Kása P, Toldi J, Farkas Z, Joó F, Wolff J R
Central Research Laboratory, Medical University, Szeged, Hungary.
Neurochem Int. 1987;11(4):443-9. doi: 10.1016/0197-0186(87)90034-9.
In the superior cervical ganglion (SCG) of rats, the interaction of sodium bromide (NaBr) with various drugs which interfere with the GABA system, such as 3-(4-chlorophenyl)-4-aminobutyrate [( + )baclofen, Bac], ( + )bicuculline (Bic), picrotoxin (Pic) and chlorpromazine (CPZ), and the effects of NaBr on the K(+)-induced release of [(3)H]acetylcholine ([(3)H]ACh) were studied in vitro. The effects on the evoked potentials induced by preganglionic stimulation were analysed in situ. The in vitro experiments revealed that 1 mM NaBr inhibits both the basal and the K(+)-induced release of [(3)H]ACh in a Ca(2+)-dependent manner. This NaBr effect was additive with the similar effect of the GABA agonist Bac, but it could not be blocked with any of the drugs applied. In vivo, 1 mM NaBr depressed the amplitude of the evoked potentials in the SCG. It is concluded that, in the SCG of rats, NaBr interacts with the presynaptic and postsynaptic membranes. The inhibitory effects of NaBr on both the [(3)H]ACh release and the potentials evoked by preganglionic stimulation cannot be attributed to a direct interference with GABA receptor complexes; some other binding site/s on the presynaptic and postsynaptic membranes might be responsible for the bromide-induced reduction of the synaptic transmission in the SCG of rats.
在大鼠的颈上神经节（SCG）中，研究了溴化钠（NaBr）与各种干扰γ-氨基丁酸（GABA）系统的药物（如3-（4-氯苯基）-4-氨基丁酸[（+）巴氯芬，Bac]、（+）荷包牡丹碱（Bic）、印防己毒素（Pic）和氯丙嗪（CPZ））的相互作用，以及NaBr对钾离子（K⁺）诱导的[³H]乙酰胆碱（[³H]ACh）释放的影响。在体分析了对节前刺激诱发的诱发电位的影响。体外实验表明，1 mM NaBr以钙（Ca²⁺）依赖的方式抑制[³H]ACh的基础释放和K⁺诱导的释放。NaBr的这种作用与GABA激动剂Bac的类似作用相加，但不能被所应用的任何药物阻断。在体内，1 mM NaBr降低了SCG中诱发电位的幅度。得出结论，在大鼠的SCG中，NaBr与突触前膜和突触后膜相互作用。NaBr对[³H]ACh释放和节前刺激诱发的电位的抑制作用不能归因于对GABA受体复合物的直接干扰；突触前膜和突触后膜上的其他一些结合位点可能是溴化物诱导大鼠SCG中突触传递减少的原因。
