AMYGDALA VS HIPPOCAMPAL BDNF FUNCTION WITH MOLECULAR GENETIC TECHNIQUES

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。 在报告期间，我们将表达Cre重组酶的新型慢病毒载体与转基因小鼠结合在一起，在转基因小鼠中，BDNF基因的两侧带有loxP位点(FLOXED)。 我们发现杏仁核内的海马区BDNF和TrkB的激活是正常消除恐惧所必需的。此外，我们发现，敲除脑源性神经营养因子，特别是在海马体中，可以防止恐惧的消退。

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.