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离子通道参与海马切片中缺氧诱导的扩散性抑制。

Ion channel involvement in hypoxia-induced spreading depression in hippocampal slices.

作者信息

Aitken P G, Jing J, Young J, Somjen G G

机构信息

Department of Cell Biology, Duke University Medical Center, Durham, NC 27710.

出版信息

Brain Res. 1991 Feb 8;541(1):7-11. doi: 10.1016/0006-8993(91)91067-b.

Abstract

Rat hippocampal tissue slices were made hypoxic in control medium and in medium containing the ion channel blockers tetraethylammonium (TEA), 4-aminopyridine (4-AP), or tetrodotoxin (TTX). Postsynaptic evoked potentials, extracellular DC potential Vec, and in some experiments extracellular potassium concentration [K+]o were monitored in stratum pyramidale of the CA1 region. TEA (10 mM) decreased the latency of hypoxia-induced spreading depression (SD), and reduced the amplitudes of the changes in Vec and [K+]o. 4-AP (50 microM) also decreased the latency of SD but had no effect on the Vec shift. In most slices, TTX (1 microM) increased SD latency but had no effect on the Vec shift. In some slices, TTX blocked the occurrence of SD.

摘要

将大鼠海马组织切片在对照培养基以及含有离子通道阻滞剂四乙铵(TEA)、4-氨基吡啶(4-AP)或河豚毒素(TTX)的培养基中进行缺氧处理。在CA1区的锥体层监测突触后诱发电位、细胞外直流电位Vec,在某些实验中还监测细胞外钾浓度[K+]o。TEA(10 mM)缩短了缺氧诱导的扩散性抑制(SD)的潜伏期,并降低了Vec和[K+]o变化的幅度。4-AP(50 microM)也缩短了SD的潜伏期,但对Vec偏移没有影响。在大多数切片中,TTX(1 microM)延长了SD潜伏期,但对Vec偏移没有影响。在一些切片中,TTX阻止了SD的发生。

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