Alcohol rapidly lowers plasma testosterone levels in the rat: Evidence that a neural brain-gonadal pathway may be important for decreased testicular responsiveness to gonadotropin

Alcohol is reported to suppress testosterone (T) secretion in the adult mal e rat. Decreases in the circulating levels of luteinizing hormone (LH) and/ or the activity of testicular steroidogenic enzymes have been proposed as p utative mechanisms underlying this inhibitory effect. We have recently prov ided functional evidence for a neural pathway between the brain and the mal e gonads that plays an important role in the ability of brain proinflammato ry cytokines to blunt testicular responsiveness to human chorionic gonadotr opin (hCG), The present work was designed to test the hypothesis that a sim ilar pathway might be implicated in the inhibitory influence of alcohol on T secretion. Alcohol, administered intraperitoneally or intragastrically, s ignificantly 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 independ ent of changes in the activity of the pituitary gonadotrophs. The lowest ef fective dose of alcohol, delivered intraperitoneally, was 2.0 g/kg. The int racerebroventricular injection of the alpha- and beta-adrenergic receptor a ntagonists phentolamine acid propranolol significantly reversed the inhibit ory influence of alcohol when it was administered 15 min, but not 60 min, b efore hCG. Collectively, our results indicate that (1) alcohol induces a ra pid and profound decrease in plasma T levels that is secondary to decreased testicular responsiveness to hCG; and (2) at least part of this acute inhi bitory action of alcohol may depend on the activation of a neural, adrenerg ic-dependent pathway between the brain and the testes.