MOLECULAR REGULATION OF GABAA RECEPTORS IN THE AMYGDALA

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 该项目的目的是检验一种假说，即GABAA受体复合体的活性依赖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应激依赖的成瘾复发。这一建议利用分子遗传学方法来检测恐惧条件作用以及苯二氮类药物急性、慢性和停药阶段后杏仁核GABAA受体突触前和突触后的调节。 在报告期间，我们完成了基线、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-Alpha1亚单位从海马体和杏仁体中删除时，对行为有显著影响。

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.