Lapin I P, Nikitina Z S, Sytinskiĭ I A
Vopr Med Khim. 1981 Jan-Feb;27(1):27-30.
Content of gamma-aminobutyric acid (GABA) was unaltered in mouse brain and cerebellum after administration of D,L-kynurenine (50 mcg), quinolinic acid (5 mcg) and nicotinic acid (50 mcg) into brain ventricles. At the same time, after administration of kinurenine, quinolinic acid and nicotinic acid activity of GABA-transaminase in brain was decreased by 39%, 40% and 48, respectively; activity of glutamate decarboxylase was decreased by 27% and 36%, respectively, in this case nicotinic acid affected only slightly. Strong clonic convulsions occurred in 60% of mice after administration of kynurenine and quinolinic acid and only in 7% of mice after treatment with nicotinic acid. Deceleration in the GABA turnover and the subsequent weakening of the brain inhibitory systems were apparently essential in development of convulsions caused by the kynurenines.
向小鼠脑室注射D,L-犬尿氨酸(50微克)、喹啉酸(5微克)和烟酸(50微克)后,小鼠脑和小脑中γ-氨基丁酸(GABA)的含量未发生改变。同时,注射犬尿氨酸、喹啉酸和烟酸后,脑中GABA转氨酶的活性分别降低了39%、40%和48%;谷氨酸脱羧酶的活性分别降低了27%和36%,在这种情况下烟酸的影响很小。注射犬尿氨酸和喹啉酸后,60%的小鼠出现强烈的阵挛性惊厥,而注射烟酸后只有7%的小鼠出现惊厥。GABA周转减慢以及随后脑抑制系统的减弱显然是犬尿氨酸引起惊厥的关键因素。