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首页> 外文期刊>Journal of Neurophysiology >Decreased afferent excitability contributes to synaptic depression during high-frequency stimulation in hippocampal area CA1
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Decreased afferent excitability contributes to synaptic depression during high-frequency stimulation in hippocampal area CA1

机译：在海马区域CA1中的高频刺激期间有助于突触抑郁症

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Longterm potentiation (LTP) is often induced experimentally by continuous high-frequency afferent stimulation (HFS), typically at 100 Hz for 1 s. Induction of LTP requires postsynaptic depolarization and voltage-dependent calcium influx. Induction is more effective if the same number of stimuli are given as a series of short bursts rather than as continuous HFS, in part because excitatory postsynaptic potentials (EPSPs) become strongly depressed during HFS, reducing postsynaptic depolarization. In this study, we examined mechanisms of EPSP depression during HFS in area CA1 of rat hippocampal brain slices. We tested for presynaptic terminal vesicle depletion by examining minimal stimulation-evoked excitatory postsynaptic currents (EPSCs) during 100-Hz HFS. While transmission failures increased, consistent with vesicle depletion, EPSC latencies also increased during HFS, suggesting a decrease in afferent excitability. Extracellular recordings of Schaffer collateral fiber volleys confirmed a decrease in afferent excitability, with decreased fiber volley amplitudes and increased latencies during HFS. To determine the mechanism responsible for fiber volley changes, we recorded antidromic action potentials in single CA3 pyramidal neurons evoked by stimulating Schaffer collateral axons. During HFS, individual action potentials decreased in amplitude and increased in latency, and these changes were accompanied by aiarge increase in the probability of action potential failure. Time derivative and phase-plane analyses indicated decreases in both axon initial segment and somato-dendritic components of CA3 neuron action potentials. Our results indicate that decreased presynaptic axon excitability contributes to depression of excitatory synaptic transmission during HFS at synapses between Schaffer collaterals and CA1 pyramidal neurons.
机译：Longterm Putiziation（LTP）通常通过连续高频传入刺激（HFS）进行实验诱导，通常在100Hz以上。 LTP的诱导需要突触后的去极化和电压依赖性钙流入。如果给予相同数量的刺激而不是作为连续的HFS，则诱导更有效，部分是因为在HFS期间兴奋性后突触电位（EPSP）变得强烈抑制，减少突触后的去极化。在这项研究中，我们在大鼠海马脑切片区CA1中HFS期间检查了EPSP抑郁的机制。通过在100HzHzHz HFS期间检查最小的刺激诱发的兴奋性突触突触电流（EPSCs），我们测试了预突触末端囊泡枯萎病。虽然传输失败增加，但与囊泡耗尽一致，EPSC延迟在HFS期间也增加，表明增强兴奋性降低。 Schaffer散纤纤维葡萄球菌的细胞外记录证实了传神兴奋性的降低，纤维排振荡减少和HFS期间的延迟增加。为了确定负责纤维排雷的机制，我们记录了通过刺激Schaffer散向诱发的单一Ca3金字塔神经元的抗染色动作电位。在HFS期间，各个动作电位在幅度下降并在延迟增加，这些变化伴随着AIARGE潜在失败的概率增加。 Ca3神经元动作电位的轴突初始段和躯体树突组分的时间衍生物和相平面分析表明。我们的结果表明，降低的突触前轴突兴奋性有助于HFS在Schaffer抵押品和Ca1金字塔神经元的突触期间的兴奋性突触传递的抑制。

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