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颗粒细胞抑制与海马门区神经元的活动

Granule cell inhibition and the activity of hilar neurons.

作者信息

Misgeld U, Bijak M, Brunner H

机构信息

I. Physiologisches Institut der Universität Heidelberg, Germany.

出版信息

Epilepsy Res Suppl. 1992;7:113-8.

PMID:1334657
Abstract

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.

摘要

来自豚鼠海马切片的电生理数据,以及关于齿状颗粒细胞 - 门区神经元回路的现有形态学信息,强烈表明门区神经元在很大程度上对颗粒细胞的突触后抑制起作用。与海马锥体细胞一样,颗粒细胞中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,进一步表明抑制颗粒细胞的门区神经元至少属于两个功能不同的组,即产生Cl依赖性抑制性突触后电位的组和产生K依赖性抑制性突触后电位的组。应用药理学工具抑制或增强门区神经元活动的实验强调了门区神经元假定的抑制作用。假定的GABAB激动剂( - )巴氯芬使门区神经元超极化与颗粒细胞的去抑制有关。如果门区神经元被4 - 氨基吡啶或苦味毒素激活而重复爆发放电,颗粒细胞会显示出反复出现的抑制性突触后电位。

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