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在使用高钾进行微透析时,齿状回中谷氨酸释放及扩散性抑制:神经胶质细胞的作用

Glutamate release and spreading depression in the fascia dentata in response to microdialysis with high K+: role of glia.

作者信息

Szerb J C

机构信息

Department of Physiology and Biophysics, Dalhousie University, Halifax, N.S., Canada.

出版信息

Brain Res. 1991 Mar 1;542(2):259-65. doi: 10.1016/0006-8993(91)91576-m.

DOI:10.1016/0006-8993(91)91576-m
PMID:1674223
Abstract

To see electrophysiological and neurochemical events during microdialysis with high [K+], direct current (DC) and excitatory postsynaptic field potentials (fEPSPs) due to perforant path stimulation were recorded in the granule cell layer of the fascia dentata, while 3, 25, 50 or 100 mM KCl was perfused through a microdialysis probe placed 1.5 mm from the recording electrode. Glutamate and glutamine content of the dialysate was measured by high performance liquid chromatography. Raising [K+] from 3 to 25 mM reduced the efflux of glutamine, without affecting that of glutamate or the electrical activity. In about 50% of experiments, 50 mM K+ induced large (20-30 mV) negative waves of spreading depression (SD), and a suppression of fEPSPs. In the other 50%, without SD, fEPSPs did not change. Glutamate efflux increased 3-fold in both groups. SD waves were produced in all experiments with 100 mM K+ which evoked a more than 10-fold increase in glutamate release. Glutamine efflux decreased equally, by about 50%, with the 3 concentrations of K+. Microdialysis with 20 mM fluoroacetate, a glial metabolic poison, decreased the spontaneous efflux of glutamine and glutamate and increased the incidence of SD waves. Results suggest that perfusion of 50 or 100 mM K+ through a microdialysis probe causes spreading depression which blocks surrounding electrical activity. The activity of glia partly protects against spreading depression caused by high [K+].

摘要

为观察高[K⁺]微透析过程中的电生理和神经化学事件,在齿状回颗粒细胞层记录了直流电(DC)和由穿通通路刺激引起的兴奋性突触后场电位(fEPSPs),同时通过置于距记录电极1.5毫米处的微透析探针灌注3、25、50或100 mM的氯化钾。通过高效液相色谱法测量透析液中的谷氨酸和谷氨酰胺含量。将[K⁺]从3 mM提高到25 mM可减少谷氨酰胺的外流,而不影响谷氨酸的外流或电活动。在约50%的实验中,50 mM K⁺诱发了大的(20 - 30 mV)扩散性抑制(SD)负波,并抑制了fEPSPs。在另外50%的实验中,没有出现SD时,fEPSPs没有变化。两组实验中谷氨酸外流均增加了3倍。在所有使用100 mM K⁺的实验中均产生了SD波,这引起了谷氨酸释放增加超过10倍。对于3种浓度的K⁺,谷氨酰胺外流均同等程度地减少了约50%。用20 mM氟乙酸(一种神经胶质代谢毒物)进行微透析,可减少谷氨酰胺和谷氨酸的自发外流,并增加SD波的发生率。结果表明,通过微透析探针灌注50或100 mM K⁺会导致扩散性抑制,从而阻断周围的电活动。神经胶质的活动部分地保护机体免受高[K⁺]引起的扩散性抑制。

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