MOLECULAR REGULATION OF GABAA RECEPTORS IN THE AMYGDALA

杏仁核中 GABAA 受体的分子调控

• 批准号: 7562649
• 负责人: Kerry J Ressler
• 金额: $ 2.37万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-05-01 至 2008-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7562649
• 关键词: Acute; Amygdaloid structure; Behavior; Benzodiazepines; Chronic; Complex; Computer Retrieval of Information on Scientific Projects Database; Down-Regulation; Extinction (Psychology); Funding; Goals; Grant; Hippocampus (Brain); Institution; Learning; Mediating; Molecular; Molecular Genetics; Phase; Regulation; Relapse; Reporting; Research; Research Personnel; Resources; Source; Stress; Synapses; United States National Institutes of Health; Withdrawal; addiction; conditioned fear; mRNA Expression; receptor

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The goal of this project is to examine the hypothesis that activity-dependent downregulation of the GABAA receptor complex is a common mechanism shared by fear conditioning and benzodiazepine use, and that this shared mechanism may mediate stress-dependent relapse of addiction. This proposal utilizes molecular genetic approaches to examining the pre- and post-synaptic regulation of amygdala GABAA receptors following fear conditioning and acute, chronic and withdrawal phases of benzodiazepine use. During the reporting period we have completed analyses of GABA-A mRNA expression at baseline, following conditioned fear learning and following extinction of conditioned fear. We have also found significant effects on behavior when the GABA-alpha1 subunit is deleted from hippocampus and amygdala.

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 本项目的目标是研究以下假设：GABAA受体复合物的活性依赖性下调是恐惧条件反射和苯二氮卓类药物使用的共同机制，并且这种共同机制可能介导成瘾的压力依赖性复发。 该提案利用分子遗传学方法来检查杏仁核GABAA受体在恐惧条件反射和苯二氮卓类药物使用的急性、慢性和戒断阶段后的突触前和突触后调节。 在本报告期间，我们完成了对基线、条件性恐惧学习和条件性恐惧消退后GABA-A mRNA表达的分析。 我们还发现，当GABA-α 1亚基从海马体和杏仁核中删除时，对行为有显著影响。