Department of Pharmacology, University of Sydney, Sydney, NSW 2006, Australia.
Brain Res. 1983 Jan 3;258(1):165-9. doi: 10.1016/0006-8993(83)91245-3.
The convulsant, 3-mercaptopropionic acid (100-1000 microM) enhanced potassium-evoked release of exogenous D-aspartate from slices of rat cerebral cortex and cerebellum, but not that from slices of hippocampus. Elevation of excitant amino acid release may contribute to the convulsant action of 3-mercaptopropionic acid. Unlike the convulsant barbiturate CHEB, 3-mercaptopropionic acid did not influence protoveratrine-stimulated release of D-aspartate and its action on potassium-evoked release appeared to be not dependent on calcium ion fluxes. Several other convulsants, including bemegride (200 microM), benzodiazepine Ro-5-3663 (100 M), nikethamide (500 microM), pentylenetetrazole (500 microM), and 4,6,6-trimethylcaprolactam (100 and 500 microM), and the glutamate decarboxylase inhibitor isoniazid (500 microM) failed to influence potassium-evoked release of D-aspartate.
激动剂 3-巯基丙酸(100-1000μM)增强了大鼠大脑皮质和小脑切片中外源 D-天冬氨酸的钾诱发释放,但对海马切片没有影响。兴奋性氨基酸释放的增加可能有助于 3-巯基丙酸的惊厥作用。与惊厥性巴比妥 CHEB 不同,3-巯基丙酸不影响原藜芦碱刺激的 D-天冬氨酸释放,其对钾诱发释放的作用似乎不依赖于钙离子流。包括苯甲曲秦(200μM)、苯二氮䓬 Ro-5-3663(100μM)、戊四氮(500μM)、4,6,6-三甲基己内酰胺(100μM 和 500μM)和谷氨酸脱羧酶抑制剂异烟肼(500μM)在内的其他几种惊厥剂均未能影响钾诱发的 D-天冬氨酸释放。