颗粒细胞的抑制作用与肺门神经元的活性。

Epilepsy research. Supplement Pub Date : 1992-01-01
U Misgeld, M Bijak, H Brunner
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引用次数: 0

摘要

来自豚鼠海马切片的电生理数据以及有关齿状颗粒细胞-门门神经元回路的现有形态学信息强烈表明,门门神经元在很大程度上有助于颗粒细胞的突触后抑制。与海马锥体细胞一样,颗粒细胞的抑制性突触后电位要么是由于cl -电导增加,要么是由于k -电导增加。因此,进一步表明门脉神经元抑制颗粒细胞至少属于两个功能不同的组,即产生cl依赖性ipsp的组和产生k依赖性ipsp的组。通过应用药理学工具抑制或增强门门神经元活动的实验,强调了假定的门门神经元的抑制作用。假定gabab激动剂(-)巴氯芬的门部神经元的超极化与颗粒细胞的去抑制有关。如果肝门神经元被4-氨基吡啶或微毒素激活以重复爆发放电,颗粒细胞表现出重复发生的抑制性突触后电位。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Granule cell inhibition and the activity of hilar neurons.

Electrophysiological data from guinea pig hippocampal slices together with available morphological information about the dentate granule cell--hilar neuron circuitry strongly suggest that hilar neurons largely contribute to postsynaptic inhibition of granule cells. As in hippocampal pyramidal cells, inhibitory postsynaptic potentials in granule cells are either due to an increase in Cl-conductance or to an increase in K-conductance. It is therefore further suggested that hilar neurons inhibiting granule cells belong to at least two functionally distinct groups, those generating Cl-dependent and those generating K-dependent IPSPs. The presumed inhibitory action of hilar neurons is underlined by experiments applying pharmacological tools to suppress or enhance hilar neuron activity. Hyperpolarization of hilar neurons by the presumed GABAB-agonist (-)baclofen is associated with disinhibition of granule cells. If hilar neurons are activated by 4-amino-pyridine or picrotoxin to discharge in repetitive bursts, granule cells display repetitively occurring inhibitory postsynaptic potentials.

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