Shiah I S, Yatham L N
Department of Psychiatry, The University of British Columbia, Vancouver, Canada.
Life Sci. 1998;63(15):1289-303. doi: 10.1016/s0024-3205(98)00241-0.
Over the past twenty years, several lines of evidence from preclinical and clinical studies has accumulated suggesting that a GABA deficit may be involved in mood disorders, particularly in depression, and that increasing GABAergic neurotransmission may exert an antidepressant effect and perhaps a mood stabilizing effect. Given that GABA has an inhibitory effect on biogenic amine neurotransmitters such as norepinephrine and serotonin and this inhibition may be involved in local circuits and interneurons, it has been suggested that the hypothesis of a GABA deficit in mood disorders does not compete with but complements the well-established hypotheses of alterations in noradrenergic and serotonergic function in mood disorders. In this paper, we systematically reviewed the results from preclinical and clinical studies of GABA function in the pathophysiology of mood disorders and in the mechanism of action of mood stabilizers, antidepressants and electroconvulsive therapy. We also discussed the unifying theory of the neurochemistry of mood disorders, which integrates the GABA hypothesis into the biogenic amine hypotheses, and indicated future directions for research.
在过去二十年中，临床前和临床研究积累了若干证据，表明γ-氨基丁酸（GABA）缺乏可能与情绪障碍有关，尤其是抑郁症，并且增强GABA能神经传递可能发挥抗抑郁作用，或许还有情绪稳定作用。鉴于GABA对去甲肾上腺素和5-羟色胺等生物胺神经递质有抑制作用，且这种抑制可能涉及局部回路和中间神经元，有人提出情绪障碍中GABA缺乏的假说并非与情绪障碍中去甲肾上腺素能和5-羟色胺能功能改变这一公认假说相互竞争，而是对其进行补充。在本文中，我们系统回顾了临床前和临床研究中关于GABA功能在情绪障碍病理生理学以及情绪稳定剂、抗抑郁药和电休克治疗作用机制方面的研究结果。我们还讨论了情绪障碍神经化学的统一理论，该理论将GABA假说纳入生物胺假说，并指出了未来的研究方向。
