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.

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