Inhibition by sodium bromide of acetylcholine release and synaptic transmission in the superior cervical ganglion of the rat.

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.