FUNCTIONAL NEUROANATOMY OF THE BASOLATERAL AMYGDALA

基底外侧杏仁核的功能神经解剖学

• 批准号: 8172376
• 负责人: DONALD G RAINNIE
• 金额: $ 4.39万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8172376
• 关键词: Amygdaloid structure; Antidepressive Agents; Computer Retrieval of Information on Scientific Projects Database; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Cytoskeleton; Dopamine D1 Receptor; Funding; Grant; Institution; Investigation; Ion Channel; Long-Term Potentiation; Maps; Neuroanatomy; Neurons; Pathway interactions; Phosphodiesterase Inhibitors; Phosphorylation; Physiological; Primates; Process; Property; Proteins; Rattus; Receptor Activation; Research; Research Personnel; Resources; Rolipram; Second Messenger Systems; Source; Synaptic Transmission; Synaptic plasticity; System; United States National Institutes of Health; Vertebral column; neuronal cell body; receptor; second messenger

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. In 2009 we continued to map the physiological properties of neurons in defined sub-regions of the rat and primate basolateral amygdala. We demonstrated that synchronized firing in BLA projection neurons and synaptic plasticity in this region is critically dependent on the cAMP second messenger cascade system, and in particular the catabolic and catabolic pathways that determine the phosphorylation state if ion channels and receptors. We have demonstrated that long-term-potentiation (LTP) of excitatory synaptic transmission in the BLA is dependent on D1 receptor activation and the activation of protein kinase A. Moreover, we have shown that PKA is compartmentalized within BLA principal neuron soma and spines by cytoskeleton anchoring proteins, and that LTP in the BLA can be disrupted by dissociating PKA from the anchoring protein. Significantly, this process is modulated by the phosphodiesterase inhibitor, and putative antidepressant agent, rolipram. We are continuing our investigations into the mechanisms of action of rolipram.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 2009 年，我们继续绘制大鼠和灵长类基底外侧杏仁核特定亚区域神经元的生理特性图。 我们证明，BLA 投射神经元的同步放电和该区域的突触可塑性严重依赖于 cAMP 第二信使级联系统，特别是决定离子通道和受体磷酸化状态的分解代谢和分解代谢途径。 我们已经证明 BLA 中兴奋性突触传递的长时程增强 (LTP) 依赖于 D1 受体激活和蛋白激酶 A 的激活。 此外，我们还发现，PKA 通过细胞骨架锚定蛋白在 BLA 主要神经元胞体和棘中划分，并且 BLA 中的 LTP 可以通过将 PKA 与锚定蛋白解离来破坏。 值得注意的是，这一过程受到磷酸二酯酶抑制剂和推定的抗抑郁药咯利普兰的调节。 我们正在继续研究咯利普兰的作用机制。