Lindgren S, Andén N E
Acta Pharmacol Toxicol (Copenh). 1984 Jul;55(1):41-9. doi: 10.1111/j.1600-0773.1984.tb01960.x.
Changes in the GABA concentration in different parts of the rat brain were studied following inhibition of the glutamic acid decarboxylase or the GABA-alpha-ketoglutaric acid aminotransferase. The GABA concentration was reduced by the decarboxylase inhibitors 4-deoxypyridoxine and isoniazid, but not by 3-mercaptopropionic acid and DL-allylglycine. The aminotransferase inhibitor gamma-acetylenic GABA increased the concentration of GABA and this effect was markedly inhibited by 3-mercaptopropionic acid and partly by 4-deoxypyridoxine and isoniazid. The 4-deoxypyridoxine-induced decrease in GABA concentration was approximately maximal after 400 mg/kg intraperitoneally and 90 min. The brain DOPA decarboxylase activity in vivo was not inhibited by 4-deoxypyridoxine. The GABA concentration in the substantia nigra was reduced by 75 per cent 4 days after section of the striato-nigral GABA neurones. In the denervated substantia nigra, 4-deoxypyridoxine did not change the concentration of GABA whereas the effect of gamma-acetylenic GABA was reduced by 70 per cent.
在抑制谷氨酸脱羧酶或γ-氨基丁酸-α-酮戊二酸转氨酶后，研究了大鼠脑不同部位γ-氨基丁酸（GABA）浓度的变化。脱羧酶抑制剂4-脱氧吡哆醇和异烟肼可降低GABA浓度，但3-巯基丙酸和DL-烯丙基甘氨酸则无此作用。转氨酶抑制剂γ-乙炔基GABA可增加GABA浓度，且该作用被3-巯基丙酸显著抑制，被4-脱氧吡哆醇和异烟肼部分抑制。腹腔注射400mg/kg 4-脱氧吡哆醇90分钟后，其诱导的GABA浓度降低作用接近最大。4-脱氧吡哆醇对体内脑多巴脱羧酶活性无抑制作用。切断纹状体-黑质GABA神经元4天后，黑质中GABA浓度降低75%。在去神经支配的黑质中，4-脱氧吡哆醇不改变GABA浓度，而γ-乙炔基GABA的作用则降低70%。
