cascade in the hippocampus, but not cortex.	Scopolamine	86-97	brain derived neurotrophic factor	Homo sapiens	136-140
30509043-10	2018	In the scopolamine-treated groups, the number of CA1 and CA3 pyramidal and dentate gyrus (DG) granular neurons was decreased significantly as compared to the control group.	Scopolamine	7-18	carbonic anhydrase 1	Rattus norvegicus	49-52
29491219-6	2018	Importantly, the usage of K252a, a selective inhibitor of tyrosine kinase B (TrkB), significantly attenuated the protective effects of SKF83959 in the scopolamine model.	Scopolamine	151-162	neurotrophic receptor tyrosine kinase 2	Homo sapiens	58-75
29491219-6	2018	Importantly, the usage of K252a, a selective inhibitor of tyrosine kinase B (TrkB), significantly attenuated the protective effects of SKF83959 in the scopolamine model.	Scopolamine	151-162	neurotrophic receptor tyrosine kinase 2	Homo sapiens	77-81
30509043-10	2018	In the scopolamine-treated groups, the number of CA1 and CA3 pyramidal and dentate gyrus (DG) granular neurons was decreased significantly as compared to the control group.	Scopolamine	7-18	carbonic anhydrase 3	Rattus norvegicus	57-60
29861525-12	2018	Pretreatment with HEZA attenuated scopolamine-induced elevation of TNF-alpha, IL-1 beta, levels in hippocampus and reversed diminished IL-10 concentrations towards normal levels in the brain.	Scopolamine	34-45	tumor necrosis factor	Rattus norvegicus	67-76
29861525-12	2018	Pretreatment with HEZA attenuated scopolamine-induced elevation of TNF-alpha, IL-1 beta, levels in hippocampus and reversed diminished IL-10 concentrations towards normal levels in the brain.	Scopolamine	34-45	interleukin 1 beta	Rattus norvegicus	78-87
28571775-11	2017	Moreover, intra-CA1 injection of sub-threshold dose of physostigmine (0.0001mug/rat) and scopolamine (0.01mug/rat) could restore the memory acquisition deficit induced by RSD, while scopolamine could restore TSD-induced amnesia.	Scopolamine	89-100	carbonic anhydrase 1	Rattus norvegicus	16-19
29157831-0	2017	Vitis labruscana leaf extract ameliorates scopolamine-induced impairments with activation of Akt, ERK and CREB in mice.	Scopolamine	42-53	mitogen-activated protein kinase 1	Mus musculus	98-101
29157831-0	2017	Vitis labruscana leaf extract ameliorates scopolamine-induced impairments with activation of Akt, ERK and CREB in mice.	Scopolamine	42-53	cAMP responsive element binding protein 1	Mus musculus	106-110
29157831-11	2017	Consistent with the cell experiment results, LEVL restored scopolamine-decreased phosphorylation of Akt, ERK, and CREB and scopolamine-reduced expression of brain-derived neuroprotective factor expression in mouse hippocampi.	Scopolamine	59-70	thymoma viral proto-oncogene 1	Mus musculus	100-103
29157831-11	2017	Consistent with the cell experiment results, LEVL restored scopolamine-decreased phosphorylation of Akt, ERK, and CREB and scopolamine-reduced expression of brain-derived neuroprotective factor expression in mouse hippocampi.	Scopolamine	59-70	mitogen-activated protein kinase 1	Mus musculus	105-108
29157831-11	2017	Consistent with the cell experiment results, LEVL restored scopolamine-decreased phosphorylation of Akt, ERK, and CREB and scopolamine-reduced expression of brain-derived neuroprotective factor expression in mouse hippocampi.	Scopolamine	59-70	cAMP responsive element binding protein 1	Mus musculus	114-118
28778589-7	2017	Most importantly, the results demonstrate that the effect of scopolamine and its prevention by protectant substances are clearly displayed in the heat capacity profiles of the brain proteome, thus identifying DSC as a powerful method in drug testing and discovery.	Scopolamine	61-72	declival sulcus of cerebellum	Mus musculus	209-212
29190426-2	2017	Our previous investigation showed that anchovy protein hydrolysate (APH) could attenuate scopolamine-induced memory deficits in mice by regulating acetylcholinesterase (AChE) activity.	Scopolamine	89-100	acylaminoacyl-peptide hydrolase	Rattus norvegicus	68-71
29190426-2	2017	Our previous investigation showed that anchovy protein hydrolysate (APH) could attenuate scopolamine-induced memory deficits in mice by regulating acetylcholinesterase (AChE) activity.	Scopolamine	89-100	acetylcholinesterase	Mus musculus	147-167
29190426-2	2017	Our previous investigation showed that anchovy protein hydrolysate (APH) could attenuate scopolamine-induced memory deficits in mice by regulating acetylcholinesterase (AChE) activity.	Scopolamine	89-100	acetylcholinesterase	Mus musculus	169-173
28830814-7	2017	p-Coumaric acid dose-dependently increased the total activity of fEPSP after high frequency stimulation and attenuated scopolamine-induced blockade of fEPSP in the hippocampal CA1 area.	Scopolamine	119-130	carbonic anhydrase 1	Rattus norvegicus	176-179
28571775-11	2017	Moreover, intra-CA1 injection of sub-threshold dose of physostigmine (0.0001mug/rat) and scopolamine (0.01mug/rat) could restore the memory acquisition deficit induced by RSD, while scopolamine could restore TSD-induced amnesia.	Scopolamine	182-193	carbonic anhydrase 1	Rattus norvegicus	16-19
28894228-6	2017	In vivo pharmacodynamic efficacy was evaluated using Morris Water Maze Test, Radial Arm Maze Test and AChE activity in scopolamine induced amnetic rats.	Scopolamine	119-130	acetylcholinesterase	Rattus norvegicus	102-106
28940173-6	2017	Furthermore, LQ markedly increased the protein level of brain-derived neurotrophic factor (BDNF) and phosphorylation of extracellular signal-regulated kinase (ERK) and cAMP response element binding (CREB) in the hippocampus of scopolamine-induced mice.	Scopolamine	227-238	brain derived neurotrophic factor	Mus musculus	56-89
28940173-6	2017	Furthermore, LQ markedly increased the protein level of brain-derived neurotrophic factor (BDNF) and phosphorylation of extracellular signal-regulated kinase (ERK) and cAMP response element binding (CREB) in the hippocampus of scopolamine-induced mice.	Scopolamine	227-238	mitogen-activated protein kinase 1	Mus musculus	120-157
28940173-6	2017	Furthermore, LQ markedly increased the protein level of brain-derived neurotrophic factor (BDNF) and phosphorylation of extracellular signal-regulated kinase (ERK) and cAMP response element binding (CREB) in the hippocampus of scopolamine-induced mice.	Scopolamine	227-238	mitogen-activated protein kinase 1	Mus musculus	159-162
28940173-6	2017	Furthermore, LQ markedly increased the protein level of brain-derived neurotrophic factor (BDNF) and phosphorylation of extracellular signal-regulated kinase (ERK) and cAMP response element binding (CREB) in the hippocampus of scopolamine-induced mice.	Scopolamine	227-238	cAMP responsive element binding protein 1	Mus musculus	168-197
28940173-6	2017	Furthermore, LQ markedly increased the protein level of brain-derived neurotrophic factor (BDNF) and phosphorylation of extracellular signal-regulated kinase (ERK) and cAMP response element binding (CREB) in the hippocampus of scopolamine-induced mice.	Scopolamine	227-238	cAMP responsive element binding protein 1	Mus musculus	199-203
28619513-0	2017	Myricetin ameliorates scopolamine-induced memory impairment in mice via inhibiting acetylcholinesterase and down-regulating brain iron.	Scopolamine	22-33	acetylcholinesterase	Mus musculus	83-103
28411153-7	2017	Intra-mPFC administration of scopolamine prior to all three phases significantly impaired fear conditioning suggesting that mPFC cholinergic function is necessary for successful CPFE performance.	Scopolamine	29-40	complement factor properdin	Mus musculus	6-10
28411153-7	2017	Intra-mPFC administration of scopolamine prior to all three phases significantly impaired fear conditioning suggesting that mPFC cholinergic function is necessary for successful CPFE performance.	Scopolamine	29-40	complement factor properdin	Mus musculus	124-128
29089996-4	2017	We proposed a hypothesis that PT3 has a neuroprotective effect against scopolamine-induced cholinergic dysfunction.	Scopolamine	71-82	zinc finger protein 135	Homo sapiens	30-33
29089996-6	2017	PT-3 (125-200 nM) inhibited scopolamine (2 mM)-induced generation of reactive oxygen species, cellular apoptosis, upregulation of acetylcholinesterase activity, downregulation of choline acetyltransferase level, and activation of p38 and JNK signalling pathways.	Scopolamine	28-39	acetylcholinesterase (Cartwright blood group)	Homo sapiens	130-150
29089996-6	2017	PT-3 (125-200 nM) inhibited scopolamine (2 mM)-induced generation of reactive oxygen species, cellular apoptosis, upregulation of acetylcholinesterase activity, downregulation of choline acetyltransferase level, and activation of p38 and JNK signalling pathways.	Scopolamine	28-39	mitogen-activated protein kinase 14	Homo sapiens	230-233
29089996-6	2017	PT-3 (125-200 nM) inhibited scopolamine (2 mM)-induced generation of reactive oxygen species, cellular apoptosis, upregulation of acetylcholinesterase activity, downregulation of choline acetyltransferase level, and activation of p38 and JNK signalling pathways.	Scopolamine	28-39	mitogen-activated protein kinase 8	Homo sapiens	238-241
27553230-1	2017	Recently, we reported a correlation of scopolamine mediated decline in memory consolidation with increase in the expression of DNA methyltransferase 1 (DNMT1) and histone deacetylase 2 (HDAC2) in the mouse hippocampus.	Scopolamine	39-50	DNA methyltransferase (cytosine-5) 1	Mus musculus	127-150
27553230-1	2017	Recently, we reported a correlation of scopolamine mediated decline in memory consolidation with increase in the expression of DNA methyltransferase 1 (DNMT1) and histone deacetylase 2 (HDAC2) in the mouse hippocampus.	Scopolamine	39-50	DNA methyltransferase (cytosine-5) 1	Mus musculus	152-157
27553230-1	2017	Recently, we reported a correlation of scopolamine mediated decline in memory consolidation with increase in the expression of DNA methyltransferase 1 (DNMT1) and histone deacetylase 2 (HDAC2) in the mouse hippocampus.	Scopolamine	39-50	histone deacetylase 2	Mus musculus	163-184
27553230-1	2017	Recently, we reported a correlation of scopolamine mediated decline in memory consolidation with increase in the expression of DNA methyltransferase 1 (DNMT1) and histone deacetylase 2 (HDAC2) in the mouse hippocampus.	Scopolamine	39-50	histone deacetylase 2	Mus musculus	186-191
28619513-3	2017	In a mouse model of AD, myricetin treatment significantly reversed scopolamine-induced cognitive deficits deriving from a novel action of inhibiting acetylcholinesterase (AChE) and down-regulating brain iron.	Scopolamine	67-78	acetylcholinesterase	Mus musculus	149-169
28619513-3	2017	In a mouse model of AD, myricetin treatment significantly reversed scopolamine-induced cognitive deficits deriving from a novel action of inhibiting acetylcholinesterase (AChE) and down-regulating brain iron.	Scopolamine	67-78	acetylcholinesterase	Mus musculus	171-175
28716085-11	2017	FCL significantly attenuated scopolamine-induced memory impairment in mice and prevented scopolamine-induced AChE activity in the hippocampus.	Scopolamine	89-100	acetylcholinesterase	Mus musculus	109-113
28449397-12	2017	Thus, these findings suggest that Vdac1-mediated disruption of energy metabolism and cytoskeleton architecture might be involved in scopolamine-induced amnesia.	Scopolamine	132-143	voltage-dependent anion channel 1	Mus musculus	34-39
29265027-11	2017	Scopolamine administration also produced a significant enhancement of brain AChE activity and oxidative stress in mice brain.	Scopolamine	0-11	acetylcholinesterase	Mus musculus	76-80
29265027-13	2017	significantly prevented scopolamine-induced learning and memory deficits along with attenuation of scopolamine-induced rise in brain AChE activity and oxidative stress level.	Scopolamine	99-110	acetylcholinesterase	Mus musculus	133-137
28792471-8	2017	Among the sub-strains, scopolamine-treated C57BL/6N strains exhibited declined step-through latency, elevated acetylcholinesterase (AChE) activity and inflammatory protein expression, associated with reduced endogenous antioxidant levels and p-CREB/BDNF expression, compared to the control and tacrine-treated groups.	Scopolamine	23-34	acetylcholinesterase	Mus musculus	110-130
28792471-8	2017	Among the sub-strains, scopolamine-treated C57BL/6N strains exhibited declined step-through latency, elevated acetylcholinesterase (AChE) activity and inflammatory protein expression, associated with reduced endogenous antioxidant levels and p-CREB/BDNF expression, compared to the control and tacrine-treated groups.	Scopolamine	23-34	acetylcholinesterase	Mus musculus	132-136
28792471-8	2017	Among the sub-strains, scopolamine-treated C57BL/6N strains exhibited declined step-through latency, elevated acetylcholinesterase (AChE) activity and inflammatory protein expression, associated with reduced endogenous antioxidant levels and p-CREB/BDNF expression, compared to the control and tacrine-treated groups.	Scopolamine	23-34	cAMP responsive element binding protein 1	Mus musculus	244-248
28792471-8	2017	Among the sub-strains, scopolamine-treated C57BL/6N strains exhibited declined step-through latency, elevated acetylcholinesterase (AChE) activity and inflammatory protein expression, associated with reduced endogenous antioxidant levels and p-CREB/BDNF expression, compared to the control and tacrine-treated groups.	Scopolamine	23-34	brain derived neurotrophic factor	Mus musculus	249-253
28713618-4	2017	Treatment with scopolamine alone impaired learning and memory function in the Morris water maze and passive avoidance tests, in addition, the treatment significantly reduced cell proliferation and neuroblast differentiation in the dentate gyrus, which were examined by immunohistochemistry for Ki-67 (a classic marker for cell proliferation) and doublecortin (a marker for neuroblasts).	Scopolamine	15-26	antigen identified by monoclonal antibody Ki 67	Mus musculus	294-299
28398193-7	2017	RESULTS: SCO administration induced memory deficit, increased oxidative stress, and increased AChE activities in the hippocampus and prefrontal cortex.	Scopolamine	9-12	acetylcholinesterase	Rattus norvegicus	94-98
28781727-14	2017	CONCLUSION: The current study findings indicated a cross state-dependent learning between SCO and morphine at CA1 level.	Scopolamine	90-93	carbonic anhydrase 1	Mus musculus	110-113
28442406-9	2017	Moreover, the activity and protein expression of AChE was significantly decreased and the content of neurotransmitter ACh was significantly increased in cerebral cortex of scopolamine-induced mice by treatment with EXT at dosages of 183, 550, 1650mg/kg and ALK at dosages of 10, 30, 90mg/kg (P&lt;0.05), compared with scopolamine-treated group.	Scopolamine	172-183	acetylcholinesterase	Mus musculus	49-53
28442406-9	2017	Moreover, the activity and protein expression of AChE was significantly decreased and the content of neurotransmitter ACh was significantly increased in cerebral cortex of scopolamine-induced mice by treatment with EXT at dosages of 183, 550, 1650mg/kg and ALK at dosages of 10, 30, 90mg/kg (P&lt;0.05), compared with scopolamine-treated group.	Scopolamine	318-329	acetylcholinesterase	Mus musculus	49-53
28102474-8	2017	Scopolamine-treated rats showed impaired learning and memory and increased activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE), adenosine deaminase (ADA), and lipid peroxidation with a concomitant decreased in levels of nitric oxide (NO) and reduced glutathione (GSH), superoxide dismutase (SOD), and catalase activities when compared with control.	Scopolamine	0-11	acetylcholinesterase	Rattus norvegicus	89-109
28137622-0	2017	The ameliorating effect of 1-palmitoyl-2-linoleoyl-3-acetylglycerol on scopolamine-induced memory impairment via acetylcholinesterase inhibition and LTP activation.	Scopolamine	71-82	acetylcholinesterase	Mus musculus	113-133
27021021-13	2017	Graphical abstract Possible molecular pathways of involvement of selenium (Se) in scopolamine (SCOP) induced apoptosis, oxidative stress, and calcium accumulation through TRPM2 and TRPV1 channels in the hippocampus neurons of aged rats.	Scopolamine	82-93	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	171-176
27021021-13	2017	Graphical abstract Possible molecular pathways of involvement of selenium (Se) in scopolamine (SCOP) induced apoptosis, oxidative stress, and calcium accumulation through TRPM2 and TRPV1 channels in the hippocampus neurons of aged rats.	Scopolamine	82-93	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	181-186
27021021-13	2017	Graphical abstract Possible molecular pathways of involvement of selenium (Se) in scopolamine (SCOP) induced apoptosis, oxidative stress, and calcium accumulation through TRPM2 and TRPV1 channels in the hippocampus neurons of aged rats.	Scopolamine	95-99	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	171-176
27021021-13	2017	Graphical abstract Possible molecular pathways of involvement of selenium (Se) in scopolamine (SCOP) induced apoptosis, oxidative stress, and calcium accumulation through TRPM2 and TRPV1 channels in the hippocampus neurons of aged rats.	Scopolamine	95-99	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	181-186
28102474-8	2017	Scopolamine-treated rats showed impaired learning and memory and increased activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE), adenosine deaminase (ADA), and lipid peroxidation with a concomitant decreased in levels of nitric oxide (NO) and reduced glutathione (GSH), superoxide dismutase (SOD), and catalase activities when compared with control.	Scopolamine	0-11	acetylcholinesterase	Rattus norvegicus	111-115
28102474-8	2017	Scopolamine-treated rats showed impaired learning and memory and increased activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE), adenosine deaminase (ADA), and lipid peroxidation with a concomitant decreased in levels of nitric oxide (NO) and reduced glutathione (GSH), superoxide dismutase (SOD), and catalase activities when compared with control.	Scopolamine	0-11	adenosine deaminase	Rattus norvegicus	152-171
28102474-8	2017	Scopolamine-treated rats showed impaired learning and memory and increased activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE), adenosine deaminase (ADA), and lipid peroxidation with a concomitant decreased in levels of nitric oxide (NO) and reduced glutathione (GSH), superoxide dismutase (SOD), and catalase activities when compared with control.	Scopolamine	0-11	adenosine deaminase	Rattus norvegicus	173-176
28275781-2	2017	This study was designed to investigate the effects of AEAS on learning, memory, and acetylcholinesterase-related activity in a scopolamine-induced model of amnesia.	Scopolamine	127-138	acetylcholinesterase	Mus musculus	84-104
28275781-6	2017	It also reversed scopolamine-induced reduction in the hippocampal brain-derived neurotrophic factor (BDNF) and the cAMP response element-binding protein (CREB) mRNA expression.	Scopolamine	17-28	brain derived neurotrophic factor	Mus musculus	66-99
28275781-6	2017	It also reversed scopolamine-induced reduction in the hippocampal brain-derived neurotrophic factor (BDNF) and the cAMP response element-binding protein (CREB) mRNA expression.	Scopolamine	17-28	brain derived neurotrophic factor	Mus musculus	101-105
28275781-6	2017	It also reversed scopolamine-induced reduction in the hippocampal brain-derived neurotrophic factor (BDNF) and the cAMP response element-binding protein (CREB) mRNA expression.	Scopolamine	17-28	cAMP responsive element binding protein 1	Mus musculus	115-152
28275781-6	2017	It also reversed scopolamine-induced reduction in the hippocampal brain-derived neurotrophic factor (BDNF) and the cAMP response element-binding protein (CREB) mRNA expression.	Scopolamine	17-28	cAMP responsive element binding protein 1	Mus musculus	154-158
28032295-8	2017	Notably, pretreatment with a dopamine D1 receptor (D1R) antagonist SCH23390 blocked the scopolamine-stimulated ERK phosphorylation in these brain regions, while a dopamine D2 receptor antagonist eticlopride did not.	Scopolamine	88-99	Eph receptor B1	Rattus norvegicus	111-114
28069458-8	2017	Loganin dose-dependently increased the total activity of fEPSP after high frequency stimulation and attenuated scopolamine-induced blockade of fEPSP in the hippocampal CA1 area.	Scopolamine	111-122	carbonic anhydrase 1	Homo sapiens	168-171
28110104-11	2017	Moreover, Q3GA significantly reversed scopolamine-induced reduction of Akt phosphorylation in the mouse hippocampus and ameliorated scopolamine-induced memory impairments.	Scopolamine	38-49	thymoma viral proto-oncogene 1	Mus musculus	71-74
26955968-5	2017	Moreover, preclinical work has shown that the antidepressant actions of ketamine and scopolamine in rodent models are caused by an increase of extracellular glutamate, elevated BDNF, activation of the mammalian target of rapamycin complex 1 (mTORC1) cascade, and increased number and function of spine synapses in the prefrontal cortex (PFC).	Scopolamine	85-96	brain derived neurotrophic factor	Homo sapiens	177-181
27470063-5	2017	Interestingly, ameliorating effect of oleanolic acid on scopolamine-induced memory impairment was abolished by N2-(2-{[(2-oxoazepan-3-yl)amino]carbonyl}phenyl)benzo[b]thiophene-2-carboxamide (ANA-12), a potent and specific inhibitor of tropomyosin receptor kinase B (TrkB), in the passive avoidance task.	Scopolamine	56-67	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	236-265
27470063-5	2017	Interestingly, ameliorating effect of oleanolic acid on scopolamine-induced memory impairment was abolished by N2-(2-{[(2-oxoazepan-3-yl)amino]carbonyl}phenyl)benzo[b]thiophene-2-carboxamide (ANA-12), a potent and specific inhibitor of tropomyosin receptor kinase B (TrkB), in the passive avoidance task.	Scopolamine	56-67	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	267-271
27470063-7	2017	Together, these results imply that oleanolic acid ameliorates scopolamine-induced memory impairment by modulating the BDNF-ERK1/2-CREB pathway through TrkB activation in mice, suggesting that oleanolic acid would be a potential therapeutic agent for the treatment of cognitive deficits.	Scopolamine	62-73	brain derived neurotrophic factor	Mus musculus	118-122
27470063-7	2017	Together, these results imply that oleanolic acid ameliorates scopolamine-induced memory impairment by modulating the BDNF-ERK1/2-CREB pathway through TrkB activation in mice, suggesting that oleanolic acid would be a potential therapeutic agent for the treatment of cognitive deficits.	Scopolamine	62-73	mitogen-activated protein kinase 3	Mus musculus	123-129
27470063-7	2017	Together, these results imply that oleanolic acid ameliorates scopolamine-induced memory impairment by modulating the BDNF-ERK1/2-CREB pathway through TrkB activation in mice, suggesting that oleanolic acid would be a potential therapeutic agent for the treatment of cognitive deficits.	Scopolamine	62-73	cAMP responsive element binding protein 1	Mus musculus	130-134
27470063-7	2017	Together, these results imply that oleanolic acid ameliorates scopolamine-induced memory impairment by modulating the BDNF-ERK1/2-CREB pathway through TrkB activation in mice, suggesting that oleanolic acid would be a potential therapeutic agent for the treatment of cognitive deficits.	Scopolamine	62-73	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	151-155
28294051-8	2017	An orally-bioavilable mTOR inhibitor (AZD8055) also attenuated the antidepressant- like effects of scopolamine and ketamine.	Scopolamine	99-110	mechanistic target of rapamycin kinase	Mus musculus	22-26
28294051-12	2017	CONCLUSION: Overall, the data substantiate and extend the idea that AMPA and mTOR signaling pathways are necessary for the antidepressant-like effects of scopolamine and ketamine, mechanisms that appear to be of general significance for TRD therapeutic agents.	Scopolamine	154-165	mechanistic target of rapamycin kinase	Mus musculus	77-81
28294051-12	2017	CONCLUSION: Overall, the data substantiate and extend the idea that AMPA and mTOR signaling pathways are necessary for the antidepressant-like effects of scopolamine and ketamine, mechanisms that appear to be of general significance for TRD therapeutic agents.	Scopolamine	154-165	t-complex distorter 1A	Mus musculus	237-240
27939357-0	2017	alpha-Isocubebenol alleviates scopolamine-induced cognitive impairment by repressing acetylcholinesterase activity.	Scopolamine	30-41	acetylcholinesterase	Mus musculus	85-105
27939357-5	2017	Acetylcholinesterase (AChE) activity was significantly decreased in the SP+ICO treated group compared with the SP+Vehicle treated group.	Scopolamine	72-74	acetylcholinesterase	Mus musculus	0-20
27939357-5	2017	Acetylcholinesterase (AChE) activity was significantly decreased in the SP+ICO treated group compared with the SP+Vehicle treated group.	Scopolamine	72-74	acetylcholinesterase	Mus musculus	22-26
27939357-5	2017	Acetylcholinesterase (AChE) activity was significantly decreased in the SP+ICO treated group compared with the SP+Vehicle treated group.	Scopolamine	72-75	acetylcholinesterase	Mus musculus	0-20
27939357-5	2017	Acetylcholinesterase (AChE) activity was significantly decreased in the SP+ICO treated group compared with the SP+Vehicle treated group.	Scopolamine	72-75	acetylcholinesterase	Mus musculus	22-26
27939357-6	2017	Additionally, significant recovery of the number of apoptotic cells and the ratio of apoptosis proteins (Bcl-2/Bax) were detected in the SP+ICO treated group than the SP+Vehicle treated group.	Scopolamine	137-139	B cell leukemia/lymphoma 2	Mus musculus	105-110
27939357-6	2017	Additionally, significant recovery of the number of apoptotic cells and the ratio of apoptosis proteins (Bcl-2/Bax) were detected in the SP+ICO treated group than the SP+Vehicle treated group.	Scopolamine	137-139	BCL2-associated X protein	Mus musculus	111-114
27939357-7	2017	Moreover, ICO treatment attenuated the decrease of ERK phosphorylation by SP treatment.	Scopolamine	74-76	mitogen-activated protein kinase 1	Mus musculus	51-54
29234406-0	2017	Amelioration of Scopolamine-Induced Learning and Memory Impairment by alpha-Pinene in C57BL/6 Mice.	Scopolamine	16-27	adiponectin, C1Q and collagen domain containing	Mus musculus	70-82
29234406-3	2017	In this study, we have investigated the neuroprotective effect of alpha-pinene (APN) against learning and memory impairment induced by scopolamine (SCO, 1 mg/kg, i.p.	Scopolamine	135-146	adiponectin, C1Q and collagen domain containing	Mus musculus	66-78
29234406-3	2017	In this study, we have investigated the neuroprotective effect of alpha-pinene (APN) against learning and memory impairment induced by scopolamine (SCO, 1 mg/kg, i.p.	Scopolamine	135-146	adiponectin, C1Q and collagen domain containing	Mus musculus	80-83
26955968-5	2017	Moreover, preclinical work has shown that the antidepressant actions of ketamine and scopolamine in rodent models are caused by an increase of extracellular glutamate, elevated BDNF, activation of the mammalian target of rapamycin complex 1 (mTORC1) cascade, and increased number and function of spine synapses in the prefrontal cortex (PFC).	Scopolamine	85-96	CREB regulated transcription coactivator 1	Mus musculus	242-248
27444169-0	2016	Timosaponin B-II ameliorates scopolamine-induced cognition deficits by attenuating acetylcholinesterase activity and brain oxidative damage in mice.	Scopolamine	29-40	acetylcholinesterase	Mus musculus	83-103
26434561-11	2016	Further, it significantly down-regulated the bax and caspase 3 and up-regulated bcl-2 expression in scopolamine intoxicated mice brains.	Scopolamine	100-111	B cell leukemia/lymphoma 2	Mus musculus	80-85
27444169-7	2016	These results indicated that TB-II offers protection against scopolamine-induced deficits in learning and memory, possibly by inhibiting AChE and preventing oxidative stress damage.	Scopolamine	61-72	acetylcholinesterase	Mus musculus	137-141
27422264-7	2016	Therefore, these findings suggest that WY14643 could improve the scopolamine-induced memory impairments, and these effects are mediated by the activation of PPAR-alpha and BDNF system, thereby exhibiting a cognition-enhancing potential.	Scopolamine	65-76	brain derived neurotrophic factor	Mus musculus	172-176
27677871-0	2016	Z-Guggulsterone Improves the Scopolamine-Induced Memory Impairments Through Enhancement of the BDNF Signal in C57BL/6J Mice.	Scopolamine	29-40	brain derived neurotrophic factor	Mus musculus	95-99
27677871-7	2016	Mechanistic studies revealed that Z-guggulsterone pretreatment reversed the scopolamine-induced increase in acetylcholinesterase (AchE) activity, as well as decreases in brain-derived neurotrophic factor (BDNF) protein expression and cAMP response element-binding protein (CREB), extracellular regulated kinase 1/2 (ERK1/2) and protein kinase B (Akt) phosphorylation levels in the hippocampus and cortex.	Scopolamine	76-87	acetylcholinesterase	Mus musculus	108-128
27677871-7	2016	Mechanistic studies revealed that Z-guggulsterone pretreatment reversed the scopolamine-induced increase in acetylcholinesterase (AchE) activity, as well as decreases in brain-derived neurotrophic factor (BDNF) protein expression and cAMP response element-binding protein (CREB), extracellular regulated kinase 1/2 (ERK1/2) and protein kinase B (Akt) phosphorylation levels in the hippocampus and cortex.	Scopolamine	76-87	acetylcholinesterase	Mus musculus	130-134
27677871-7	2016	Mechanistic studies revealed that Z-guggulsterone pretreatment reversed the scopolamine-induced increase in acetylcholinesterase (AchE) activity, as well as decreases in brain-derived neurotrophic factor (BDNF) protein expression and cAMP response element-binding protein (CREB), extracellular regulated kinase 1/2 (ERK1/2) and protein kinase B (Akt) phosphorylation levels in the hippocampus and cortex.	Scopolamine	76-87	cAMP responsive element binding protein 1	Mus musculus	234-271
27677871-7	2016	Mechanistic studies revealed that Z-guggulsterone pretreatment reversed the scopolamine-induced increase in acetylcholinesterase (AchE) activity, as well as decreases in brain-derived neurotrophic factor (BDNF) protein expression and cAMP response element-binding protein (CREB), extracellular regulated kinase 1/2 (ERK1/2) and protein kinase B (Akt) phosphorylation levels in the hippocampus and cortex.	Scopolamine	76-87	cAMP responsive element binding protein 1	Mus musculus	273-277
27677871-7	2016	Mechanistic studies revealed that Z-guggulsterone pretreatment reversed the scopolamine-induced increase in acetylcholinesterase (AchE) activity, as well as decreases in brain-derived neurotrophic factor (BDNF) protein expression and cAMP response element-binding protein (CREB), extracellular regulated kinase 1/2 (ERK1/2) and protein kinase B (Akt) phosphorylation levels in the hippocampus and cortex.	Scopolamine	76-87	mitogen-activated protein kinase 3	Mus musculus	316-322
27677871-7	2016	Mechanistic studies revealed that Z-guggulsterone pretreatment reversed the scopolamine-induced increase in acetylcholinesterase (AchE) activity, as well as decreases in brain-derived neurotrophic factor (BDNF) protein expression and cAMP response element-binding protein (CREB), extracellular regulated kinase 1/2 (ERK1/2) and protein kinase B (Akt) phosphorylation levels in the hippocampus and cortex.	Scopolamine	76-87	thymoma viral proto-oncogene 1	Mus musculus	346-349
27677871-9	2016	Therefore, these findings demonstrate that Z-guggulsterone attenuates the scopolamine-induced memory impairments mainly through activation of the CREB-BDNF signaling pathway, thereby exhibiting memory-improving effects.	Scopolamine	74-85	cAMP responsive element binding protein 1	Mus musculus	146-150
27677871-9	2016	Therefore, these findings demonstrate that Z-guggulsterone attenuates the scopolamine-induced memory impairments mainly through activation of the CREB-BDNF signaling pathway, thereby exhibiting memory-improving effects.	Scopolamine	74-85	brain derived neurotrophic factor	Mus musculus	151-155
27481223-7	2016	This reduction in protein degradation led to an increased amount of p70 S6 kinase (p70S6k), which was abolished in the presence of mAChR antagonist scopolamine.	Scopolamine	148-159	ribosomal protein S6 kinase B1	Homo sapiens	68-81
27568232-0	2016	The dual-acting AChE inhibitor and H3 receptor antagonist UW-MD-72 reverses amnesia induced by scopolamine or dizocilpine in passive avoidance paradigm in rats.	Scopolamine	95-106	acetylcholinesterase (Cartwright blood group)	Homo sapiens	16-20
27481223-7	2016	This reduction in protein degradation led to an increased amount of p70 S6 kinase (p70S6k), which was abolished in the presence of mAChR antagonist scopolamine.	Scopolamine	148-159	ribosomal protein S6 kinase B1	Homo sapiens	83-89
27760517-0	2016	Neuroprotective effects of HTR1A antagonist WAY-100635 on scopolamine-induced delirium in rats and underlying molecular mechanisms.	Scopolamine	58-69	5-hydroxytryptamine receptor 1A	Rattus norvegicus	27-32
27568232-0	2016	The dual-acting AChE inhibitor and H3 receptor antagonist UW-MD-72 reverses amnesia induced by scopolamine or dizocilpine in passive avoidance paradigm in rats.	Scopolamine	95-106	histamine receptor H3	Rattus norvegicus	35-46
27149969-7	2016	Furthermore, it was observed that scopolamine-induced memory impairment was coupled by alterations in neurotransmitters, acetylcholinesterase activity and oxidative stress markers.	Scopolamine	34-45	acetylcholinesterase	Rattus norvegicus	121-141
27273555-6	2016	The estimated scopolamine population mean apparent central and peripheral volume of distribution was 2.66 +- 1.050 l and 62.10 +- 10.100 l, respectively and the clearance was 1.09 +- 0.096 l min(-1) .	Scopolamine	14-25	CD59 molecule (CD59 blood group)	Homo sapiens	191-197
27346436-0	2016	Lactucopicrin ameliorates oxidative stress mediated by scopolamine-induced neurotoxicity through activation of the NRF2 pathway.	Scopolamine	55-66	nuclear factor, erythroid derived 2, like 2	Mus musculus	115-119
27346436-7	2016	Our results revealed that 1 h scopolamine pre-treatment induced cytotoxicity by increasing apoptotic cell death via oxidative stress-mediated caspase 3 activation and mitochondrial dysfunction.	Scopolamine	30-41	caspase 3	Mus musculus	142-151
27346436-8	2016	Scopolamine also downregulated the expression the antioxidant enzymes superoxide dismutase, glutathione peroxidase, and catalase, and the transcription factor NRF2.	Scopolamine	0-11	catalase	Mus musculus	120-128
27346436-8	2016	Scopolamine also downregulated the expression the antioxidant enzymes superoxide dismutase, glutathione peroxidase, and catalase, and the transcription factor NRF2.	Scopolamine	0-11	nuclear factor, erythroid derived 2, like 2	Mus musculus	159-163
27346436-12	2016	Our study is the first to show that lactucopicrin, a potential neuroprotective agent, ameliorates scopolamine-induced cholinergic dysfunction via NRF2 activation and subsequent expression of antioxidant enzymes.	Scopolamine	98-109	nuclear factor, erythroid derived 2, like 2	Mus musculus	146-150
27180103-0	2016	beta-glucan attenuated scopolamine induced cognitive impairment via hippocampal acetylcholinesterase inhibition in rats.	Scopolamine	23-34	acetylcholinesterase	Rattus norvegicus	80-100
27230394-5	2016	Bilateral microinjection of the cannabinoid CB1 receptor agonist, arachydonilcyclopropylamide (ACPA; 1-4ng/rat), into the BLA significantly improved scopolamine-induced memory consolidation impairment.	Scopolamine	149-160	cannabinoid receptor 1	Rattus norvegicus	44-47
27230394-9	2016	Moreover, the blockade of the BLA CB1 receptors by 0.3ng/rat of AM251 prevented ACPA-induced improvement of the scopolamine response.	Scopolamine	112-123	cannabinoid receptor 1	Rattus norvegicus	34-37
27230394-10	2016	In view of the known actions of the drugs used, the present data pointed to the involvement of the BLA CB1 receptors in scopolamine-induced memory consolidation impairment.	Scopolamine	120-131	cannabinoid receptor 1	Rattus norvegicus	103-106
27108935-4	2016	5-HT3 receptor-responses were reversibly inhibited by scopolamine with an IC50 of 2.09 muM.	Scopolamine	54-65	latexin	Homo sapiens	87-90
27343058-0	2016	Effects of Chronic Scopolamine Treatment on Cognitive Impairments and Myelin Basic Protein Expression in the Mouse Hippocampus.	Scopolamine	19-30	myelin basic protein	Mus musculus	70-90
27343058-3	2016	In this study, we first examined changes in the distribution of MBP-immunoreactive myelinated fibers and MBP levels according to hippocampal subregion in mice following chronic systemic treatment with 1 mg/kg scopolamine (SCO) for 4 weeks.	Scopolamine	209-220	myelin basic protein	Mus musculus	64-67
27343058-3	2016	In this study, we first examined changes in the distribution of MBP-immunoreactive myelinated fibers and MBP levels according to hippocampal subregion in mice following chronic systemic treatment with 1 mg/kg scopolamine (SCO) for 4 weeks.	Scopolamine	209-220	myelin basic protein	Mus musculus	105-108
27343058-3	2016	In this study, we first examined changes in the distribution of MBP-immunoreactive myelinated fibers and MBP levels according to hippocampal subregion in mice following chronic systemic treatment with 1 mg/kg scopolamine (SCO) for 4 weeks.	Scopolamine	222-225	myelin basic protein	Mus musculus	64-67
27270172-8	2016	Moreover, knockdown of M1-AChR in SST interneurons in the mPFC demonstrated that M1-AChR expression in these neurons is required for the rapid antidepressant-like effects of scopolamine.	Scopolamine	174-185	somatostatin	Mus musculus	34-37
26323488-0	2016	Neuropeptide S ameliorates olfactory spatial memory impairment induced by scopolamine and MK801 through activation of cognate receptor-expressing neurons in the subiculum complex.	Scopolamine	74-85	neuropeptide S	Mus musculus	0-14
26323488-3	2016	The present study was undertaken to investigate effects of NPS on the scopolamine- or MK801-induced impairment of olfactory spatial memory using computer-assisted 4-hole-board spatial memory test, and by monitoring Fos expression in the subiculum complex in mice.	Scopolamine	70-81	neuropeptide S	Mus musculus	59-62
26323488-5	2016	Intracerebroventricular administration of NPS (0.5 nmol) significantly increased the number of visits to switched odorants in recall trial in mice suffering from odor-discriminating inability induced by scopolamine, a selective muscarinic cholinergic receptor antagonist, or MK801, a N-methyl-D-aspartate receptor antagonist, after training trials.	Scopolamine	203-214	neuropeptide S	Mus musculus	42-45
26323488-9	2016	The present findings demonstrate that NPS, via selective activation of the neurons bearing NPSR in the subiculum complex, ameliorates olfactory spatial memory impairment induced by scopolamine and MK801 in mice.	Scopolamine	181-192	neuropeptide S	Mus musculus	38-41
27168840-11	2016	To conclude, the expression levels of PAI-1 were significantly elevated in mice with scopolamine-induced cognitive impairment, which may be associated with the downregulation of miR-30b.	Scopolamine	85-96	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	38-43
27178852-9	2016	RESULTS: A statistically significant decrease in p13 latency was found after administration of scopolamine compared with baseline (14.46ms vs. 15.09ms, p=0.0049), with significant prolongation of the binaural average inter-latency in this group.	Scopolamine	95-106	H3 histone pseudogene 6	Homo sapiens	49-52
26703089-10	2016	Differential expression profiles of the immediate early gene cFos indicated hippocampal involvement in the inference process while localized microinfusions of the muscarinic antagonist, scopolamine, into the dorsal hippocampus caused rats to behave as if only one light was present.	Scopolamine	186-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-65
27133261-8	2016	D. superbus also inhibited AChE levels in the hippocampi of the scopolamine-injected mice.	Scopolamine	64-75	acetylcholinesterase	Mus musculus	27-31
27168840-11	2016	To conclude, the expression levels of PAI-1 were significantly elevated in mice with scopolamine-induced cognitive impairment, which may be associated with the downregulation of miR-30b.	Scopolamine	85-96	microRNA 30b	Mus musculus	178-185
27012214-4	2016	Further, memory deficit induced by scopolamine was restored by compound K, which did not inhibit acetylcholine esterase, in C57BL/6 mice but not in Nrf2 knockout mice as assessed by passive avoidance test, Y-maze and water maze tests, suggesting that scopolamine-induced memory impairment was overcome by the induction of Nrf2-mediated antioxidant enzymes by the compound K. Overall, our data indicate that compound K could be useful in prevention and treatment of reactive oxygen species-induced neurological disorders such as Alzheimer"s disease.	Scopolamine	35-46	nuclear factor, erythroid derived 2, like 2	Mus musculus	322-326
26646000-7	2016	Therefore, these findings suggest that P7C3 could improve the scopolamine-induced learning and memory impairment possibly through activation of BDNF signaling pathway, thereby exhibiting a cognition-enhancing potential.	Scopolamine	62-73	brain derived neurotrophic factor	Mus musculus	144-148
26677075-9	2016	BME administration also ameliorated scopolamine effect by down-regulating AChE and up-regulating BDNF, muscarinic M1 receptor and CREB expression in brain hippocampus confirms the potent neuroprotective role and these results are in corroboration with the earlier in vitro studies.	Scopolamine	36-47	acetylcholinesterase	Rattus norvegicus	74-78
26677075-9	2016	BME administration also ameliorated scopolamine effect by down-regulating AChE and up-regulating BDNF, muscarinic M1 receptor and CREB expression in brain hippocampus confirms the potent neuroprotective role and these results are in corroboration with the earlier in vitro studies.	Scopolamine	36-47	brain-derived neurotrophic factor	Rattus norvegicus	97-101
26677075-9	2016	BME administration also ameliorated scopolamine effect by down-regulating AChE and up-regulating BDNF, muscarinic M1 receptor and CREB expression in brain hippocampus confirms the potent neuroprotective role and these results are in corroboration with the earlier in vitro studies.	Scopolamine	36-47	cAMP responsive element binding protein 1	Rattus norvegicus	130-134
26946964-4	2016	It was found that 5-hydroxy-3-indoleacetic acid (5-HIAA), 3,4-dihydroxyphenylacetic acid, and homovanillic acid concentrations in the CSF of scopolamine-induced delirium rats were significantly increased, among which 5-HIAA was also increased in hippocampus and basolateral amygdala (BLA), and 5-HT(1A) receptor was significantly higher in the hippocampuses and BLA than other brain regions.	Scopolamine	141-152	5-hydroxytryptamine receptor 1A	Rattus norvegicus	294-301
26946964-7	2016	Altogether, these results suggest that delirium rats induced by scopolamine may be correlated with an increased cerebral concentration of 5-HT and dopamine neurotransmitters system; the selective 5-HT(1A) antagoniszts can reverse the delirium symptoms at some extent through tendering PI3K/Akt/mammalian target of rapamycin complex 1 (mTOR) activation-induced NLRP3 activity and then reducing IL-1beta release.	Scopolamine	64-75	mechanistic target of rapamycin kinase	Homo sapiens	335-339
26946964-7	2016	Altogether, these results suggest that delirium rats induced by scopolamine may be correlated with an increased cerebral concentration of 5-HT and dopamine neurotransmitters system; the selective 5-HT(1A) antagoniszts can reverse the delirium symptoms at some extent through tendering PI3K/Akt/mammalian target of rapamycin complex 1 (mTOR) activation-induced NLRP3 activity and then reducing IL-1beta release.	Scopolamine	64-75	5-hydroxytryptamine receptor 1A	Rattus norvegicus	196-203
26946964-7	2016	Altogether, these results suggest that delirium rats induced by scopolamine may be correlated with an increased cerebral concentration of 5-HT and dopamine neurotransmitters system; the selective 5-HT(1A) antagoniszts can reverse the delirium symptoms at some extent through tendering PI3K/Akt/mammalian target of rapamycin complex 1 (mTOR) activation-induced NLRP3 activity and then reducing IL-1beta release.	Scopolamine	64-75	NLR family pyrin domain containing 3	Homo sapiens	360-365
26946964-7	2016	Altogether, these results suggest that delirium rats induced by scopolamine may be correlated with an increased cerebral concentration of 5-HT and dopamine neurotransmitters system; the selective 5-HT(1A) antagoniszts can reverse the delirium symptoms at some extent through tendering PI3K/Akt/mammalian target of rapamycin complex 1 (mTOR) activation-induced NLRP3 activity and then reducing IL-1beta release.	Scopolamine	64-75	AKT serine/threonine kinase 1	Rattus norvegicus	290-293
26946964-7	2016	Altogether, these results suggest that delirium rats induced by scopolamine may be correlated with an increased cerebral concentration of 5-HT and dopamine neurotransmitters system; the selective 5-HT(1A) antagoniszts can reverse the delirium symptoms at some extent through tendering PI3K/Akt/mammalian target of rapamycin complex 1 (mTOR) activation-induced NLRP3 activity and then reducing IL-1beta release.	Scopolamine	64-75	interleukin 1 beta	Rattus norvegicus	393-401
26780350-9	2016	These results suggest that erucic acid has an ameliorative effect in mice with scopolamine-induced memory deficits and that the effect of erucic acid is partially due to the activation of PI3K-PKCzeta-ERK-CREB signaling as well as an increase in phosphorylated Akt in the hippocampus.	Scopolamine	79-90	protein kinase C, zeta	Mus musculus	193-200
26700245-6	2016	In Neuro2a cells with endogenous expression of PAC1 and its ligands, doxycycline not only promoted the proliferation of Neuro2a cells but also protected the cells from scopolamine induced apoptosis, which was inhibited by cAMP-PKA signal pathway inhibitor H-89, PAC1 shRNA or PACAP antagonist PACAP(6-38).	Scopolamine	168-179	adenylate cyclase activating polypeptide 1 receptor 1	Mus musculus	47-51
27023569-3	2016	In addition, fucoxanthin significantly reversed the scopolamine-induced increase of acetylcholinesterase (AChE) activity and decreased both choline acetyltransferase activity and brain-derived neurotrophic factor (BDNF) expression.	Scopolamine	52-63	acetylcholinesterase	Mus musculus	84-104
27023569-3	2016	In addition, fucoxanthin significantly reversed the scopolamine-induced increase of acetylcholinesterase (AChE) activity and decreased both choline acetyltransferase activity and brain-derived neurotrophic factor (BDNF) expression.	Scopolamine	52-63	acetylcholinesterase	Mus musculus	106-110
27023569-3	2016	In addition, fucoxanthin significantly reversed the scopolamine-induced increase of acetylcholinesterase (AChE) activity and decreased both choline acetyltransferase activity and brain-derived neurotrophic factor (BDNF) expression.	Scopolamine	52-63	brain derived neurotrophic factor	Mus musculus	214-218
26780350-9	2016	These results suggest that erucic acid has an ameliorative effect in mice with scopolamine-induced memory deficits and that the effect of erucic acid is partially due to the activation of PI3K-PKCzeta-ERK-CREB signaling as well as an increase in phosphorylated Akt in the hippocampus.	Scopolamine	79-90	mitogen-activated protein kinase 1	Mus musculus	201-204
26780350-9	2016	These results suggest that erucic acid has an ameliorative effect in mice with scopolamine-induced memory deficits and that the effect of erucic acid is partially due to the activation of PI3K-PKCzeta-ERK-CREB signaling as well as an increase in phosphorylated Akt in the hippocampus.	Scopolamine	79-90	cAMP responsive element binding protein 1	Mus musculus	205-209
26780350-9	2016	These results suggest that erucic acid has an ameliorative effect in mice with scopolamine-induced memory deficits and that the effect of erucic acid is partially due to the activation of PI3K-PKCzeta-ERK-CREB signaling as well as an increase in phosphorylated Akt in the hippocampus.	Scopolamine	79-90	thymoma viral proto-oncogene 1	Mus musculus	261-264
25216329-8	2016	These results suggest that fermented GT reduced scopolamine-induced amnesia in mice through AChE inhibition.	Scopolamine	48-59	acetylcholinesterase	Mus musculus	92-96
27556046-6	2016	STS decreased the activity of acetylcholinesterase (AChE) and increased the activity of choline acetyltransferase (ChAT) in the hippocampus and cortex of SCOP-treated mice.	Scopolamine	154-158	choline acetyltransferase	Mus musculus	88-113
27556046-6	2016	STS decreased the activity of acetylcholinesterase (AChE) and increased the activity of choline acetyltransferase (ChAT) in the hippocampus and cortex of SCOP-treated mice.	Scopolamine	154-158	choline acetyltransferase	Mus musculus	115-119
26497539-10	2016	The adverse effect of scopolamine on the task was attenuated in apoE4 mice compared to apoE2 and apoE3.	Scopolamine	22-33	apolipoprotein E	Homo sapiens	64-69
26685899-0	2015	alpha-Melanocyte-stimulating hormone ameliorates ocular surface dysfunctions and lesions in a scopolamine-induced dry eye model via PKA-CREB and MEK-Erk pathways.	Scopolamine	94-105	proopiomelanocortin	Rattus norvegicus	0-36
26685899-0	2015	alpha-Melanocyte-stimulating hormone ameliorates ocular surface dysfunctions and lesions in a scopolamine-induced dry eye model via PKA-CREB and MEK-Erk pathways.	Scopolamine	94-105	cAMP responsive element binding protein 1	Rattus norvegicus	136-140
26685899-0	2015	alpha-Melanocyte-stimulating hormone ameliorates ocular surface dysfunctions and lesions in a scopolamine-induced dry eye model via PKA-CREB and MEK-Erk pathways.	Scopolamine	94-105	Eph receptor B1	Rattus norvegicus	149-152
26685899-4	2015	Here we applied alpha-Melanocyte-stimulating hormone (alpha-MSH) twice a day to the ocular surface of a scopolamine-induced dry eye rat model.	Scopolamine	104-115	proopiomelanocortin	Rattus norvegicus	16-52
26685899-4	2015	Here we applied alpha-Melanocyte-stimulating hormone (alpha-MSH) twice a day to the ocular surface of a scopolamine-induced dry eye rat model.	Scopolamine	104-115	proopiomelanocortin	Rattus norvegicus	54-63
26481535-0	2015	The effect of GABA transporter 1 (GAT1) inhibitor, tiagabine, on scopolamine-induced memory impairments in mice.	Scopolamine	65-76	solute carrier family 6 (neurotransmitter transporter, GABA), member 1	Mus musculus	14-32
26670184-4	2016	Likewise, both PDE5-I and PDE4-I reversed the scopolamine deficit model when administered within 2 min after the learning trial.	Scopolamine	46-57	phosphodiesterase 5A	Homo sapiens	15-19
26408985-9	2015	Additionally, it prevented against scopolamine-induced expression of iNOS and COX-2.	Scopolamine	35-46	nitric oxide synthase 2, inducible	Mus musculus	69-73
26408985-9	2015	Additionally, it prevented against scopolamine-induced expression of iNOS and COX-2.	Scopolamine	35-46	cytochrome c oxidase II, mitochondrial	Mus musculus	78-83
26315944-6	2015	We also found that the increase in the number of oligodendrocytes observed following donepezil treatment was significantly inhibited by the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine, but not by the muscarinic acetylcholine receptor antagonist scopolamine.	Scopolamine	266-277	cholinergic receptor nicotinic alpha 4 subunit	Homo sapiens	140-172
26315944-6	2015	We also found that the increase in the number of oligodendrocytes observed following donepezil treatment was significantly inhibited by the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine, but not by the muscarinic acetylcholine receptor antagonist scopolamine.	Scopolamine	266-277	cholinergic receptor nicotinic alpha 4 subunit	Homo sapiens	174-179
26481535-0	2015	The effect of GABA transporter 1 (GAT1) inhibitor, tiagabine, on scopolamine-induced memory impairments in mice.	Scopolamine	65-76	solute carrier family 6 (neurotransmitter transporter, GABA), member 1	Mus musculus	34-38
26400617-10	2015	CONCLUSIONS: Taken together, our results suggested that the hydroalcoholic extract of Emilia coccinae ameliorated the cognitive dysfunction in scopolamine treated rats through the blockage of the oxidative effect of scopolamine and inhibition of AChE activity.	Scopolamine	143-154	acetylcholinesterase	Rattus norvegicus	246-250
26463268-5	2015	By using scopolamine-induced rats and APPswe mice representing AD-like cholinergic deficits and amyloidosis, respectively, we found that intraperitoneal administration of the peptide significantly improved spatial memory with activation of the TrkB/ERK1/2/Akt pathway and restoration of several memory-associated proteins in both models.	Scopolamine	9-20	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	244-248
26102021-1	2015	Clinical studies demonstrate that scopolamine, a non-selective muscarinic acetylcholine receptor (mAchR) antagonist, produces rapid therapeutic effects in depressed patients, and preclinical studies report that the actions of scopolamine require glutamate receptor activation and the mechanistic target of rapamycin complex 1 (mTORC1).	Scopolamine	34-45	CREB regulated transcription coactivator 1	Mus musculus	327-333
26102021-1	2015	Clinical studies demonstrate that scopolamine, a non-selective muscarinic acetylcholine receptor (mAchR) antagonist, produces rapid therapeutic effects in depressed patients, and preclinical studies report that the actions of scopolamine require glutamate receptor activation and the mechanistic target of rapamycin complex 1 (mTORC1).	Scopolamine	226-237	CREB regulated transcription coactivator 1	Mus musculus	327-333
26102021-2	2015	The present study extends these findings to determine the role of the medial prefrontal cortex (mPFC) and specific muscarinic acetylcholine receptor (M-AchR) subtypes in the actions of scopolamine.	Scopolamine	185-196	complement factor properdin	Mus musculus	96-100
26102021-3	2015	The administration of scopolamine increases the activity marker Fos in the mPFC, including the infralimbic (IL) and prelimbic (PrL) subregions.	Scopolamine	22-33	complement factor properdin	Mus musculus	75-79
26102021-7	2015	Taken together, these findings indicate that mPFC is a critical mediator of the behavioral actions of scopolamine and identify the M1-AChR as a therapeutic target for the development of novel and selective rapid-acting antidepressants.	Scopolamine	102-113	complement factor properdin	Mus musculus	45-49
26352794-6	2015	Statistical analysis of the temporospatial factor scores indicated that in most conditions the amplitude of the classic P300 was increased by clonidine and scopolamine.	Scopolamine	156-167	E1A binding protein p300	Homo sapiens	120-124
26233262-11	2015	When participants were classified as having an abnormal response to scopolamine (based on change score at 5-hours post dose >0), 100% were correctly classified as Abeta+ and 67% as Abeta-.	Scopolamine	68-79	amyloid beta precursor protein	Homo sapiens	163-168
26233262-11	2015	When participants were classified as having an abnormal response to scopolamine (based on change score at 5-hours post dose >0), 100% were correctly classified as Abeta+ and 67% as Abeta-.	Scopolamine	68-79	amyloid beta precursor protein	Homo sapiens	181-186
24390152-4	2015	Here, we discuss the modulatory capacity of stress and corticosteroid hormones on hippocampal plasticity and neuronal viability in late life depression as well as the anti-depressive of ketamine and scopolamine mediated by stimulation of the mammalian target of rapamycin, increased inhibitory phosphorylation of GSK-3beta, and increased synaptogenesis.	Scopolamine	199-210	mechanistic target of rapamycin kinase	Homo sapiens	242-271
26168780-5	2015	Decreased activities of superoxide dismutase, glutathione peroxidase and catalase along with increase of acetylcholinesterase activity and decrease of total content of reduced glutathione were observed in the rat hippocampal homogenates of scopolamine-treated animals as compared with control.	Scopolamine	240-251	acetylcholinesterase	Rattus norvegicus	105-125
23406953-7	2015	Scopolamine (2 mg/kg ip) group showed significant increase in AChE reactivity and glutamate level and reduced monoamines (norepinephrine, dopamine and serotonin) and gamma-aminobutyric acid contents in cortex, hippocampus and striatum.	Scopolamine	0-11	acetylcholinesterase	Rattus norvegicus	62-66
26317078-0	2015	A comparative study of neuroprotective effect of angiotensin converting enzyme inhibitors against scopolamine-induced memory impairments in rats.	Scopolamine	98-109	angiotensin I converting enzyme	Rattus norvegicus	49-78
26191403-0	2015	Discovery of a low affinity thyrotropin-releasing hormone (TRH)-like peptide that exhibits potent inhibition of scopolamine-induced memory impairment in mice.	Scopolamine	112-123	thyrotropin releasing hormone	Mus musculus	28-57
26191403-0	2015	Discovery of a low affinity thyrotropin-releasing hormone (TRH)-like peptide that exhibits potent inhibition of scopolamine-induced memory impairment in mice.	Scopolamine	112-123	thyrotropin releasing hormone	Mus musculus	59-62
25982413-5	2015	Scopolamine administration drastically up-regulated DNA methyltransferases (DNMT1) and HDAC2 expression while CREB-binding protein (CBP), DNMT3a and DNMT3b remained unaffected.	Scopolamine	0-11	DNA methyltransferase 1	Homo sapiens	76-81
25982413-5	2015	Scopolamine administration drastically up-regulated DNA methyltransferases (DNMT1) and HDAC2 expression while CREB-binding protein (CBP), DNMT3a and DNMT3b remained unaffected.	Scopolamine	0-11	histone deacetylase 2	Homo sapiens	87-92
25982413-8	2015	Taken together, we showed for the first time that scopolamine-induced up-regulation of chromatin-modifying enzymes, HDAC2 and DNMT1, leads to gene expression changes and consequent decline in memory consolidation.	Scopolamine	50-61	histone deacetylase 2	Homo sapiens	116-121
25982413-8	2015	Taken together, we showed for the first time that scopolamine-induced up-regulation of chromatin-modifying enzymes, HDAC2 and DNMT1, leads to gene expression changes and consequent decline in memory consolidation.	Scopolamine	50-61	DNA methyltransferase 1	Homo sapiens	126-131
25982413-10	2015	We propose the following putative pathway for scopolamine-mediated memory impairment; scopolamine up-regulates hippocampal DNMT1 and HDAC2 expression, induces methylation and deacetylation of BDNF and Arc promoter, represses gene expression and eventually impairs memory consolidation.	Scopolamine	46-57	DNA methyltransferase 1	Homo sapiens	123-128
25982413-10	2015	We propose the following putative pathway for scopolamine-mediated memory impairment; scopolamine up-regulates hippocampal DNMT1 and HDAC2 expression, induces methylation and deacetylation of BDNF and Arc promoter, represses gene expression and eventually impairs memory consolidation.	Scopolamine	46-57	histone deacetylase 2	Homo sapiens	133-138
25982413-10	2015	We propose the following putative pathway for scopolamine-mediated memory impairment; scopolamine up-regulates hippocampal DNMT1 and HDAC2 expression, induces methylation and deacetylation of BDNF and Arc promoter, represses gene expression and eventually impairs memory consolidation.	Scopolamine	46-57	brain derived neurotrophic factor	Homo sapiens	192-196
25982413-10	2015	We propose the following putative pathway for scopolamine-mediated memory impairment; scopolamine up-regulates hippocampal DNMT1 and HDAC2 expression, induces methylation and deacetylation of BDNF and Arc promoter, represses gene expression and eventually impairs memory consolidation.	Scopolamine	86-97	DNA methyltransferase 1	Homo sapiens	123-128
25982413-10	2015	We propose the following putative pathway for scopolamine-mediated memory impairment; scopolamine up-regulates hippocampal DNMT1 and HDAC2 expression, induces methylation and deacetylation of BDNF and Arc promoter, represses gene expression and eventually impairs memory consolidation.	Scopolamine	86-97	histone deacetylase 2	Homo sapiens	133-138
25982413-10	2015	We propose the following putative pathway for scopolamine-mediated memory impairment; scopolamine up-regulates hippocampal DNMT1 and HDAC2 expression, induces methylation and deacetylation of BDNF and Arc promoter, represses gene expression and eventually impairs memory consolidation.	Scopolamine	86-97	brain derived neurotrophic factor	Homo sapiens	192-196
25982413-12	2015	We elucidate the action of scopolamine as an epigenetic modulator and hope that DNMT1 and HDAC2 would be ideal therapeutic targets for memory disorders.	Scopolamine	27-38	histone deacetylase 2	Homo sapiens	90-95
25974329-7	2015	Pretreatment with PNE increased the proliferating cells and immature neurons against hippocampal neurogenesis suppressed by scopolamine, which was confirmed by ki67- and DCX-positive stained cells.	Scopolamine	124-135	antigen identified by monoclonal antibody Ki 67	Mus musculus	160-164
25974329-7	2015	Pretreatment with PNE increased the proliferating cells and immature neurons against hippocampal neurogenesis suppressed by scopolamine, which was confirmed by ki67- and DCX-positive stained cells.	Scopolamine	124-135	doublecortin	Mus musculus	170-173
27307953-4	2015	Therefore the present study was designed to investigate the effects of walnuts consumption (2%, 6% and 9% walnut diets) on memory enhancement and acetylcholinesterase (AChE) activity of brain in scopolamine-induced amnesic rats.	Scopolamine	195-206	acetylcholinesterase	Rattus norvegicus	146-166
27307953-7	2015	Moreover, the potential of walnuts to prevent scopolamine neurotoxicity was also reflected by the decreased AChE activity in the whole brain in comparison with the scopolamine group.	Scopolamine	46-57	acetylcholinesterase	Rattus norvegicus	108-112
27307953-4	2015	Therefore the present study was designed to investigate the effects of walnuts consumption (2%, 6% and 9% walnut diets) on memory enhancement and acetylcholinesterase (AChE) activity of brain in scopolamine-induced amnesic rats.	Scopolamine	195-206	acetylcholinesterase	Rattus norvegicus	168-172
25705233-6	2015	Mice that received scopolamine alone showed impairments in acquisition and retention in Morris water maze task and increased activity of AChE in the hippocampus.	Scopolamine	19-30	acetylcholinesterase	Mus musculus	137-141
25837935-0	2015	Novel 5-HT5A receptor antagonists ameliorate scopolamine-induced working memory deficit in mice and reference memory impairment in aged rats.	Scopolamine	45-56	5-hydroxytryptamine receptor 5A	Rattus norvegicus	6-12
25546299-12	2015	Furthermore, scopolamine-induced oxidative damage of neurons in hippocampal CA1 and CA3 regions were prevented by DBE treatment.	Scopolamine	13-24	carbonic anhydrase 1	Mus musculus	76-79
25546299-12	2015	Furthermore, scopolamine-induced oxidative damage of neurons in hippocampal CA1 and CA3 regions were prevented by DBE treatment.	Scopolamine	13-24	carbonic anhydrase 3	Mus musculus	84-87
25705233-7	2015	Mice that received F. mume and scopolamine showed no scopolamine-induced memory impairment and increased activity of AChE.	Scopolamine	31-42	acetylcholinesterase	Mus musculus	117-121
26635888-6	2015	In addition, Western blot analysis and Immunohistochemistry revealed that AEM reversed scopolamine-decreased phosphorylation of Akt and extracellular signal-regulated kinase (ERK).	Scopolamine	87-98	thymoma viral proto-oncogene 1	Mus musculus	128-131
26635888-6	2015	In addition, Western blot analysis and Immunohistochemistry revealed that AEM reversed scopolamine-decreased phosphorylation of Akt and extracellular signal-regulated kinase (ERK).	Scopolamine	87-98	mitogen-activated protein kinase 1	Mus musculus	136-173
26635888-6	2015	In addition, Western blot analysis and Immunohistochemistry revealed that AEM reversed scopolamine-decreased phosphorylation of Akt and extracellular signal-regulated kinase (ERK).	Scopolamine	87-98	mitogen-activated protein kinase 1	Mus musculus	175-178
26413117-0	2015	A Special Extract of Bacopa monnieri (CDRI-08) Restores Learning and Memory by Upregulating Expression of the NMDA Receptor Subunit GluN2B in the Brain of Scopolamine-Induced Amnesic Mice.	Scopolamine	155-166	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	132-138
26413117-1	2015	In the present communication, we have investigated effects of the CDRI-08, a well characterized extract of Bacopa monnieri, on expression of the GluN2B subunit of NMDAR in various brain regions of the scopolamine-induced amnesic mice.	Scopolamine	201-212	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	145-151
26413117-3	2015	Our RT-PCR and immunoblotting data revealed that the scopolamine treatment resulted in a significant downregulation of the NMDAR GluN2B subunit expression in prefrontal cortex and hippocampus.	Scopolamine	53-64	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	129-135
26413117-5	2015	Further, oral administration of the CDRI-08 to scopolamine-treated amnesic mice restored the spatial memory which was found to be associated with significant upregulation of the GluN2B subunit expression and decline in the acetylcholinesterase activity in prefrontal cortex as well as hippocampus towards their levels in the normal control mice.	Scopolamine	47-58	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	178-184
26413129-6	2015	Pre- and postadministration of CDRI-08 ameliorated amnesic effect of scopolamine by decreasing acetyl cholinesterase activity and drastically upregulating the mRNA and protein expression of BDNF, Arc, and GFAP in mouse cerebrum.	Scopolamine	69-80	brain derived neurotrophic factor	Mus musculus	190-194
26413129-6	2015	Pre- and postadministration of CDRI-08 ameliorated amnesic effect of scopolamine by decreasing acetyl cholinesterase activity and drastically upregulating the mRNA and protein expression of BDNF, Arc, and GFAP in mouse cerebrum.	Scopolamine	69-80	glial fibrillary acidic protein	Mus musculus	205-209