• Sayumi Fujimori and Yukio Yoneda.
• Laboratory of Molecular Pharmacology, Kanazawa University Graduate School of Natural Science and Technology, Kakuma-machi, Kanazawa 920-1192, Japan.
• Nihon Shinkei Seishin Yakurigaku Zasshi. 2004 Oct 1; 24 (5): 265-71.

AbstractIn the mammalian central nervous system (CNS), the inhibitory GABAergic system is composed of different signaling molecules such as glutamate decaroxylase, vesicular GABA transporters, GABA receptors, GABA transporters and GABA transaminase. A prevailing view is that the balance between excitatory signaling mediated by glutamate and inhibitory signaling mediated by GABA plays a pivotal role in mechanisms underlying the modulation and maintenance of a variety of neural functions. Therefore, abnormalities in a GABAergic signaling molecule would lead to a crisis of severe symptoms relevant to a number of neuropsychiatric disorders. These include epilepsy, depression, schizophrenia, stiff-person syndrome, drug addiction and so on. In this review article, we will summarize recent studies on the relationship between the malfunction of GABAergic signaling molecules and the etiology of these neuropsychiatric disorders. We will also refer to novel strategies on GABAergic signaling molecules other than GABA receptors for therapeutic usefulness in the future.

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