Abstract

A model has been developed in which acute cocaine administration results in an enhanced T-dependent antibody response to sheep erythrocytes. This enhancement occurs when cocaine (30 mg/kg, twice in 1 day) is administered 1 or 2 days before sensitization with antigen, in mice older than 16 wk. Acute cocaine has been shown to elicit a rise in serum corticosterone, and the administration of exogenous corticosterone, under similar conditions as cocaine, also results in a similar immunoenhancement. Further evidence in support of a role by corticosterone is the lack of an enhancement in adrenalectomized mice and the ability of α-helical corticotropin releasing factor to block the enhancement by cocaine. The role of concomitant epinephrine release from the adrenal was addressed by adrenal demedullation. Eliminating epinephrine, but not corticosterone release, had no effect on the cocaine-induced immunoenhancement. The evidence presented provides support for a major role by corticosterone in mediating cocaine’s effects on at least one measure of immune function, the T-dependent antibody response.