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蛋白激酶C同工酶作为滥用药物敏感性和自我给药的调节因子——转基因小鼠研究

Protein kinase C isozymes as regulators of sensitivity to and self-administration of drugs of abuse-studies with genetically modified mice.

作者信息

Olive Michael Foster, Newton Philip M

机构信息

Department of Psychiatry, Medical University of South Carolina, Charleston, South Carolina 29425, USA.

出版信息

Behav Pharmacol. 2010 Sep;21(5-6):493-9. doi: 10.1097/FBP.0b013e32833d8bb7.

Abstract

Studies using targeted gene deletion in mice have revealed distinct roles for individual isozymes of the protein kinase C (PKC) family of enzymes in regulating sensitivity to various drugs of abuse. These changes in drug sensitivity are associated with altered patterns of drug self-administration. The purpose of this review is to summarize behavioral studies conducted on mice carrying targeted deletions of genes encoding specific PKC isozymes (namely the beta, gamma, delta, and epsilon isozymes), and to critically evaluate the possibility of using pharmacological inhibitors of specific PKC isozymes as modulators of the sensitivity to various drugs of abuse, as well as potential aids in the treatment of substance use disorders.

摘要

利用小鼠进行的靶向基因缺失研究揭示了蛋白激酶C(PKC)家族酶的各个同工酶在调节对各种滥用药物的敏感性方面具有不同作用。药物敏感性的这些变化与药物自我给药模式的改变有关。本综述的目的是总结对携带编码特定PKC同工酶(即β、γ、δ和ε同工酶)基因靶向缺失的小鼠进行的行为学研究,并严格评估使用特定PKC同工酶的药理学抑制剂作为各种滥用药物敏感性调节剂以及物质使用障碍治疗潜在辅助手段的可能性。

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