Apoptotic molecules in synapse plasticity

突触可塑性中的凋亡分子

• 批准号: 7594605
• 负责人: Zheng Li
• 金额: $ 54.23万
• 依托单位: NATIONAL INSTITUTE OF MENTAL HEALTH
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/7594605
• 关键词: Amino Acids; Antibodies; Apoptosis; Apoptotic; Behavior; Brain; Caspase; Chromosome Pairing; Cleaved cell; Cognition; Development; Endocytosis; Goals; Hippocampus (Brain); Immunoprecipitation; Knowledge; Lead; Long-Term Depression; Mediating; Mental Depression; Mental disorders; Mitochondria; Modification; Molecular; Neurons; Propionic Acids; Propionic acid; Protein Binding; Protein Overexpression; Proteins; Structure; Synapses; Synaptic Transmission; caspase-3; experience; improved; neural circuit; receptor; research study

The release of apoptotic molecules from mitochondria is activated by the pro-apoptotic Bcl-2 proteins in programmed cell death. We first ask whether the pro-apoptotic Bcl-2 proteins activate mitochondria in long-term depression (LTD). We will alter the expression of pro-apoptotic Bcl-2 proteins in hippocampal neurons, then examine -amino-3-hydroxy-5-methylisoxazole-4- propionic acid (AMPA) receptor endocytosis and LTD in these neurons. To investigate how casapses mediate AMPA receptor endocytosis, we will use antibodies against caspase-3 to immunoprecipitate proteins that bind to caspase-3 in LTD. We have made a construct to overexpress caspase-3 in hippocampal neurons and are performing the immunoprecipitation experiment.

在程序性细胞死亡中，凋亡分子从线粒体的释放被促凋亡Bcl-2蛋白激活。我们首先询问促凋亡Bcl-2蛋白是否在长期抑郁症（LTD）中激活线粒体。我们将改变海马神经元中促凋亡蛋白Bcl-2的表达，然后检测这些神经元中-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）受体的内吞和LTD。为了研究casapses如何介导AMPA受体的内吞作用，我们将使用抗体对caspase-3的免疫沉淀蛋白，结合到caspase-3在LTD。我们已经提出了一个结构过度表达caspase-3在海马神经元，并正在进行免疫沉淀实验。