PRESYNAPTIC MECHANISMS OF SOME NEURONAL PLASTICITIES

一些神经元可塑性的突触前机制

• 批准号: 2266960
• 负责人: GEORGE Davis BITTNER
• 金额: $ 13.96万
• 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/2266960
• 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.

我们的长期目标是确定电生理和生物物理 负责突触前可塑性的机制， 易化、增强、强直后增强和长期 增强作用 所有这些同突触可塑体将被检查 使用小龙虾开启器兴奋神经元，其神经末梢可以 距离发射器双倍穿透一个空间常数的分数 可以记录其诱发和自发释放的释放部位， 大的，可识别的突触后肌肉细胞。 使用该制剂，我们 建议检查钙电流的增加， 几个钾电导，和/或增加内部钙或 钠浓度有助于任何或所有这些同源突触 塑料。 电生理学和生物物理学范式已经被 精心设计来测量每一种离子特性。 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， 几乎可以肯定的是， 哺乳动物突触（包括人类）。 这些知识很重要 因为突触可塑性的促进，增强， 强直后增强可能负责这种行为 长时程增强效应（long-term potentiation） 可能是学习和记忆的神经基础。