Mechanisms of glutamate release from astrocytes: gap junction "hemichannels", purinergic receptors and exocytotic release

被引：132

作者：

Parpura, V ^{[1
]}

Scemes, E ^{[1
]}

Spray, DC ^{[1
]}

机构：

[1] Yeshiva Univ Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA

来源：

NEUROCHEMISTRY INTERNATIONAL | 2004年 / 45卷 / 2-3期

关键词：

astrocytes; glutamate release; P2X receptors; connexin "hemichannels; Ca2+; vesicular glutamate transporters; SNAREs; exocytosis;

D O I：

10.1016/j.neuint.2003.12.011

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Neuronal exocytotic release of glutamate at synapses involves a highly specialized vesicular apparatus, consisting of a variety of proteins connected to the vesicles or required for vesicular fusion to the presynaptic membrane. Astrocytes also release glutamate, and recent evidence indicates that this release can modify neuronal function. Several mechanisms have been proposed for astrocytic release of glutamate under pathological conditions, such as reversal of glutamate transporters and opening of volume sensitive ion channels. In this review we limit our discussion to findings supporting the exocytotic release of glutamate, as well as two new pathways implicated in this release, the ionotropic (P2X) purinergic receptors and gap junction hemichannels. (C) 2004 Elsevier Ltd. All rights reserved.

引用

页码：259 / 264

页数：6

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