The development and maintenance of tolerance to the physiological and behavioral effects of repeated exposure to ethanol can be altered markedly by the presence of arginine vasopressin (AVP). In addition, AVP has been implicated in the etiology of convulsions, including those induced by exposure to high ambient temperatures. In light of these findings, experiments were conducted to determine the role, if any, that AVP might play in the pathogenesis of alcohol-withdrawal convulsions. Thirty-two male Long Evans (LE) rats and 32 age-matched male homozygous Brattleboro (DI) rats (genetically deficient in AVP) were exposed to ethanol vapor concentrations adjusted to maintain blood alcohol levels of each rat at 150-350 mg/dl. Following at least 5 days of ethanol exposure, the animals were withdrawn. From 3-24 hr after cessation of ethanol administration, withdrawal severity was assessed by observing the response of each animal to a 60-120 sec period of auditory stimulation. No significant differences were observed in either latency to onset or severity of the convulsions in LE and DI rats upon ethanol withdrawal. Thus, alcohol-withdrawal convulsions, unlike hyperthermia-induced convulsions, may be mediated by a neurochemical substrate other than AVP.