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.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 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。 2009年，我们继续绘制大鼠和灵长类动物基底外侧杏仁核特定亚区域神经元的生理特性。 我们证明了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，在BLA的兴奋性突触传递的长时程增强（LTP）是依赖于D1受体的激活和蛋白激酶A的激活。 此外，我们已经表明，PKA是BLA主神经元索马和脊髓内的细胞骨架锚定蛋白，并在BLA的LTP可以被破坏从锚定蛋白解离PKA。 值得注意的是，这一过程是由磷酸二酯酶抑制剂和公认的抗抑郁药咯利普兰调节的。 我们正在继续调查咯利普兰的作用机制。