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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此，可以在其他清晰的条目中表示。列出的机构是 对于中心，这不一定是调查员的机构。 2009年，我们继续绘制大鼠和灵长类基底外侧杏仁核的定义子区域中神经元的生理特性。 我们证明，在BLA投影神经元中的同步发射和该区域的突触可塑性取决于CAMP第二信使级联系统，尤其是确定离子通道和受体的磷酸化状态的分解代谢和分解代谢途径。 我们已经证明，BLA中兴奋性突触传播的长期训练（LTP）取决于D1受体激活和蛋白激酶A的激活。 此外，我们已经表明，PKA在BLA主神经元体内被划分为细胞骨骼锚定蛋白，而BLA中的LTP可以通过从锚固蛋白中分离PKA来破坏BLA中的LTP。 值得注意的是，该过程由磷酸二酯酶抑制剂和假定的抗抑郁药Rolipram调节。 我们正在继续研究Rolipram的作用机理。