Differences in inhibitory synaptic input between layer II-III and layer V neurons of the cat neocortex.
Differences in inhibitory synaptic input between layer II-III and layer V neurons of the cat neocortex.
复制标题
猫新皮质的 II-III 层和 V 层神经元之间抑制性突触输入的差异。
DOI：
10.1152/jn.1995.74.3.1149
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发表时间：
1995
影响因子：
2.5
通讯作者：
Spain,WJ
中科院分区：
文献类型：
--
作者：
vanBrederode,JF;Spain,WJ
1.本研究的目的是比较猫运动皮层不同层次的内在抑制性突触输入的相对有效性。在离体条件下，通过局部细胞外刺激，在位于浅层（Ⅱ-Ⅲ层）或深层（Ⅴ层）的神经元中诱发突触后电位（PSP）。电生理特性和细胞内充盈表明所记录的神经元为锥体细胞。2.诱发的PSP的形状和时间过程不同。第II-III层细胞表现出由快速兴奋性PSP（fEPSP）和快速和缓慢抑制性PSP（分别为fIPSP和sIPSP）组成的定型三相PSP。相反，第V层细胞中的PSP变化更大，主要是在静息膜电位下去极化，并且在84%的静息测试神经元中缺乏超极化IPSP。3.用6-氰基-7-硝基喹喔啉-2，3-二酮（CNQX）和D-2-氨基-5-膦酰基戊酸（AP 5）阻断多巴胺能神经传递后发现，通过局部刺激浅层或深层，甚至在对照灌注液中显示小或无IPSP的那些细胞中，fIPSP也可以在所有V层细胞中被诱发。当刺激深层时，仅在五分之一的V层细胞中诱发小的（< 1 mV）孤立的sIPSP，当刺激浅层时，在约一半的V层细胞中诱发小的（< 1 mV）孤立的sIPSP。在II-III层细胞中，刺激表层总是导致fIPSP-sIPSP组合。阻断多巴胺后，刺激深层神经元不能诱发Ⅱ-Ⅲ层神经元的IPSPs。选择性阻断γ-氨基丁酸-A（GABAA）或GABAB受体介导的神经传递表明，在这两种细胞类型中，fIPSP是由于GABAA受体刺激，而sIPSP是由GABAB受体介导的。4.在含有CNQX、AP 5和GABAB拮抗剂CGP 35348的灌注液中记录分离的fIPSP。第II-III层细胞中fIPSPs的上升和衰减时间显著长于第V层细胞中的fIPSPs。上升和衰减时间归一化的膜时间常数的差异没有显着不同，但是，这表明突触后膜的内在膜特性的fIPSP在这两种细胞类型的时间过程中的差异。5.选择性阻断内向整流电流Ih与细胞外Cs+表明，这种电导的功能，以缩短和衰减fIPSPs在第V层细胞。相反，Ih在II-III层细胞中不存在或很小，因此，Cs+对这些细胞中诱发的fIPSPs几乎没有影响。（400字处截断摘要）
1. The goal of this study was to compare the relative effectiveness of intrinsic inhibitory synaptic inputs in different layers of the cat motor cortex. Postsynaptic potentials (PSPs) were evoked in neurons located in the superficial (layer II-III) or deep layers (layer V) by local extracellular stimulation in vitro. Electrophysiological properties and intracellular filling indicated that the recorded neurons were pyramidal cells. 2. The shape and time course of the evoked PSPs differed. Layer II-III cells showed stereotyped triphasic PSPs consisting of a fast excitatory PSP (fEPSP) and a fast and slow inhibitory PSP (fIPSP and sIPSP, respectively). PSPs in layer V cells, in contrast, were much more variable, mainly depolarizing at resting membrane potential, and lacked a hyperpolarizing IPSP in 84% of neurons tested at rest. 3. Blockade of glutaminergic neurotransmission with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D-2-amino-5-phosphonovaleric acid (AP5) revealed that fIPSPs could be evoked in all layer V cells by local stimulation of the superficial or deep layers, even in those that showed small or no IPSPs in control perfusate. Small (< 1 mV) isolated sIPSPs were evoked in only one-fifth of layer V cells when the deep layers were stimulated, and in about one-half of the layer V cells when the superficial layers were stimulated. In layer II-III cells, stimulation of the superficial layers always resulted in fIPSP-sIPSP combinations. No IPSPs could be evoked in layer II-III neurons by stimulating the deep layers after glutaminergic blockade. Selective blockade of gamma-aminobutyric acid-A (GABAA) or GABAB receptor-mediated neurotransmission showed that in both cell types fIPSPs were due to GABAA receptor stimulation, whereas sIPSPs were mediated by GABAB receptors. 4. Isolated fIPSPs were recorded in perfusate containing CNQX, AP5, and the GABAB antagonist CGP 35348. The rise and decay times of the fIPSPs in layer II-III cells were significantly longer than those in layer V cells. Rise and decay times normalized for differences in membrane time constant were not significantly different, however, suggesting that the intrinsic membrane properties of the postsynaptic membrane account for the difference in time course of the fIPSPs in these two cell types. 5. Selective blockade of the inward rectifier current Ih with extracellular Cs+ showed that this conductance functions to shorten and attenuate fIPSPs in layer V cells. In contrast, Ih is absent or small in layer II-III cells, and, consequently, Cs+ had little or no effect on the fIPSPs evoked in these cells.(ABSTRACT TRUNCATED AT 400 WORDS)