Accumbens GABA-ergic innervation contributes to the stressor-induced locomotor depression in rats.

The effect of intra-accumbens injections of drugs changing the function of GABA-A and GABA-B receptor systems on stressor-induced motor depression, was studied in rats. Local injections of picrotoxin and baclofen, but not of midazolam and muscimol, attenuated the inhibitory effect of inescapable footshock on locomotor activity in the open field test, examined 24 h after a single exposure of rats to the stressful event. The results obtained with picrotoxin may be related to the general disinhibitory properties of the convulsant on brain neuronal activity, in a period of time important for consolidation of central processes evoked by inescapable shock. The lack of effects of muscimol and midazolam, further underlines the minor and/or indirect role of accumbens GABA-A receptor-related innervation in the neural processes generated by stressful event. On the other hand, the results obtained with baclofen confirm the reports indicating an inverse relationship between the number of GABA-B receptors in the frontal cortex and the development of helpless behavior in rats. It is also noteworthy that most antidepressant drugs which have been shown to prevent or reverse behavioral deficits after inescapable shock, upregulate GABA-B receptors in the frontal cortex. Hence, it appears that GABA-B receptor-related systems within the nucleus accumbens, may contribute to the footshock-induced behavioral depression, including locomotor inhibition. The reduction of stress effect by baclofen does not seem to reflect changes in fear and anxiety, since the drug was given after the stress session, and the anxiolytic midazolam appeared to be ineffective in this test.