Abstract
In the presence of the reuptake blocker, nomifensine (1 μM), neurotensin caused a dose-dependent increase in the 25 mM K +-evoked release of [ 3H]dopamine ([ 3H]-DA) from rat nucleus accumbens slices. Chronic desipramine (DMI)-treatment (20 mg DMI/kg/day, orally for 28 days) caused a significant reduction in the K +-stimulated release of [ 3H]DA from rat nucleus accumbens slices. This could possibly have resulted from increased DA autoreceptor-mediated inhibition of DA release. Superfusion of the DMI-treated rat tissue with buffer-containing neurotensin (100 nM) resulted in an increase in the K +-evoked release of [ 3H]DA to a level which was higher than that observed with tissue obtained from untreated rats. A similar enhanced effect of neurotensin on DA release was observed when the DA agonist, apomorphine (APO), and ascorbate were included in the superfusion buffer. These findings are consistent with DMI treatment giving rise to impaired DA release possibly due to DA autoreceptor-mediated inhibition of DA release and cancellation of this effect by neurotensin.
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