Function of glutamate and GABA in schizophrenia

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  • 統合失調症患者におけるグルタミン酸・GABAの動態
  • トウゴウ シッチョウショウ カンジャ ニ オケル グルタミンサン ・ GABA ノ ドウタイ

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Abstract

The N-methyl-D-aspartic acid (NMDA) hypofunction model of schizophrenia is based on the ability of NMDA receptor antagonists to mimic schizophrenic symptoms. Glutamate system and gamma- amino butyric acid (GABA) system have functional correlation. NMDA receptor hypofunction on GABAergic neuron could cause hypofunction of GABA system, and may lead to disinhibition of pyramidal neurons, cortical excitation and neural toxity. The proton magnetic resonance spectroscopy (1H-MRS) technique can evaluate the metabolites levels in the region of interest of brain. Recently, new techniques of MRS become available which allow separated determination of glutamate, glutamine and GABA from its close spectral position. The aim of this article is to provide an overview of existing MRS studies which support the NMDA hypofunction model of schizophrenia.

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