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 负责突触前可塑性的机制 促进、增强、强直后增强和长期 增强作用。 所有这些同突触塑化物都将被检查 使用小龙虾开瓶器兴奋神经元，其神经末梢可以是 双重穿透远离发射机的空间常数的一小部分 可以记录诱发和自发释放的释放位点 大的、已识别的突触后肌细胞。 使用这种制剂，我们 建议检查钙电流是否增加，钙电流是否减少 一些钾电导，和/或内部钙的增加或 钠浓度有助于任何或所有这些同突触 增塑剂。 电生理学和生物物理学范式已被 精心设计用于测量这些离子特性。 鉴于许多其他细胞/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/分子机制发现于 几乎肯定会在以下位置找到小龙虾开启器兴奋性突触 哺乳动物突触（包括人类）。 这些知识很重要 因为促进、增强和突触可塑性 强直后增强可能是造成这种行为的原因 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元基础。