ROLE OF CORTICOSTERONE IN THE ENHANCEMENT OF THE ANTIBODY-RESPONSE AFTER ACUTE COCAINE ADMINISTRATION

A model has been developed in which acute cocaine administration resul ts in an enhanced T-dependent antibody response to sheep erythrocytes. This enhancement occurs when cocaine (30 mg/kg, twice in 1 day) is ad ministered 1 or 2 days before sensitization with antigen, in mice olde r than 16 wk. Acute cocaine has been shown to elicit a rise in serum c orticosterone, and the administration of exogenous corticosterone, und er similar conditions as cocaine, also results in a similar immunoenha ncement. Further evidence in support of a role by corticosterone is th e lack of an enhancement in adrenalectomized mice and the ability of a lpha-helical corticotropin releasing factor to block the enhancement b y cocaine. The role of concomitant epinephrine release from the adrena l was addressed by adrenal demedullation. Eliminating epinephrine, but not corticosterone release, had no effect on the cocaine-induced immu noenhancement. The evidence presented provides support for a major rol e by corticosterone in mediating cocaine's effects on at least one mea sure of immune function, the T-dependent antibody response.