Postsynaptic membrane shifts during frequency potentiation of the hippocampal EPSP.
Postsynaptic membrane shifts during frequency potentiation of the hippocampal EPSP.
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海马 EPSP 频率增强过程中突触后膜发生变化。
DOI：
10.1152/jn.1987.58.4.866
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发表时间：
1987
影响因子：
2.5
通讯作者：
Landfield,PW
中科院分区：
文献类型：
--
作者：
Pitler,TA;Landfield,PW
1.在某些类型的中枢神经元中，重复的突触刺激诱导突触后膜的实质性变化，连同兴奋性突触后电位（EPSP）的稳健频率增强。然而，这些突触后膜移位的性质和时间过程，或它们对EPSP频率增强的可能贡献（例如，通过改变驱动力或电流路径），还没有被广泛地研究。因此，我们研究了海马切片CA 1神经元在4分钟10 Hz单突触刺激过程中复合EPSP振幅、突触后输入电阻（Rin）和突触后膜电位的同时变化模式。将切片保持在含有对照（4 mM）或高浓度（6.5mM）K+的培养基中。2.增强的EPSP，超极化的膜，和下降的Rin，都迅速发展，在10 Hz的突触刺激，这些反应达到最高水平的5-15秒的刺激列车。在大多数细胞中，膜去极化相发生在刺激的15和45秒之间，然后通过1分钟的刺激再超极化。在去极化阶段，EPSP增强和Rin的下降保持接近最大。没有显着差异被视为K+浓度的函数。3.这些结果表明，超极化并不总是与EPSP频率增强的时间。此外，如果驱动力和膜电导的变化被认为是近似相似的大树突和索马，那么驱动力的增加，由于膜超极化是不足以解释的三倍和四倍的增加EPSP振幅在频率增强。此外，基于类似的假设和EPSP衰减的树突模型，Rin的下降应该会降低树突突触部位的EPSP振幅，并在更大程度上降低索马的EPSP振幅。4.在研究中，膜超极化与注入电流约IPSP逆转电位，或在其中荷包牡丹碱甲碘应用于切片，表明抑郁症的IPSP的重复刺激不占频率增强的EPSP振幅。5.因此，这些数据是一致的结论，复合EPSP在中枢神经元的频率增强依赖于突触前机制，而不是广义的突触后变化。然而，我们的研究结果并不排除受体或棘的局部突触后变化作为可能的影响因素。（400字处截断摘要）
1. In some classes of central neurons, repetitive synaptic stimulation induces substantial changes in the postsynaptic membrane, in conjunction with robust frequency potentiation of the excitatory postsynaptic potential (EPSP). However, the nature and time course of these postsynaptic membrane shifts, or their possible contributions to EPSP frequency potentiation (e.g., by altering driving force or current pathways), have not been examined extensively. We therefore studied the simultaneous patterns of change in composite EPSP amplitude, postsynaptic input resistance (Rin), and postsynaptic membrane potential during a 4-min train of 10-Hz monosynaptic stimulation in CA1 neurons of hippocampal slices. Slices were maintained in media containing either control (4 mM) or high (6.5 mM) concentrations of K+. 2. Potentiation of the EPSP, hyperpolarization of the membrane, and a decline of Rin, all developed rapidly during 10-Hz synaptic stimulation; these responses reached maximal levels by 5-15 s of the stimulation train. In most cells, a membrane depolarization phase occurred between 15 and 45 s of stimulation, followed by rehyperpolarization by 1 min of stimulation. During the depolarization phase, both EPSP potentiation and the decline in Rin remained near maximal. No significant differences were seen as a function of K+ concentrations. 3. These results show that hyperpolarization is not invariably associated temporally with EPSP frequency potentiation. Moreover, if driving force and membrane conductance changes are assumed to be approximately similar in large dendrites and soma, then the increase in driving force due to membrane hyperpolarization was not sufficient to account for the three- and fourfold increases in EPSP amplitude seen during frequency potentiation. Further, based on similar assumptions and on dendritic models of EPSP attenuation, the decline in Rin should reduce EPSP amplitude at the dendritic synaptic site and, to a proportionately greater extent, at the soma. 4. Studies in which the membrane was hyperpolarized with injected current to approximately the IPSP reversal potential, or in which bicuculline methiodide was applied to the slices, indicated that depression of the IPSP by repetitive stimulation did not account for frequency potentiation of EPSP amplitude. 5. These data are therefore consistent with the conclusion that the frequency potentiation of composite EPSPs in central neurons depends on presynaptic mechanisms, rather than on generalized postsynaptic changes. However, our findings do not rule out localized postsynaptic changes in receptors or spines as possible contributing factors.(ABSTRACT TRUNCATED AT 400 WORDS)