A chronic stress that impairs reactivity in rats also decreases dopaminergic transmission in the nucleus accumbens: A microdialysis study

Chronic stress induces in rats a decreased reactivity toward noxious stimul i (escape deficit), which can be reverted by antidepressant treatments. The present study reports that this condition of behavioral deficit is accompa nied by a decreased level of extracellular dopamine in the nucleus accumben s shell. To assess whether this finding was the result of a decreased relea se or of an enhanced removal of dopamine, we acutely administered cocaine, and 2 h later d-amphetamine, to stressed and control rats. The increases in dopamine output observed in stressed animals after cocaine administration were significantly lower than those observed in control rats; whereas the t otal amount of dopamine released after d-amphetamine administration was sim ilar in both groups of rats. These data suggest a reduced activity of dopam inergic neurons as the possible mechanism underlying dopamine basal level r eduction in stressed animals. It is interesting that the stress group showe d a locomotor response to cocaine not different from control rats, thus sug gesting a condition of sensitization to dopamine receptor stimulation. Imip ramine administered daily concomitantly with stress exposure completely rev erted the escape deficit condition of chronically stressed rats. Moreover, stressed rats treated with imipramine showed basal and cocaine stimulated l evels of extraneuronal dopamine similar to those observed in control animal s.