ROLE OF GAMMA-AMINOBUTYRIC ACID IN ANXIETY
ROLE OF GAMMA-AMINOBUTYRIC ACID IN ANXIETY
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DOI：
10.1159/000284073
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发表时间：
1984-01-01
期刊：
影响因子：
3.6
通讯作者：
ENNA, SJ
中科院分区：
文献类型：
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作者：
ENNA, SJ
抗焦虑选择性药物的发展使得研究焦虑的生化基础成为可能。电生理学分析表明，苯二氮卓类药物选择性增强γ-氨基丁酸（GABA）神经传递。随后的工作证明了神经元膜上存在特定群的苯二氮卓结合位点。这些位点似乎与某些 GABA 受体相关，因此苯二氮卓成分的占据揭示了一组可能对神经递质更敏感的 GABA 识别位点。这些数据，再加上巴比妥率可能至少部分通过与 GABA 受体偶联氯离子通道相互作用的发现，表明对 GABA 系统的药理学操作可以减轻焦虑症状。苯二氮卓类药物的抗焦虑选择性可能与它们仅激活特定群体的 GABA 受体有关，而巴比妥类药物可以增强大多数这些位点。这些发现表明 GABA 系统的改变可能部分解释焦虑的神经化学基础。
The development of anxioselective agents has made it possible to examine the biochemical basis of anxiety. Electrophysiological analysis revealed that benzodiazepines selectively enhance y-aminobutyric acid (GABA) neurotransmission. Subsequent work dem onstrated the presence of a specific population of benzodiazepine binding sites on neuronal membranes. These sites appear to be linked to certain GABA receptors such that occupation of the benzodiazepine component reveals a group of GABA recognition sites that may be more sensitive to the neurotransmitter. These data, coupled with the findings that barbitu rates may act, at least in part, by interacting with the GABA receptor-coupled chloride chan nel, suggest that pharmacological manipulations of the GABA system can alleviate the symp toms of anxiety. The anxioselectivity of the benzodiazepines may be related to the fact that they activate only a certain population of GABA receptors, whereas barbiturates can poten tiate the majority of these sites. These discoveries point to the possibility that alterations in the GABA system may partially explain the neurochemical basis of anxiety.