短期抑制时gaba释放的量子参数分析及突触传递的促进作用。

O. Kolesnyk, S. Fedulova, N. Veselovsky
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引用次数: 0

摘要

采用突触后神经元全细胞膜片钳技术和单个突触前轴突局部胞外电配对脉冲刺激技术,研究了培养大鼠海马神经元诱发抑制性突触后电流(eIPSCs)振幅的变化。在43个神经元中观察到成对脉冲抑制(PPD)和成对脉冲促进(PPF)。方差系数(CV)分析发现,抑郁期第二反应的CV比第一反应大57% (n = 26),促进期第二反应的CV比第一反应小27% (n = 17)。因此,只有突触前机制是短期抑郁和促进的基础。我们还估计了量子参数,假设发射机释放被合理地描述为二项分布。我们发现在我们的实验条件下,PPD和PPF期间GABA释放概率没有明显变化。第一对刺激的平均量子含量和平均递质释放位点数相同,抑制组为9.7,突触传递促进组为5。第二次刺激的值在PPD期间分别显著降低了28%和26%,在PPF期间分别显著提高了14%和11%。因此,表征短期抑制时GABA释放和突触传递促进的量子参数存在显著差异。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
ANALYSIS OF QUANTAL PARAMETERS OF GABA RELEASE DURING SHORT-TERM DEPRESSION AND FACILITATION OF SYNAPTIC TRANSMISSION.
Changes in amplitudes of evoked inhibitory postsynaptic currents (eIPSCs) from rat cultured hippocampal neurons were studied using whole-cell patch-clamp technique in postsynaptic neuron and local extracellular electrical paired pulse stimulation of single presynaptic axon. Paired pulse depression (PPD) and paired pulse facilitation (PPF) were observed in studied 43 neurons. According to coefficient of variance (CV) analysis was found that CV of second respond was significantly larger than CV first by 57 % (n 26) during depression and significanty smaller by 27 % (n = 17) during facilitation. Thus, only presynaptic mechanism underlies short-term depression and facilitation. We also estimated quantal parameters assuming that transmitter release is reasonably described by a binomial distribution. We found that under our experimental conditions there were no significant changes in GABA release probability during PPD and PPF. The values of mean quantal content and mean number of sites of transmitter release were the same for first stimulus in pair and were equal 9.7 in depression and 5 in facilitation of synaptic transmission. The values both of them for second stimulus were significant decreased by 28 and 26% during PPD and were significant increased by 14 and 11% during PPF, respectively. Thus, there is significant difference in quantal parameters characterizing GABA release during short-term depression and facilitation of synaptic transmission.
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