Bartholini G
Schweiz Arch Neurol Neurochir Psychiatr. 1979;125(2):265-9.
Several pieces of evidence support the view that GABA neurons inhibit the DA system both in extrapyramidal and limbic regions. This inhibition is exerted on cell bodies and terminals of DA neurons and is involved in the regulation of their activity. A recently synthesized GABAmimetic compound SL 76.002 has considerably helped in elucidating the role of GABA in this regulation as well as the therapeutic implication of changes of GABAergic transmission in human brain. Thus, impairment of dopaminergic transmission by SL 76.002 has been shown to be effective in iatrogenic extrapyramidal syndromes such as L-DOPA-induced involuntary movements in parkinsonian patients and neuroleptic-induced tardive dyskinesias: the first attributed to an exaggerated formation and liberation of DA, the second to supersensitivity of target cells of DA neurons. Furthermore, GABAergic medication has been confirmed to be useful in Huntington's chorea in which some symptoms originate from degeneration of striatal GABAergic neurons. Finally, GABAergic inhibition on cellular excitability has been proved to ameliorate epilepsy. However, SL 76.002, contrary to the expectation, was not effective in schizophrenia suggesting that GABA does not play a major role in the pathogenesis of this disorder.
多条证据支持这样一种观点，即γ-氨基丁酸（GABA）能神经元在锥体外系和边缘系统区域均对多巴胺（DA）系统起抑制作用。这种抑制作用作用于DA能神经元的细胞体和终末，并参与其活动的调节。最近合成的一种GABA模拟化合物SL 76.002在阐明GABA在这种调节中的作用以及GABA能传递变化在人脑中的治疗意义方面有很大帮助。因此，已表明SL 76.002对多巴胺能传递的损害在医源性锥体外系综合征中有效，如帕金森病患者中左旋多巴诱导的不自主运动以及抗精神病药物引起的迟发性运动障碍：前者归因于DA过度生成和释放，后者归因于DA能神经元靶细胞的超敏反应。此外，已证实GABA能药物对亨廷顿舞蹈病有用，其中一些症状源于纹状体GABA能神经元的变性。最后，已证明GABA能对细胞兴奋性的抑制可改善癫痫。然而，与预期相反，SL 76.002在精神分裂症中无效，这表明GABA在该疾病的发病机制中不发挥主要作用。
