Pasantes-Morales H, Arzate M E, Quesada O, Huxtable R J
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, D.F.
Neuropharmacology. 1987 Dec;26(12):1721-5. doi: 10.1016/0028-3908(87)90123-7.
The susceptibility of rats made deficient of taurine by treatment with guanidinoethane sulfonate (GES), to seizures induced by 4-aminopyridine was examined. Guanidinoethane sulfonate, at a concentration of 1% was administered to pregnant rats, in the drinking water 2-3 days prior to delivery and the treatment was continued during nursing. Pups were weaned to the same treatment until 6 weeks of age. This treatment decreased levels of taurine in the cerebral cortex by 70%. 4-Aminopyridine was injected intraperitoneally at doses ranging from 4-7 mg/kg. Taurine-deficient rats showed a greater susceptibility to seizures, as demonstrated by a lowered latency for clonic seizures, an increased incidence of tonic seizures and a higher postseizure mortality. These results suggest an involvement of endogenous taurine in nervous excitability.
研究了用胍基乙烷磺酸盐(GES)处理使牛磺酸缺乏的大鼠对4-氨基吡啶诱导的癫痫发作的易感性。在分娩前2-3天,将浓度为1%的胍基乙烷磺酸盐加入孕鼠饮用水中给药,并在哺乳期间持续该处理。幼崽断奶后接受相同处理直至6周龄。该处理使大脑皮层中的牛磺酸水平降低了70%。以4-7mg/kg的剂量腹腔注射4-氨基吡啶。牛磺酸缺乏的大鼠对癫痫发作表现出更高的易感性,表现为阵挛性发作的潜伏期缩短、强直性发作的发生率增加以及癫痫发作后的死亡率更高。这些结果表明内源性牛磺酸参与神经兴奋性调节。