Alcohol is reported to suppress testosterone (T) secretion in the adult male rat. Decreases in the circulating levels of luteinizing hormone (LH) and/or the activity of testicular steroidogenic enzymes have been proposed as putative mechanisms underlying this inhibitory effect. We have recently provided functional evidence for a neural pathway between the brain and the male gonads that plays an important role in the ability of brain proinflammatory cytokines to blunt testicular responsiveness to human chorionic gonadotropin (hCG). The present work was designed to test the hypothesis that a similar pathway might be implicated in the inhibitory influence of alcohol on T secretion. Alcohol, administered intraperitoneally or intragastrically, significantly prevented the T response to the gonadotropin. This effect was significant within 15 min of drug treatment. In the intragastric model (the only one used for this type of experiment), the effect of alcohol was not altered by prior blockade of LH release, which suggests that it is independent of changes in the activity of the pituitary gonadotrophs. The lowest effective dose of alcohol, delivered intraperitoneally, was 2.0 g/kg. The intracerebroventricular injection of the alpha- and beta-adrenergic receptor antagonists phentolamine and propranolol significantly reversed the inhibitory influence of alcohol when it was administered 15 min, but not 60 min, before hCG. Collectively, our results indicate that (1) alcohol induces a rapid and profound decrease in plasma T levels that is secondary to decreased testicular responsiveness to hCG; and (2) at least part of this acute inhibitory action of alcohol may depend on the activation of a neural, adrenergic-dependent pathway between the brain and the testes.