FUNCTIONAL NEUROANATOMY OF THE BASOLATERAL AMYGDALA

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 2010年，我们完成了对我们的父母R01(杏仁基底外侧核的功能神经解剖学)的研究，并使用从父母拨款中产生的初步数据，我们成功地向NIH申请了继续资助R01的资金(杏仁基底外侧核中的恐惧和多巴胺)。根据我们以前的研究，我们知道BLA中间神经元的一个亚群，即含有小白蛋白的细胞，是BLA中同步神经活动的关键调节因素。这项研究的结果发表在《生理学杂志》上。目前正在修订中(Jasnow等人，修订中)。我们以前的研究结果也表明，小白蛋白中间神经元的兴奋性受到瞬时外向钾电流IA表达的严格控制。这些通道与包括钾通道相互作用蛋白(KChIP)在内的伴侣分子形成大分子复合体。我们已经检测了KChIPs(KChIP1，KChIP4)在BLA中的相对分布，并注意到KChIP1选择性地在神经元亚群中表达。我们扩展了这项研究，以表明KChIP1几乎只在表达小白蛋白的中间神经元中表达。此外，我们还完成了对LTP在BLA主神经元诱导的多巴胺依赖性的研究。此外，我们扩展了这些研究，以表明多巴胺、脑源性神经生长因子和突触释放的锌之间的共同作用是LTP诱导的先决条件，并通过外推形成恐惧记忆。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. In 2010 we concluded the studies for our parent R01 (Functional Neuroanatomy of the Basolateral Amygdala) and using preliminary data generated from the parent grant we successfully applied to NIH for continuing R01 funding (Fear and Dopamine in the Basolateral Amygdala). Based on our previous studies, we knew that a subpopulation of BLA interneurons, the parvalbumin containing cells, were key regulators of synchronized neural activity in the BLA. The results of this study were submitted to the Journal of Physiology [Lond.] and are currently being revised (Jasnow et al., in revision). The results of our previous studies had also suggested that the excitability of the parvalbumin interneurons was tightly controlled by expression of the transient outward potassium current, IA. These channels form macromolecular complexes with chaperone molecules, including the potassium channel interacting proteins (KChIPs). We have examined the relative distribution of KChIPs (KChIP1  KChIP4) in the BLA and noted that KChIP1 was selectively expressed in a subpopulation of neurons. We have extended this study to show that KChiP1 is almost exclusively expressed in the population of parvalbumin expressing interneurons. In addition, we completed our study into the dopamine-dependence of LTP induction in principal neurons of the BLA. Moreover, we extended these studies to show that a synaergistic interaction between dopamine, brain derived nerve growth factor, and synaptically released zinc, are a prerequisite for LTP induction, and by extrapolation fear memory formation.