Schwartz R D, Skolnick P, Hollingsworth E B, Paul S M
FEBS Lett. 1984 Sep 17;175(1):193-6. doi: 10.1016/0014-5793(84)80597-9.
The effects of various barbiturates and picrotoxin in modifying the efflux of chloride (36Cl-) was studied in a novel subcellular preparation from rat cerebral cortex, the 'synaptoneurosome'. Dilution of synaptoneurosomes pre-loaded with 36Cl- resulted in rapid efflux of 36Cl- that could be measured as early as 10 s following dilution. In the presence of barbiturates such as pentobarbital and hexobarbital there was a significant increase in 36Cl- efflux which was not observed with the pharmacologically-inactive barbiturate, barbital. The effect of barbiturates in enhancing 36Cl- efflux was also stereospecific [(-)-DMBB greater than (+)-DMBB] and reversed by picrotoxin. By contrast, picrotoxin alone significantly inhibited 36Cl- efflux. These data demonstrate pharmacologically relevant Cl- transport for the first time in a subcellular brain preparation.
在一种从大鼠大脑皮层分离出的新型亚细胞制剂“突触神经小体”中,研究了各种巴比妥酸盐和印防己毒素对氯化物(³⁶Cl⁻)外流的影响。预先加载³⁶Cl⁻的突触神经小体稀释后,³⁶Cl⁻迅速外流,早在稀释后10秒就可检测到。在戊巴比妥和己巴比妥等巴比妥酸盐存在的情况下,³⁶Cl⁻外流显著增加,而药理活性不高的巴比妥酸盐巴比妥则未观察到这种现象。巴比妥酸盐增强³⁶Cl⁻外流的作用也是立体特异性的[(-)-DMBB大于(+)-DMBB],并被印防己毒素逆转。相比之下,单独使用印防己毒素会显著抑制³⁶Cl⁻外流。这些数据首次在亚细胞脑制剂中证明了与药理学相关的氯离子转运。