Díaz-Muñoz M, Tapia R
Departamento de Neurociencias, Universidad Nacional Autónoma de México, México, D. F.
Neurochem Res. 1988 Jan;13(1):37-44. doi: 10.1007/BF00971852.
Hepatic coma was induced in rats chronically treated with CCl4, by means of a single injection of ammonium acetate. The activities of glutamate decarboxylase (GAD) and GABA transaminase (GABA-T), as well as the synaptosomal uptake and release of [3H]GABA, were measured in the following brain areas of the comatose rats: cortex, striatum, hypothalamus, hippocampus, midbrain and cerebellum. Hepatic coma was associated with a general decrease of GAD activity, whereas GABA-T activity was diminished only in the hypothalamus, striatum and midbrain. During hepatic coma, the K+-stimulated [3H]GABA release was notably diminished in the striatum and cerebellum, whereas a significant increase was observed in the hippocampus. [3H]GABA uptake increased in most regions after CCl4 treatment, independently of the presence of coma. The results indicate that GABAergic transmission seems to be decreased in most cerebral regions during hepatic coma.
通过单次注射醋酸铵，在长期用四氯化碳处理的大鼠中诱发肝昏迷。在昏迷大鼠的以下脑区测量谷氨酸脱羧酶（GAD）和GABA转氨酶（GABA-T）的活性，以及[3H]GABA的突触体摄取和释放：皮层、纹状体、下丘脑、海马、中脑和小脑。肝昏迷与GAD活性普遍降低有关，而GABA-T活性仅在下丘脑、纹状体和中脑降低。在肝昏迷期间，纹状体和小脑中钾离子刺激的[3H]GABA释放明显减少，而海马中则观察到显著增加。四氯化碳处理后，大多数区域的[3H]GABA摄取增加，与昏迷状态无关。结果表明，在肝昏迷期间，大多数脑区的GABA能传递似乎减少。
