ROLE OF BDNF AND TRKB IN CONDITIONED DEFEAT

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。本研究使用病毒载体介导的基因转移，在仓鼠的杏仁核中过度表达TrkB受体的截断形式，TrkB受体是BDNF的主要负受体，以暴露于社会失败。我们假设BDNF信号的阻断会阻止条件失败的获得，而不是表达，条件失败是仓鼠在社会失败后观察到的一种行为变化。早期的结果是有希望的，这笔拨款还资助了一篇关于BDNF ？杏仁核中TrkB的相互作用。

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. This study used viral vector-mediated gene transfer to over-express a truncated form of the TrkB receptor, which served as a dominant negative receptor for BDNF, in the amygdala of hamsters to expose to social defeat. We hypothesized that a blockade of BDNF signaling will block the acquisition, but not the expression, of conditioned defeat, a behavioral change observed following social defeat in hamsters. Early results are promising, and this grant has also funded the publication of a review manuscript on the BDNF ? TrkB interaction in amygdala.