Chronic desipramine treatment selectively potentiates somatostatin-induceddopamine release in the nucleus accumbens

Dopamine and somatostatin have been implicated in the pathophysiology of de pression. We have employed in vivo microdialysis to investigate the regulat ion of dopamine release by somatostatin in the nucleus accumbens and the st riatum of awake, freely moving rats, and to ascertain how this regulation m ay be affected by desipramine treatment. Somatostatin-14 (10(-4) M) infusio n induced an increase in the release of dopamine and a decrease in the rele ase of its metabolites in both the nucleus accumbens (568% of basal) and th e striatum (546% of basal). Chronic desipramine treatment resulted in an ex aggerated somatostatin-induced increase of dopamine levels, specifically in the nucleus accumbens (3542% compared with 564% of basal in the striatum), whereas acute desipramine treatment had no effect (582% of basal) compared with saline treated rats. Basal concentrations of dopamine and metabolites were not influenced by either chronic or acute treatment of desipramine in either brain area. These results demonstrate that somatostatin regulates d opamine release in the nucleus accumbens and the striatum. Chronic antidepr essant treatment influences somatostatin's actions on dopamine function sel ectively in the nucleus accumbens.