Skerritt J H, Willow M, Johnston G A
Brain Res. 1983 Jan 10;258(2):271-6. doi: 10.1016/0006-8993(83)91150-2.
The effects of a convulsant barbiturate, 5(2-cyclohexylidine-ethyl)-5-ethyl barbituric acid (CHEB), and phenobarbitone (PhB) on the release of exogenous D-aspartate and GABA from slices of rat cerebral cortex were investigated. While PhB inhibited potassium-evoked release of D-aspartate more so than that of GABA, CHEB potently inhibited potassium-evoked GABA release and stimulated evoked D-aspartate release, in a concentration-dependent manner. These actions are consistent with the observed in vivo convulsant and anticonvulsant properties of these barbiturates. CHEB, but not PhB also elevated spontaneous efflux of both amino acids. The actions of these barbiturates were further studied in calcium- and sodium-free media, and in the presence of tetrodotoxin and ruthenium red, agents known to alter ion flux across neuronal membranes. The results obtained indicate that different ionic mechanisms may be involved in the release of excitatory and inhibitory amino acid transmitters.
研究了惊厥性巴比妥酸盐5-(2-环己叉基-乙基)-5-乙基巴比妥酸(CHEB)和苯巴比妥(PhB)对大鼠大脑皮质切片中外源性D-天冬氨酸和GABA释放的影响。与GABA相比,PhB对钾诱发的D-天冬氨酸释放的抑制作用更强,而CHEB则以浓度依赖的方式强烈抑制钾诱发的GABA释放,并刺激诱发的D-天冬氨酸释放。这些作用与这些巴比妥酸盐在体内观察到的惊厥和抗惊厥特性一致。CHEB而非PhB还提高了两种氨基酸的自发流出量。在无钙和无钠培养基中,以及在已知会改变跨神经元膜离子通量的河豚毒素和钌红存在的情况下,对这些巴比妥酸盐的作用进行了进一步研究。获得的结果表明,兴奋性和抑制性氨基酸递质的释放可能涉及不同的离子机制。