STRESS AND THE FUNCTION OF THE CL CHANNEL COUPLED TO THE GABA RECEPTOR
Several lines of evidence indicate that the GABA/benzodiazepine receptor complex is coupled to a chloride ionophore (24). Thus electrophysiological studies have demonstrated that GABA produces its inhibitory effect on neurotransmission by enhancing the flux of chloride ions across its specific channel on the nerve membrane (22). Recently it has been shown that using the synaptoneurosomes, a novel subcellular brain membrane preparation, it is possible to study the membrane per 
meability to chloride ions by measuring the changes in chloride efflux induced by different drugs acting at the level of the GABA/benzodiazepine receptor / СП ionophore complex (31). Hence, by using this biochemical technique, we evaluated the effect of foot-shock stress on 36 C1 efflux from cerebral cortex synap-toneurosomes of handling-habituated and naive rats. As shown in Table 4 foot-shock stress decreased 36 C1 efflux from synapto-neurosomes of handling-habituated rats, but failed to modify the 36 СГ exchange from the membranes of naive rats. The presence in the dilution buffer of pentobarbital, a drug that facilitates the chloride transport by increasing the opening time of the GAB A receptor-coupled chloride channel (21,34) reversed the stress-induced decrease of 36 С l efflux from synaptoneurosomes of handling-habituated rats. Moreover, pentobarbital also stimulated 36 Cl efflux from cerebral cortex synaptoneurosomes of naive rats. Thus the function of the СГ channel coupled to the GABA/benzodiazepine receptors is decreased by foot-shock stress. This finding is in line with our previous results showing that foot-shock stress markedly decreases the density of low affinity GABA receptors in the cerebral cortex of handling-habituated rats.