PRESYNAPTIC MECHANISMS OF SOME NEURONAL PLASTICITIES

一些神经元可塑性的突触前机制

• 批准号: 3415014
• 负责人: GEORGE Davis BITTNER
• 金额: $ 14.75万
• 依托单位: UNIVERSITY OF TEXAS AT AUSTIN
• 依托单位国家: 美国
• 财政年份: 1992
• 资助国家: 美国
• 起止时间: 1992-12-01 至 1995-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3415014
• 关键词: action potentials; alternatives to animals in research; biophysics; calcium channel blockers; calcium flux; crayfish; electrical conductance; electrophysiology; evoked potentials; long term potentiation; magnetic recording system; neural facilitation; neural plasticity; neuropharmacology; neurotransmitter transport; phosphorylation; potassium; potassium channel; sodium; voltage /patch clamp

Our long-term objective is to define electrophysiological and biophysical mechanisms which are responsible for the presynaptic plasticities of facilitation, augmentation, post-tetanic potentiation and long-term potentiation. All of these homosynaptic plasticides will be examined using the crayfish opener excitor neuron whose nerve terminals can be doubly penetrated a fraction of a space constant away from transmitter release sites whose evoked and spontaneous release can be recorded from large, identified postsynaptic muscle cells. Using this preparation, we propose to examine whether increases in calcium currents, decreases in several potassium conductances, and/or increases in internal calcium or sodium concentrations contribute to any or all of these homosynaptic plasticides. Electrophysiological and biophysical paradigms have been carefully designed to measure each of these ionic properties. Given the conservative evolution of many other cellular/molecular mechanisms (including axonal conduction and synaptic transmission), cellular/molecular mechanisms of these synaptic plasticities found at crayfish opener excitor synapses will almost certainly be found at mammalian synapses (including humans). Such knowledge is important because the synaptic plasticities of facilitation, augmentation, and post-tetanic potentiation are probably responsible for such behavioral phenomena as arousal and sensitization, whereas long-term potentiation may be the neuronal basis for learning and memory.

我们的长期目标是定义电生理学和生物物理学 突触前可塑性的机制 易化、增强、强直后增强和长期 增强功能。所有这些同型突触增塑剂都将被检查 使用小龙虾开放兴奋神经元，其神经末梢可以 双倍穿透远离发射机的一小部分空间常数 可记录其诱发和自发释放的释放部位 突触后的大型肌细胞。利用这种准备，我们 建议研究钙电流的增加，是否会减少 几种钾电导，和/或体内钙或 钠浓度对这些同源突触中的任何一个或全部起作用 增塑剂。电生理和生物物理范式已经被 精心设计来测量这些离子的每一个性质。 考虑到许多其他细胞/分子的保守进化 机制(包括轴突传导和突触传递)， 这些突触可塑性的细胞/分子机制可在 小龙虾启动子兴奋性突触几乎肯定会在 哺乳动物的突触(包括人类)。这样的知识很重要 因为突触的易化、增强和可塑性 强直后增强可能是导致这种行为的原因 觉醒和敏化等现象，而长时程增强 可能是学习和记忆的神经基础。