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和生物物理 负责导致突触前可塑性的机制 促进，增强，转机后增强和长期 增强。 所有这些同性突触塑料将被检查 使用小龙虾揭示仪的神经元，其神经终端可以是 双重穿透远离发射器的空间的一部分 释放网站的诱发和自发释放可以从 大型，鉴定出突触后肌肉细胞。 使用此准备，我们 建议检查钙电流的增加，减少 几种钾电导和/或增加内部钙或/或 钠浓度有助于任何或全部同性突触 塑料。 电生理和生物物理范例已经 仔细设计以测量这些离子特性中的每一个。 鉴于许多其他细胞/分子的保守演变 机制（包括轴突传导和突触传播）， 这些突触可塑性的细胞/分子机制 小龙虾揭幕战兴奋剂突触几乎可以肯定会在 哺乳动物突触（包括人类）。 这样的知识很重要 因为促进，增强和 tetanic增强可能是导致这种行为的原因 现象是唤醒和敏化的，而长期增强 可能是学习和记忆的神经元基础。