期刊
BEHAVIOURAL PHARMACOLOGY
卷 21, 期 5-6, 页码 514-522出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/FBP.0b013e32833d41b2
关键词
cystine/glutamate exchanger; drug seeking; glial glutamate transporter; glutamate homeostasis
资金
- NIH [DA015369, DA012513, DA003906]
- NATIONAL INSTITUTE ON DRUG ABUSE [P50DA015369, R01DA012513, F32DA026254, R37DA003906, R01DA003906] Funding Source: NIH RePORTER
Well-developed cellular mechanisms exist to preserve glutamate homeostasis and regulate extrasynaptic glutamate levels. Accumulating evidence indicates that disruptions in glutamate homeostasis are associated with addictive disorders. The disruptions in glutamate concentrations observed after prolonged exposure to drugs of abuse are associated with changes in the function and activity of several key components within the homeostatic control mechanism, including the cystine/glutamate exchanger xc(-) and the glial glutamate transporter, EAAT2/GLT-1. Changes in the balance between synaptic and extrasynaptic glutamate levels in turn influence signaling through presynaptic and postsynaptic glutamate receptors, and thus affect synaptic plasticity and circuit-level activity. In this review, we describe the evidence for impaired glutamate homeostasis as a critical mediator of long-term drug-seeking behaviors, how chronic neuroadaptations in xc(-) and the glutamate transporter, GLT-1, mediate a disruption in glutamate homeostasis, and how targeting these components restores glutamate levels and inhibits drug-seeking behaviors. Behavioural Pharmacology 21:514-522 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据