PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26256075-2 2015 In mouse studies, nonselective nAChR antagonist mecamylamine blocks cocaine-induced conditioned place preference (CPP) and behavioral sensitization. Cocaine 68-75 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 31-36 26256075-3 2015 Among subtype-selective nAChR antagonists, the beta2-selective antagonist dihydrobetaerythroidine and alpha7 antagonist methyllycaconitine (MLA), but not MLA alone prevent behavioral sensitization to cocaine. Cocaine 200-207 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 24-29 26256075-3 2015 Among subtype-selective nAChR antagonists, the beta2-selective antagonist dihydrobetaerythroidine and alpha7 antagonist methyllycaconitine (MLA), but not MLA alone prevent behavioral sensitization to cocaine. Cocaine 200-207 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 102-108 26256075-9 2015 These results indicate that the alpha3beta4 nAChR play a role in the rewarding and behavioral effects of cocaine, and that selective alpha3beta4 nAChR ligands can attenuate cocaine-induced behavioral phenomena. Cocaine 105-112 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 44-49 26256075-9 2015 These results indicate that the alpha3beta4 nAChR play a role in the rewarding and behavioral effects of cocaine, and that selective alpha3beta4 nAChR ligands can attenuate cocaine-induced behavioral phenomena. Cocaine 105-112 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 145-150 26256075-9 2015 These results indicate that the alpha3beta4 nAChR play a role in the rewarding and behavioral effects of cocaine, and that selective alpha3beta4 nAChR ligands can attenuate cocaine-induced behavioral phenomena. Cocaine 173-180 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 145-150 20580908-3 2010 Recently, it is demonstrated that mecamylamine, a nAChR antagonist blocks cocaine-, d-amphetamine-, ephedrine-, nicotine-, and methylphenidate-induced psychomotor sensitization. Cocaine 74-81 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 50-55 20890227-2 2010 This study aimed to further assess the role of beta2 and coexpressed nAChR subunits in the brain (alpha4, alpha6 and alpha7) to control monoamine-mediated locomotor response, that is, response to novelty, saline, nicotine with tranylcypromine pretreatment, cocaine, d-amphetamine and morphine treatments. Cocaine 257-264 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 69-74 20890227-4 2010 In contrast, alpha7 KO mice were hyporeactive to tranylcypromine and cocaine. Cocaine 69-76 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 13-19 22568685-2 2012 This study was designed to assess the contribution of different nAChR subtypes to the behavioural and neurochemical effects of chronic cocaine treatment. Cocaine 135-142 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 64-69 22568685-6 2012 Quantitative autoradiography was used to examine the effect of cocaine exposure on alpha7 and alpha4beta2* nAChRs, and on the high-affinity choline transporter. Cocaine 63-70 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 83-89 22568685-7 2012 KEY RESULTS: MLA+cocaine administration induced an intense self-grooming behaviour, indicating a likely role for alpha7 nAChRs in modulating this anxiogenic, compulsive-like effect of cocaine. Cocaine 17-24 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 113-119 17061109-2 2007 OBJECTIVES AND METHODS: The aim of this paper is to study the effects of local perfusions (through the microdialysis cannula) of nicotinic acetylcholine receptor (nAChR) antagonists in the ventral tegmental area (VTA, where mesolimbic DA cell bodies are located) or nucleus accumbens (nAc, where mesolimbic DA nerve terminals project) on cocaine-elicited increase in DA levels in the nAc of mice using intracerebral microdialysis. Cocaine 338-345 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 163-168 17061109-6 2007 CONCLUSIONS: These results show that intra-nAc and intra-VTA perfusion of nAChR antagonists differentially affect cocaine-elicited increase in DA levels in a region and subtype-specific manner. Cocaine 114-121 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 74-79 11282258-5 2001 In addition, mice lacking the high affinity nAChR containing the beta2 subunit showed decreased place preference to 5 mg/kg cocaine, although higher doses of cocaine could condition a place preference in these knock out animals. Cocaine 124-131 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 44-49 16826402-7 2006 CONCLUSIONS: These data indicate that inhibition of both alpha7* and beta2* nAChRs is necessary to prevent development of sensitization of cocaine-elicited increases in extracellular dopamine levels in the ventral striatum of mice. Cocaine 139-146 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 57-64 16826402-0 2006 Inhibition of both alpha7* and beta2* nicotinic acetylcholine receptors is necessary to prevent development of sensitization to cocaine-elicited increases in extracellular dopamine levels in the ventral striatum. Cocaine 128-135 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 19-26 16826402-2 2006 OBJECTIVES: The current study examined the hypothesis that nicotinic acetylcholine receptor (nAChR) blockade influences the ability of cocaine to elicit increases in extracellular dopamine levels. Cocaine 135-142 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 59-91 16826402-2 2006 OBJECTIVES: The current study examined the hypothesis that nicotinic acetylcholine receptor (nAChR) blockade influences the ability of cocaine to elicit increases in extracellular dopamine levels. Cocaine 135-142 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 93-98 15287742-0 2004 Mechanism-based discovery of small molecules that prevent noncompetitive inhibition by cocaine and MK-801 mediated by two different sites on the nicotinic acetylcholine receptor. Cocaine 87-94 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 145-177 11282258-5 2001 In addition, mice lacking the high affinity nAChR containing the beta2 subunit showed decreased place preference to 5 mg/kg cocaine, although higher doses of cocaine could condition a place preference in these knock out animals. Cocaine 158-165 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 44-49 11282258-9 2001 Induction of chronic fos-related antigens by cocaine was also reduced in mutant mice as compared to their wild type siblings, implying that downstream actions of cocaine were also affected by inactivation of the high affinity nAChR. Cocaine 162-169 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 226-231 11282258-10 2001 These data indicate that activation of the high affinity nAChR may contribute to cocaine reinforcement. Cocaine 81-88 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 57-62 10578459-0 1999 Selective alpha 7 nicotinic receptor stimulation normalizes chronic cocaine-induced loss of hippocampal sensory inhibition in C3H mice. Cocaine 68-75 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 10-36