惊厥后大鼠脑区γ-氨基丁酸（GABA）合成速率的抑制。
Inhibition of the rate of GABA synthesis in regions of rat brain following a convulsion.
作者信息
Green A R, Metz A, Minchin M C, Vincent N D
机构信息
MRC Clinical Pharmacology Unit, Radcliffe Infirmary, Oxford.
出版信息
Br J Pharmacol. 1987 Sep;92(1):5-11. doi: 10.1111/j.1476-5381.1987.tb11288.x.
Abstract
1 The rate of synthesis of gamma-aminobutyric acid (GABA) in the cortex, hippocampus and striatum of rat brain was assessed by measuring the linear rate of accumulation of GABA following injection of amino-oxyacetic acid (AOAA). 2 Five min after a single electrically induced seizure there was a rise in GABA content in these brain regions and an almost total inhibition of the rate of synthesis. 3 Five min after seizure induced by the inhalant convulsant flurothyl there was no rise in GABA content in these brain regions but a similar marked degree of inhibition of GABA synthesis. 4 Two hours after the convulsion the rate of GABA synthesis had returned to control values in all three brain regions. 5 A single convulsion did not alter the glutamic acid decarboxylase activity in these brain regions either in the absence or presence of added co-factor (pyridoxal phosphate). 6 Evidence for an inhibition of GABA release following a convulsion which may be associated with the inhibition of GABA synthesis is presented in the following paper.
摘要
1 通过测量注射氨氧基乙酸（AOAA）后γ-氨基丁酸（GABA）的线性积累速率，评估大鼠大脑皮质、海马体和纹状体中GABA的合成速率。2 单次电诱发癫痫发作5分钟后，这些脑区的GABA含量升高，合成速率几乎完全受到抑制。3 吸入性惊厥剂氟代乙酰胺诱发癫痫发作5分钟后，这些脑区的GABA含量没有升高，但GABA合成受到类似程度的显著抑制。4 惊厥发作两小时后，所有三个脑区的GABA合成速率均恢复到对照值。5 单次惊厥发作在不存在或存在添加的辅因子（磷酸吡哆醛）的情况下，均未改变这些脑区的谷氨酸脱羧酶活性。6 下一篇论文将提供惊厥发作后GABA释放受到抑制的证据，这可能与GABA合成的抑制有关。
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