ELECTROPHYSIOLOGICAL PROPERTIES AND SYNAPTIC RESPONSES IN THE DEEP LAYERS OF THE HUMAN EPILEPTOGENIC NEOCORTEX INVITRO
ELECTROPHYSIOLOGICAL PROPERTIES AND SYNAPTIC RESPONSES IN THE DEEP LAYERS OF THE HUMAN EPILEPTOGENIC NEOCORTEX INVITRO
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DOI：
10.1152/jn.1989.61.3.589
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发表时间：
1989-03-01
影响因子：
2.5
通讯作者：
OLIVIER, A
中科院分区：
文献类型：
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作者：
AVOLI, M;OLIVIER, A
人类癫痫患者为缓解顽固性癫痫发作而切除的第一、第二颞回和额叶的新皮质切片，在体外维持在35。1. degree.c。深层神经元的电生理特性（1800 - 2600 .mu）。用常规的细胞内记录和刺激技术研究了枕部表面下的M。细胞外局灶刺激诱发突触反应。用荧光染料路西法黄在细胞内注射的一些细胞显示出大的刺锥体神经元。不同皮质区神经元的输入电阻、静息膜电位（Vm）和动作电位幅值相似。当神经元按照皮层组织原位显示的癫痫样电图活动程度分组时，这些参数也相似。当神经元以5 ~ 15 mV向静息Vm正极性去极化时，发生向内整流。细胞外应用河豚毒素(TTX, 1。M)，但在Ca2+通道阻滞剂Cd2+ (2 mM)的存在下仍然观察到。超极化电流脉冲引起缓慢发展的向内整流，称为异常整流，对TTX不敏感，但被细胞外应用Cs+ (1-2 mM)阻断。细胞内注射去极化方形脉冲电流（0.1 ~ 4 s）可诱发重复放电。在大多数细胞中，放电速率在达到稳定水平之前会平稳地下降几十毫秒（即适应）。重复发射频率与注入电流之间的关系图（f-I曲线）在早期间隔以及适应和/或稳定发射中显示出两个线性段。在早期间隔和适应射击期间计算的f-I曲线的初始，更陡峭的线性段的斜率为163 .+-。51和56，+-。27 (SD) Hz/nA。在去极化电流方形脉冲诱发的重复放电之后，出现了持续时间长达8 s的后超极化（AHP）。它的振幅与注入电流的大小成正比，对Vm的变化很敏感，其平衡电位负10-40 mV。这个值加上AHP可以用充满kcl的微电极记录的事实表明，这是由对K+离子的电导增加引起的。Ca2+通道阻滞剂Cd2+ (2mm)或Mn2+ (2mm)的浴液应用减少并最终阻断AHP。这些变化伴随着放电适应性的显著降低，表明Ca2+依赖的K+电导是AHP的原因。
Neocortical slices of the first and second temporal gyrus and frontal lobe, removed in human epileptic patients for the relief of intractable seizures, were maintained in vitro at 35 .+-. 1.degree.C. Electrophysiological properties of neurons in the deep layers (1,800-2,600 .mu.m below the pial surface) were studied with conventional intracellular recording and stimulation techniques. Synaptic responses were evoked by extracellular focal stimuli. Intracellular injections of some cells with the fluorescent dye Lucifer yellow revealed large spiny pyramidal neurons. Values of input resistance, resting membrane potential (Vm), and action-potential amplitude were similar for neurons in different cortical region. These parameters were also similar when neurons were grouped in accordance to the degree of electrographic epileptiform activity displayed by the cortical tissue in situ. Inward rectification occurred when neurons were depolarized by 5-15 mV positive to the resting Vm. This rectification was abolished by extracellular application of tetrodotoxin (TTX, 1 .mu.M), but was still observed in the presence of the Ca2+-channel blocker Cd2+ (2 mM). Pulses of hyperpolarizing current elicited a slowly developing inward rectification, called anomalous rectification, which was insenstive to TTX, but blocked by extracellular application of Cs+ (1-2 mM). Intracellular injection of depolarizing square pulses of current (0.1-4 s) evoked repetitive firing. In most cells the firing rate decreased smoothly for tens of milliseconds (i.e., it adapted) before reaching a steady level. Plots of the relation between frequency of the repetitive firing and injected current (f-I curve) displayed two linear segments for the early intervals as well as for the adapted and/or the steady firing. The slope of the initial, steeper linear segment of the f-I curve computed during the early intervals and during the adapted firing was 163 .+-. 51 and 56.+-. 27 (SD) Hz/nA, respectively. A long-lasting (upt to 8 s) afterhyperpolarization (AHP) followed the repetitive firing induced by square pulses of depolarizing current. Its amplitude was directly proportional to the amount of current injected, it was sensitive to changes in the Vm, and its had an equilibrium potential 10-40 mV negative to the resting Vm. This value plus the fact that the AHP could be recorded with KCl-filled microelectrodes suggested that it was caused by an increase in conductance to K+ ions. Bath applications of the Ca2+ channel blockers Cd2+ (2 mM) or Mn2+ (2 mM) decreased and eventually blocked the AHP. These changes, which were accompanied by a marked decrease in the adaptation of firing, indicate that a Ca2+-dependent K+ conductance was responsible for the AHP.