VOLTAGE DEPENDENCE OF 5-HYDROXYTRYPTAMINE RELEASE AT A SYNAPSE BETWEEN IDENTIFIED LEECH NEURONS IN CULTURE
VOLTAGE DEPENDENCE OF 5-HYDROXYTRYPTAMINE RELEASE AT A SYNAPSE BETWEEN IDENTIFIED LEECH NEURONS IN CULTURE
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DOI：
10.1113/jphysiol.1986.sp016004
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发表时间：
1986-03-01
影响因子：
5.5
通讯作者：
NICHOLLS, JG
中科院分区：
文献类型：
--
作者：
DIETZEL, ID;DRAPEAU, P;NICHOLLS, JG
本文用电压钳技术研究了从水蛭中枢神经系统分离的Retzius和压力（P）感觉神经元所形成的突触前末梢5-羟色胺（5-HT）释放。并保持在组织培养物中。在这些突触促进，抑郁症和释放的调制发生与动作电位和电压钳脉冲。Retzius细胞从一个恒定的保持电位通过不同幅度的步骤（持续时间为5 ms）的去极化引起5-HT的分级释放。使用这些短测试脉冲释放的陡峭传递函数类似于在鱿鱼的巨大突触中看到的：突触电位随着突触前去极化超过-25 mV而显著增加，并且随着大的去极化脉冲超过+40 mV而降低。当电压钳制的Retzius细胞的稳定保持电位突然移位到一个新的值（-40 mV ~-85 mV）时，突触后P细胞膜电位也随之发生缓慢但较小的同向变化。在约40 ms的初始延迟后，突触后电位以指数时间过程和0.7 s的时间常数达到其新的水平。由于Retzius和P细胞没有电耦合，这些效应可以通过改变递质的紧张性释放来解释。突触前保持电位向更去极化水平的变化导致P细胞中记录的电压噪声增加。相反，去极化水平的超极化降低了噪声。噪声分析表明，这些变化可以占量子事件的平均幅度约为0.15 mV。这个值是类似的自发微型电位和量子波动Retzius和P细胞之间的突触观察。稳态保持电位的变化也有显着的效果后，观察到的Retzius细胞的短暂去极化脉冲的传递函数。当Retzius细胞的保持电位从静息值-45 mV增加到-75 mV时，由去极化至0 mV（脉冲持续时间为5 ms）诱发的突触后反应的幅度降低。例如，从-45 mV开始去极化至0 mV诱发的突触电位比从-75 mV开始去极化至0 mV诱发的突触电位大十倍。在保持电位的阶跃去极化或超极化的情况下，对由短脉冲诱发的释放的影响在指数时间过程上累积到0 mV，类似于保持电位对紧张性释放的影响（τ）。= 0.7 s）。频率依赖性的促进tarnsmission发生与成对的刺激（约100毫秒）的脉冲和电压钳条件下。易化衰减的时间过程与保持电位无关。它的结论是，两个休克促进和调制释放的静息电位的变化取决于不同的突触前机制。
The release of 5-hydroxytryptamine (5-HT) from presynaptic terminals has been studied by the voltage-clamp technique at synapses made by isolated Retzius and pressure (P) sensory neurones dissected from the leech C.N.S. and maintained in tissue culture. At these synapses facilitation, depression and modulation of release occur with action potentials and with voltage-clamp pulses. Depolarization of Retzius cells from a constant holding potential by steps of varying amplitude (5 ms in duration) caused graded release of 5-HT. The steep transfer function for release using these short test pulses resembled that seen at the giant synapse of the squid: synaptic potentials increased markedly with presynaptic depolarizations beyond -25 mV and decreased with large depolarizing pulses beyond +40 mV. When the steady holding potential of voltage-clamped Retzius cells was suddenly displaced to a new value within the range of -40 mV to -85 mV, there followed a slow but smaller change of the post-synaptic P-cell membrane potential in the same direction. After an initial delay of about 40 ms, the post-synaptic potential reached its new level with an exponential time course and a time constant of 0.7 s. Since Retzius and P cells are not electrically coupled, these effects can be accounted for by alterations in tonic release of transmitter. Changes of presynaptic holding potential to a more depolarized level resulted in an increase in voltage noise recorded in the P cell. Conversely, hyperpolarization from a depolarized level reduced noise. Noise analysis showed that these changes could be accounted for by quantal events with a mean amplitude of about 0.15 mV. This value is similar to that for spontaneous miniature potentials and quantal fluctuations observed at synapses between Retzius and P cells. Changes in steady holding potential also had marked effects upon the transfer function observed with brief depolarizing pulses of the Retzius cell. The post-synaptic responses evoked by depolarizations to 0 mV with pulses of 5 ms duration were reduced in amplitude as the holding potential of the Retzius cell was increased from the resting value of -45 to -75 mV. For example, depolarization to 0 mV starting from -45 mV evoked synaptic potentials as much as ten times larger than those evoked by depolarizations to 0 mV starting from -75 mV. With step depolarizations or hyperpolarizations of the holding potential, the effect on release evoked by brief pulses to 0 mV built up over an exponential time course similar to that found for the effect of holding potential on tonic release (.tau. = 0.7 s). Frequency-dependent facilitation of tarnsmission occurred with paired stimuli (approximately 100 ms) with impulses and under voltage-clamp conditions. The time course of the decay of facilitation was independent of the holding potential. It is concluded that two-shock facilitation and modulation of release by changes in the resting potential depend on different presynaptic mechanisms.