Evidence for GABAergic inhibitory deficits in major depressive disorder

被引：114
|
作者：
Croarkin, Paul E. [2 ]
Levinson, Andrea J.
Daskalakis, Zafiris J. [1 ]
机构：
[1] Univ Toronto, Fac Med, Ctr Addict & Mental Hlth, Dept Psychiat, Toronto, ON M5T 1R8, Canada
[2] Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA
来源：
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS | 2011年 / 35卷 / 03期
基金：
美国国家卫生研究院; 加拿大健康研究院;
关键词：
Major depressive disorder; Cortical inhibition; GABA; Transcranial magnetic stimulation; Interneuron; GAMMA-AMINOBUTYRIC-ACID; TRANSCRANIAL MAGNETIC STIMULATION; MOTOR CORTEX EXCITABILITY; INCREASED CORTICAL INHIBITION; OCCIPITAL CORTEX; GABA CONCENTRATIONS; SILENT PERIOD; SUICIDE BRAIN; RECEPTORS; SEROTONIN;
D O I：
10.1016/j.neubiorev.2010.10.002
中图分类号：
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号：
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要：
Converging evidence suggests that deficits in gamma-aminobutyric acid (GABA) functioning are implicated in the pathophysiology of major depressive disorder (MDD). This is highlighted by research investigating cortical inhibition (Cl), a process whereby GABAergic interneurons selectively attenuate pyramidal neurons. Transcranial magnetic stimulation (TMS) paradigms evaluate this marker of neuronal inhibitory activity in the cortex. This review will examine the neuroanatomic and neurophysiological evidence from neuroimaging, molecular, treatment, and TMS studies linking dysfunctional GABAergic neurotransmission to MDD. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码：818 / 825
页数：8
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