A characterization of excitatory postsynaptic potentials in the avian nucleus magnocellularis.
A characterization of excitatory postsynaptic potentials in the avian nucleus magnocellularis.
复制标题
禽类大细胞核兴奋性突触后电位的表征。
DOI：
10.1152/jn.1994.72.2.705
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发表时间：
1994
影响因子：
2.5
通讯作者：
Trussell,LO
中科院分区：
文献类型：
--
作者：
Zhang,S;Trussell,LO
1. 本文研究了第8神经刺激对鸡大细胞核（nMAG）电流箝位神经元的激活作用。单个突触前刺激产生快速上升的、阈值以上的兴奋性突触后电位（epsp），突触延迟约为0.4 ms。在对照的细胞外溶液和存在河豚毒素（TTX）的情况下，自发的微型EPSPs （mepsp）很明显。2. EPSP由一个对α -氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体拮抗剂敏感的大而短的组分和一个对n -甲基- d -天冬氨酸（NMDA）和AMPA受体拮抗剂敏感的小而缓慢衰变的组分组成。3. 在接近静息电位的电位处，注入去极化电流的步骤显示出膜电导的强烈向外整流。因此，在当前步骤中，神经元只能激发单一的ttx敏感动作电位。负责这种整流的电导对1毫米4-氨基吡啶敏感，但对1毫米四乙基铵不敏感。4. 在去极化电流脉冲终止后，膜电位以半衰期（t1/2）衰减，半衰期随着去极化电流的增加而减小，从剩余的20 mV去极化时达到约0.25 ms。epsp衰减的t1/2与膜t1/2相匹配，表明底层突触电导的衰减比膜t1/2更快。5. EPSP的慢相总是比t1/2膜长，并且随着超极化而增大。这一结果与AMPA受体对慢速和快速EPSP的贡献是一致的。6. 从EPSP的上升时间、EPSP分流动作电位的程度以及环噻嗪延长突触传导后EPSP的大小可以看出，低频刺激下传递的安全系数较大。7. 在重复的突触刺激过程中，缓慢的EPSPs叠加产生10-20 mV的平台去极化。平台电位仅被NMDA受体拮抗剂部分阻断。8. 在刺激序列中，更快的epsp在平台电位之上，可以在短时间内以高达500赫兹的速率驱动动作电位。在训练过程中，突触抑制很明显，例如，在超过200 Hz的5-10次刺激后，epsp经常低于阈值。在50赫兹的频率下，epsp可以在几秒钟内保持高于阈值。（摘要删节为400字）
1. The activation of current-clamped neurons in the chick nucleus magnocellularis (nMAG) by eighth nerve stimulation has been studied in a brain slice preparation using patch electrodes. Single presynaptic stimuli produced rapidly rising, suprathreshold, excitatory postsynaptic potentials (EPSPs) with a synaptic delay of approximately 0.4 ms. Spontaneous, miniature EPSPs (mEPSPs) were evident in control extracellular solution and in the presence of tetrodotoxin (TTX). 2. The EPSP was composed of a large, brief component that was sensitive to antagonists of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, and a smaller, slowly decaying component that was sensitive to both N-methyl-D-aspartate (NMDA) and AMPA receptor antagonists. 3. Injection of depolarizing current steps revealed a strong outward rectification of the membrane conductance at potentials close to the resting potential. Consequently, neurons could fire only a single, TTX-sensitive action potential during a current step. The conductance responsible for this rectification was sensitive to 1 mM 4-aminopyridine but not to 1 mM tetraethylammonium. 4. Following the termination of depolarizing current pulses, membrane potential decayed with a half-time (t1/2) that decreased as the depolarizing current increased, reaching approximately 0.25 ms for a depolarization from rest of 20 mV. The t1/2 for the decay of EPSPs matched the membrane t1/2, indicating that the underlying synaptic conductance decays more quickly than the membrane t1/2. 5. The slow phase of the EPSP was always longer than the membrane t1/2 and increased in size with hyperpolarization. This result is consistent with the contribution of AMPA receptors to the slow, as well as fast, EPSP. 6. The safety factor for transmission with low-frequency stimuli was large, as indicated by the rise time of the EPSP, the extent to which the EPSP shunted the action potential, and the size of EPSPs after prolongation of the synaptic conductance by cyclothiazide. 7. During repetitive synaptic stimulation, the slow EPSPs summated to produce a plateau depolarization of 10–20 mV. The plateau potential was only partially blocked by NMDA receptor antagonists. 8. During trains of stimuli, the faster EPSPs rode atop the plateau potential and could drive action potentials at rates up to 500 Hz for short periods. Synaptic depression was evident during trains, such that EPSPs often fell below threshold after 5–10 stimuli at rates above 200 Hz. EPSPs could remain suprathreshold for several seconds at 50 Hz.(ABSTRACT TRUNCATED AT 400 WORDS)