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A Chronic Stress that Impairs Reactivity in Rats Also Decreases Dopaminergic Transmission in the Nucleus Accumbens: A Microdialysis Study
Author(s) -
Gambarana Carla,
Masi Flavio,
Tagliamonte Alessandro,
Scheggi Simona,
Ghiglieri Ombretta,
Graziella De Montis Maria
Publication year - 1999
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1999.0722039.x
Subject(s) - nucleus accumbens , dopamine , microdialysis , dopaminergic , medicine , endocrinology , amphetamine , imipramine , stimulation , sensitization , catecholamine , chemistry , psychology , neuroscience , alternative medicine , pathology
Chronic stress induces in rats a decreased reactivity toward noxious stimuli (escape deficit), which can be reverted by antidepressant treatments. The present study reports that this condition of behavioral deficit is accompanied by a decreased level of extracellular dopamine in the nucleus accumbens shell. To assess whether this finding was the result of a decreased release 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 total amount of dopamine released after d ‐amphetamine administration was similar in both groups of rats. These data suggest a reduced activity of dopaminergic neurons as the possible mechanism underlying dopamine basal level reduction in stressed animals. It is interesting that the stress group showed a locomotor response to cocaine not different from control rats, thus suggesting a condition of sensitization to dopamine receptor stimulation. Imipramine administered daily concomitantly with stress exposure completely reverted the escape deficit condition of chronically stressed rats. Moreover, stressed rats treated with imipramine showed basal and cocaine stimulated levels of extraneuronal dopamine similar to those observed in control animals.