Studies on the relation of gamma-hydroxybutyric acid (GHB) to gamma-aminobutyric acid (GABA). Evidence that GABA is not the sole source for GHB in rat brain.
Studies on the relation of gamma-hydroxybutyric acid (GHB) to gamma-aminobutyric acid (GABA). Evidence that GABA is not the sole source for GHB in rat brain.
复制标题
γ-羟基丁酸（GHB）与γ-氨基丁酸（GABA）关系的研究。
DOI：
10.1016/0006-2952(82)90310-0
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发表时间：
1982
影响因子：
5.8
通讯作者：
Bearden,LJ
中科院分区：
文献类型：
--
作者：
Snead3rd,OC;Liu,CC;Bearden,LJ
本文研究了γ-氨基丁酸（GABA）-α-酮戊二酸氨基转移酶（GABA-T）抑制剂、谷氨酸脱羧酶（GAD）抑制剂和抗癫痫药对γ-羟丁酸（GHB）和GABA的影响。抗惊厥药和GABA-T抑制剂治疗导致GHB和GABA的稳态脑水平增加。GAD抑制剂产生显着降低脑GABA水平，但GHB浓度没有变化。对完全由GABA衍生的GHB的研究表明，GABA-T抑制剂可提高脑中GHB的稳态水平，也可降低GABA衍生的GHB。脑室内（i. c. v.）GABA、腐胺和1，4-丁二醇的给药均产生脑GHB的显著升高，但GABA-T抑制剂阻断了GABA和腐胺的这种作用。这些数据表明，除了GABA外，脑中可能还有另一种GHB来源，并提出了1，4-丁二醇可能是该来源的可能性。
The effects of γ-aminobutyric acid (GABA)-α-oxoglutarate aminotransferase (GABA-T) inhibitors,l-glutamic acid decarboxylase (GAD) inhibitors, and antipetit mal anticonvulsants on γ-hydroxybutyric acid (GHB) and GABA were studied. Treatment with anticonvulsants and GABA-T inhibitors resulted in an increase in steady-state brain levels of both GHB and GABA. GAD inhibitors produced markedly decreased levels of brain GABA but no change in GHB concentrations. Studies of GHB derived exclusively from GABA showed that GABA-T inhibitors which produced an elevation of steady-state levels of GHB in brain also resulted in a decrease in GABA-derived GHB. Intracere-broventricular (i.c.v.) administration of GABA, putrescine, and 1,4-butanediol all produced significant elevations in brain GHB, but GABA-T inhibitors blocked this effect of GABA and putrescine. These data suggest that there may be another source for GHB in brain in addition to GABA and raise the possibility that 1,4-butanediol may be that source.