PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33182055-8 2020 However, a nAChR antagonist, mecamylamine, strongly inhibited the expression of these genes. Mecamylamine 29-41 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 11-16 34038754-5 2021 Nicotine withdrawal symptoms were precipitated by an acute injection of mecamylamine, a nonspecific nAChR antagonist, following chronic nicotine consumption. Mecamylamine 72-84 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 100-105 32726882-11 2021 Furthermore, the effects of sinomenine were abolished by the alpha7 nAChR antagonist mecamylamine and the allosteric modulator PNU-120596, but no change occurred when the mice were pretreated with the muscarinic acetylcholine receptor antagonist atropine. Mecamylamine 85-97 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 61-73 33414685-12 2020 Scratch-wound assay showed marked reduction in proliferation/migration of nicotine and palmitate-treated breast cancer cells with mecamylamine (MEC), a nicotine acetylcholine receptor (nAchR) antagonist. Mecamylamine 130-142 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 152-183 33414685-12 2020 Scratch-wound assay showed marked reduction in proliferation/migration of nicotine and palmitate-treated breast cancer cells with mecamylamine (MEC), a nicotine acetylcholine receptor (nAchR) antagonist. Mecamylamine 130-142 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 185-190 33414685-12 2020 Scratch-wound assay showed marked reduction in proliferation/migration of nicotine and palmitate-treated breast cancer cells with mecamylamine (MEC), a nicotine acetylcholine receptor (nAchR) antagonist. Mecamylamine 144-147 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 152-183 33414685-12 2020 Scratch-wound assay showed marked reduction in proliferation/migration of nicotine and palmitate-treated breast cancer cells with mecamylamine (MEC), a nicotine acetylcholine receptor (nAchR) antagonist. Mecamylamine 144-147 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 185-190 32959891-8 2020 The nicotine-effect was abolished by the nAChR inhibitor mecamylamine. Mecamylamine 57-69 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 41-46 32304995-5 2020 Nicotine-induced PTS acceleration was sensitive to the general nAChR inhibitors mecamylamine and d-tubocurarine as well as to the alpha3beta4-nAChR antagonist alpha-conotoxin AulB, but not to other antagonists primarily addressing alpha3beta2-nAChR or alpha4-, alpha7- and alpha9-containing nAChR. Mecamylamine 80-92 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 63-68 32691528-8 2020 Furthermore, the nonselective nAChR antagonist, mecamylamine, reversed nicotine effects on sociability and increased repetitive behaviors in BTBR T + tf/J mice. Mecamylamine 48-60 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 30-35 30062776-9 2018 We observed that short- and long-term nicotine/cotinine exposure significantly decreased neuronal glucose utilization in ischemic conditions and the non-specific nAChR antagonist, mecamylamine reversed this effect. Mecamylamine 180-192 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 162-167 32092237-0 2020 Unexpected loss of sensitivity to the nicotinic acetylcholine receptor antagonist activity of mecamylamine and dihydro-beta-erythroidine in nicotine-tolerant mice. Mecamylamine 94-106 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 38-70 29549391-3 2018 OBJECTIVES: This study aimed to investigate the impact of alpha7 nAChR pharmacological modulation on mecamylamine-precipitated nicotine withdrawal behaviors in mice by using positive allosteric modulators (PAMs). Mecamylamine 101-113 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 58-70 29549391-8 2018 Nicotine withdrawal signs were precipitated upon administration of the non-selective nAChR antagonist mecamylamine (3.5 mg/kg, i.p.). Mecamylamine 102-114 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 85-90 29549391-12 2018 CONCLUSIONS: Taken together, our results suggest that modulation of the alpha7 nAChR can play important roles in mecamylamine-precipitated nicotine withdrawal behaviors in mice. Mecamylamine 113-125 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 72-84 26471256-5 2016 Local infusion of the non-competitive non-selective nAChR antagonist mecamylamine or viral-mediated downregulation of the beta2 or alpha7 nAChR subunit in the amygdala all induced robust anxiolytic- and antidepressant-like effects in several mouse behavioral models. Mecamylamine 69-81 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 52-57 28398760-3 2017 To neutralize the effects of nicotine in CS extract, we used a competitive inhibitor to the nicotinic acetylcholine receptor (nAChR)-mecamylamine-as well as macrophages derived from mice with genetic disruption of specific subunits of nAChR. Mecamylamine 133-145 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 92-124 28398760-3 2017 To neutralize the effects of nicotine in CS extract, we used a competitive inhibitor to the nicotinic acetylcholine receptor (nAChR)-mecamylamine-as well as macrophages derived from mice with genetic disruption of specific subunits of nAChR. Mecamylamine 133-145 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 126-131 28271317-11 2017 Mecamylamine abolished the reduction of DAI, MPO activity and IL-6 by AN917 and rivastigmine, indicating they were mediated by alpha7nAChR. Mecamylamine 0-12 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 127-138 28457878-11 2017 Importantly, treatment of control and BCCAO mice with the non-selective nAChR antagonist mecamylamine (MEC: 1.0 mg/kg, i.p.) Mecamylamine 89-101 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 72-77 26921469-11 2016 The general nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine blocked the decline in LIDs with longer optical pulses showing it was nAChR-mediated. Mecamylamine 64-76 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 12-44 26921469-11 2016 The general nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine blocked the decline in LIDs with longer optical pulses showing it was nAChR-mediated. Mecamylamine 64-76 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 46-51 26921469-11 2016 The general nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine blocked the decline in LIDs with longer optical pulses showing it was nAChR-mediated. Mecamylamine 64-76 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 147-152 26999808-7 2016 The effect of NNK on MTPPT function is mediated through the nonneuronal alpha7-nicotinic acetylcholine receptor (alpha7-nAChR), as indicated by both in vitro (using the nAChR antagonist mecamylamine) and in vivo (using an alpha7-nAchR(-/-) mouse model) studies. Mecamylamine 186-198 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 72-111 26999808-7 2016 The effect of NNK on MTPPT function is mediated through the nonneuronal alpha7-nicotinic acetylcholine receptor (alpha7-nAChR), as indicated by both in vitro (using the nAChR antagonist mecamylamine) and in vivo (using an alpha7-nAchR(-/-) mouse model) studies. Mecamylamine 186-198 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 113-125 26471256-5 2016 Local infusion of the non-competitive non-selective nAChR antagonist mecamylamine or viral-mediated downregulation of the beta2 or alpha7 nAChR subunit in the amygdala all induced robust anxiolytic- and antidepressant-like effects in several mouse behavioral models. Mecamylamine 69-81 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 131-143 26775017-4 2016 The present study was designed to examine the effects of nicotine withdrawal induced by mecamylamine, a non-specific nicotinic receptor (nAChR) antagonist, on cognitive control processes in mice using an operant strategy switching task. Mecamylamine 88-100 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 137-142 26361040-8 2015 The effects of SS on apoptosis were attenuated by the nAChR antagonist mecamylamine. Mecamylamine 71-83 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 54-59 26256075-2 2015 In mouse studies, nonselective nAChR antagonist mecamylamine blocks cocaine-induced conditioned place preference (CPP) and behavioral sensitization. Mecamylamine 48-60 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 31-36 25813704-10 2015 However, the nAChR antagonist mecamylamine (1mg/kg ip 30min before l-dopa) reduced l-dopa-induced AIMs in both alpha6L9S and WT mice. Mecamylamine 30-42 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 13-18 24643637-7 2014 Furthermore, the nonspecific nAChR antagonist mecamylamine (2 mg/kg) blocked the effects of ethanol in the core in vivo. Mecamylamine 46-58 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 29-34 24800895-8 2014 The nAChR antagonist mecamylamine (3.2 mg/kg) antagonized the discriminative stimulus effects of epibatidine and RTI-7527-102, as well as the hypothermic effects of every drug except cytisine. Mecamylamine 21-33 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 4-9 25430056-5 2015 Nicotine induced dose- and time-dependent upregulation of IP3 R-1 protein following its mRNA increase, and the latter was significantly suppressed by a nonselective nicotinic acetylcholine receptors (nAChR) antagonist, mecamylamine. Mecamylamine 219-231 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 165-198 25430056-5 2015 Nicotine induced dose- and time-dependent upregulation of IP3 R-1 protein following its mRNA increase, and the latter was significantly suppressed by a nonselective nicotinic acetylcholine receptors (nAChR) antagonist, mecamylamine. Mecamylamine 219-231 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 200-205 22932776-10 2013 The galantamine-induced increase in the hippocampal IGF2 mRNA levels was blocked by mecamylamine, a nonselective nicotinic acetylcholine (ACh) receptor (nAChR) antagonist, and methyllycaconitine, a selective alpha7 nAChR antagonist, but not by telenzepine, a preferential M(1) muscarinic ACh receptor antagonist. Mecamylamine 84-96 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 153-158 23958450-7 2013 Additionally, CHT+/- mice displayed greater SAT-disrupting effects of reverse dialysis of the nAChR antagonist mecamylamine. Mecamylamine 111-123 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 94-99 23958943-3 2013 MATERIALS AND METHODS: Effects of acute (0.03125-0.5 mg/kg SC) or chronic (24 mg/kg per day; osmotic minipump) nicotine and mecamylamine-precipitated withdrawal on intracranial self-stimulation (ICSS) thresholds were assessed in wild-type and alpha5 nAChR subunit knockout mice. Mecamylamine 124-136 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 250-255 23757602-6 2013 Importantly, concomitant exposure to SS and the nAChR antagonist mecamylamine during gestation blocked the development of BPD. Mecamylamine 65-77 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 48-53 23995055-4 2013 The nicotine-induced (1.0 mg/kg, s.c.) improvement was significantly abolished by the nAChR antagonist mecamylamine (1.0 mg/kg, i.p.). Mecamylamine 103-115 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 86-91 22614008-4 2013 This nicotine-mediated MUC4 overexpression was via the alpha7 subunit of nicotinic acetylcholine receptor (nAChR) stimulation and subsequent activation of the JAK2/STAT3 downstream signaling cascade in cooperation with the MEK/ERK1/2 pathway; this effect was blocked by the alpha7nAChR antagonists, alpha-bungarotoxin and mecamylamine, and by specific siRNA-mediated STAT3 inhibition. Mecamylamine 322-334 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 107-112 22932776-10 2013 The galantamine-induced increase in the hippocampal IGF2 mRNA levels was blocked by mecamylamine, a nonselective nicotinic acetylcholine (ACh) receptor (nAChR) antagonist, and methyllycaconitine, a selective alpha7 nAChR antagonist, but not by telenzepine, a preferential M(1) muscarinic ACh receptor antagonist. Mecamylamine 84-96 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 208-220 22506481-4 2012 Acetylcholine-evoked [(3) H]-GABA release from SuSC crude synaptosomal preparations is calcium dependent, blocked by the voltage-sensitive calcium channel blocker, cadmium, and the nAChR antagonist mecamylamine, but is unaffected by muscarinic, glutamatergic, P2X and 5-HT3 receptor antagonists. Mecamylamine 198-210 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 181-186 22480510-9 2012 The general nAChR inhibitor mecamylamine enhances muscarinic and purinergic responses. Mecamylamine 28-40 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 12-17 22138237-7 2012 The effect of nicotine on weight loss in mice on an HFD was completely blocked by mecamylamine, a nonselective nicotinic acetylcholine receptor (nAChR) antagonist, but only partially blocked by the alpha4beta2 nAChR partial agonist/antagonist, varenicline. Mecamylamine 82-94 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 111-143 22009521-6 2012 Administration of a low dose of the nAChR antagonist mecamylamine induced threshold elevations in alpha7(-/-), but not alpha7(+/+), mice, whereas the highest dose tested only elevated thresholds in alpha7(+/+) mice. Mecamylamine 53-65 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 36-41 22009521-6 2012 Administration of a low dose of the nAChR antagonist mecamylamine induced threshold elevations in alpha7(-/-), but not alpha7(+/+), mice, whereas the highest dose tested only elevated thresholds in alpha7(+/+) mice. Mecamylamine 53-65 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 98-104 22009521-10 2012 The mecamylamine-precipitated withdrawal data suggest that compensatory adaptations may occur in constitutive alpha7(-/-) mice or that mecamylamine may interact with other receptors besides nAChRs in these mice. Mecamylamine 4-16 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 110-116 22241831-8 2012 Effects of the highest dose studied were blocked by mecamylamine (general nAChR antagonist) and partially antagonized by hexamethonium (largely peripheral nAChR antagonist). Mecamylamine 52-64 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 74-79 22138237-7 2012 The effect of nicotine on weight loss in mice on an HFD was completely blocked by mecamylamine, a nonselective nicotinic acetylcholine receptor (nAChR) antagonist, but only partially blocked by the alpha4beta2 nAChR partial agonist/antagonist, varenicline. Mecamylamine 82-94 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 145-150 22138237-7 2012 The effect of nicotine on weight loss in mice on an HFD was completely blocked by mecamylamine, a nonselective nicotinic acetylcholine receptor (nAChR) antagonist, but only partially blocked by the alpha4beta2 nAChR partial agonist/antagonist, varenicline. Mecamylamine 82-94 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 210-215 21487659-5 2011 The role of beta2* nAChRs was confirmed by results showing: (1) reversal of sazetidine"s antidepressant-like effects in the forced swim test by nAChR antagonists mecamylamine and dihydro-beta-erythroidine; (2) absence of sazetidine"s effect in mice lacking the beta2 subunit of the nAChR; and (3) a high correspondence between behaviorally active doses of sazetidine and beta2* receptor occupancy. Mecamylamine 162-174 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 144-149 21640128-5 2011 The nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine decreased responding for nicotine, but not food rewards, verifying that nAChRs regulate nicotine self-administration in mice. Mecamylamine 56-68 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 4-36 21640128-5 2011 The nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine decreased responding for nicotine, but not food rewards, verifying that nAChRs regulate nicotine self-administration in mice. Mecamylamine 56-68 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 38-43 20580908-3 2010 Recently, it is demonstrated that mecamylamine, a nAChR antagonist blocks cocaine-, d-amphetamine-, ephedrine-, nicotine-, and methylphenidate-induced psychomotor sensitization. Mecamylamine 34-46 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 50-55 20933579-5 2010 treatment with the non-selective centrally active nAChR antagonist, mecamylamine decreased fasting-induced food intake in both mice and rats. Mecamylamine 68-80 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 50-55 20168214-2 2010 Therefore, this study evaluated the effects of mecamylamine, a nAChR antagonist, on ethanol withdrawal signs. Mecamylamine 47-59 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 63-68 20168214-7 2010 In addition, chronic administration of mecamylamine into ethanol diet-fed mice markedly attenuated the ethanol withdrawal sign scores, thus supporting the contention that nAChR is involved in ethanol dependence. Mecamylamine 39-51 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 171-176 20168214-8 2010 In conclusion, our results suggest that mecamylamine exhibited inhibitory effects on ethanol withdrawal signs which could be mediated through nAChR. Mecamylamine 40-52 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 142-147 18786574-2 2009 In rodents, antidepressant-like effects of both nicotine and the non-selective nAChR antagonist mecamylamine have been reported. Mecamylamine 96-108 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 79-84 19501109-3 2009 The current studies examined the influence of the nAChR antagonist mecamylamine (MEC) on operant ethanol self-administration using a procedure that independently assessed appetitive and consumptive processes, and compared these findings to effects of MEC on sucrose self-administration. Mecamylamine 81-84 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 50-55 17666046-5 2007 Nicotine-induced ERK phosphorylation was inhibited by high concentrations of mecamylamine, however it was not blocked by other broad nicotinic acetylcholine receptor (nAChR) inhibitors (including hexamethonium and chlorisondamine) or nAChR subtype selective inhibitors (such as methyllycaconitine, alpha-bungarotoxin, dihydro-beta-erythroidine, and alpha-conotoxin Au1B). Mecamylamine 77-89 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 234-239 18452957-3 2008 Nicotine withdrawal was induced by termination of chronic nicotine delivery through osmotic minipumps or precipitated with the nicotinic acetylcholine receptor (nAChR) antagonists mecamylamine or dihydro-beta-erythroidine (DHbetaE). Mecamylamine 180-192 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 127-159 18452957-3 2008 Nicotine withdrawal was induced by termination of chronic nicotine delivery through osmotic minipumps or precipitated with the nicotinic acetylcholine receptor (nAChR) antagonists mecamylamine or dihydro-beta-erythroidine (DHbetaE). Mecamylamine 180-192 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 161-166 18385094-6 2008 RESULTS: Several nAChR isoforms were identified in retinal and choroidal microvascular endothelial cells, and the ability of these cells to form tubules when grown in growth factor-reduced basement membrane matrix and supplemented with VEGF was suppressed by the nAChR antagonist mecamylamine. Mecamylamine 280-292 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 17-22 17920082-5 2007 A single intraperitoneal injection of the nAChR antagonists mecamylamine (MEC) or methyllycaconitine (MLA) was used to precipitate withdrawal. Mecamylamine 60-72 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 42-47 17920082-5 2007 A single intraperitoneal injection of the nAChR antagonists mecamylamine (MEC) or methyllycaconitine (MLA) was used to precipitate withdrawal. Mecamylamine 74-77 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 42-47 17632185-8 2007 The synergistic behavioral effect was abolished by a dopamine-D1 receptor antagonist, SCH 23390, and a nAChR antagonist, mecamylamine, but not a muscarinic AChR (mAChR) antagonist, scopolamine. Mecamylamine 121-133 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 103-108 15356218-8 2005 In that respect, dextrometorphan seems to behave as another mecamylamine, a noncompetitive nicotinic receptor antagonist with a preferential activity to alpha(3)beta(4)(*) neuronal nAChR subtypes. Mecamylamine 60-72 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 181-186 17133263-5 2007 The effects of nicotine on the extracellular dopamine release were potentiated by galantamine, but antagonized by mecamylamine, a nAChR antagonist. Mecamylamine 114-126 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 130-135 17016705-3 2006 OBJECTIVES: We determined whether the noncompetitive nAChR antagonist mecamylamine had antidepressant-like effects in the forced swim test (FST) and tail suspension test (TST). Mecamylamine 70-82 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 53-58 16781069-5 2006 injection of non-selective nAChR antagonist mecamylamine and alpha4beta2 subtype-selective antagonist dihydro-beta-erythroidine (DHbetaE) dose-dependently induced thermal and mechanical hyperalgesia in mice while the alpha7-selective antagonist methyllycaconitine (MLA) had no effect. Mecamylamine 44-56 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 27-32 12551757-6 2002 Mecamylamine (negative allosteric modulator of nAChR; 2.0 mg/kg, i.p.) Mecamylamine 0-12 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 47-52 15522249-2 2004 METHODS: Antidepressant properties of the noncompetitive nAChR antagonist mecamylamine in the forced swim test were tested alone and in combination with the tricyclic antidepressant amitriptyline. Mecamylamine 74-86 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 57-62 7913497-6 1994 The memory-enhancing effect of ABT 418 was prevented by the nAChR channel blocker, mecamylamine. Mecamylamine 83-95 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 60-65 9084060-4 1997 The (-)-nicotine (1.0 mg/kg)-induced changes in monoamine turnover were blocked by pretreatment with the centrally acting nACh-R channel blocker mecamylamine (2.0 mg/kg i.p.) Mecamylamine 145-157 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 122-128 9084060-10 1997 Pretreatment with mecamylamine completely blocked the THA-induced increase in NA and 5-HT turnover, but not in DA turnover, suggesting that the nACh-R system is involved in the THA-induced increase in brain NA and 5-HT turnover. Mecamylamine 18-30 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 144-150 7965777-7 1994 Both functional effects were blocked by the nAChR channel blocker, mecamylamine (100 microM). Mecamylamine 67-79 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 44-49 34193682-5 2021 Intra-mPFC infusion of mecamylamine, a non-selective nicotinic acetylcholine receptor (nAChR) antagonist, 5 min before nicotine administration blocked the effect of nicotine. Mecamylamine 23-35 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 53-85 34193682-5 2021 Intra-mPFC infusion of mecamylamine, a non-selective nicotinic acetylcholine receptor (nAChR) antagonist, 5 min before nicotine administration blocked the effect of nicotine. Mecamylamine 23-35 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 87-92