Evidence of glutamatergic deficiency in schizophrenia
Evidence of glutamatergic deficiency in schizophrenia
复制标题
精神分裂症谷氨酸能缺乏的证据
DOI：
10.1016/0304-3940(91)90653-b
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发表时间：
1991
影响因子：
2.5
通讯作者：
R. Waziri
中科院分区：
文献类型：
--
作者：
A. Sherman;A. Davidson;S. Baruah;T. S. Hegwood;R. Waziri
使用精神分裂症患者和对照组大脑的冷冻切片进行氨基酸释放的研究。通过在聚蔗糖中差速离心制备突触体，从而可以测量藜芦定诱导的天冬氨酸、谷氨酸、甘氨酸和 GABA 的释放。精神分裂症患者突触体中谷氨酸和 γ-氨基丁酸 (GABA) 的释放减少。这种下降可以通过突触体与氟哌啶醇的预孵育来部分逆转。此外，氟哌啶醇预孵育降低了谷氨酸脱羧酶的活性并部分恢复了其活性。这些数据与精神分裂症中谷氨酸/GABA能缺陷的假设一致。
Studies of amino acid release were carried out using frozen sections from brains of schizophrenics and controls. Synaptosomes were prepared via differential centrifugation in Ficoll allowing the veratridine-induced release of aspartate, glutamate, glycine, and GABA to be measured. The release of glutamate and γ-aminobutyric acid (GABA) was reduced in the synaptosomes from schizophrenics. This decrease could be reversed partially by pre-incubation of the synaptosomes with haloperidol. Additionally, the activity of glutamate decarboxylase was decreased and partially restored by haloperidol pre-incubation. These data are consistent with the hypothesis of a glutamatergic/GABAergic deficit in schizophrenia.