AMYGDALA VS HIPPOCAMPAL BDNF FUNCTION WITH MOLECULAR GENETIC TECHNIQUES

这个子项目是许多利用 由NIH/NCRR资助的中心赠款提供的资源。子项目及 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。 在报告期间，我们将表达Cre重组酶的新型慢病毒载体与其中BDNF基因侧翼为LoxP位点的转基因小鼠（Floxed）相结合。 我们发现杏仁核内海马体bdnf和trkB的激活是恐惧正常消退所必需的。 此外，我们发现，敲除bdnf，特别是海马体内的bdnf，可以阻止恐惧的消失。

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. During the reporting period, we combined a novel lentivirus vector that expresses the Cre recombinase with transgenic mice in which the BDNF gene has been flanked by LoxP sites (Floxed). We found that hippocampal bdnf and trkB activation within the amygdala are required for the normal extinction of fear. Additionally, we found that knocking out bdnf, specifically within the hippocampus, prevents extinction of fear.