Ethanol-induced neurological changes produce aversive withdrawal symptoms that often promote further ethanol abuse as a way of suppressing these unwanted conditions. Efforts to treat alcoholism must address the pervasive physiological alterations that result in withdrawal symptoms in order to effectively reduce the probability of further abuse episodes. Although most alcohol research, to date, has focused primarily upon ethanol-induced disruptions in glutamate homeostasis, changes in the neuroendocrine control of systemic osmolarity also appears to exist as a contributing factor of withdrawal severity. However, the beta-amino acid taurine, with recognized functions in osmoregulation and calcium modulation, might ameliorate these ethanol-provoked alterations and reduce overall withdrawal severities. This proposed investigation will examine the ability of taurine treatment in reducing ethanol withdrawal severity, determined by measures of withdrawal-induced seizures, in male C3H mice made ethanol dependent through both continuous and intermittent vapor inhalation methods. In addition, during time points of peak withdrawal severity, quantification of the major neuroendocrine regulator of systemic osmolarity, arginine vasopressin (AVP), will determine whether any changes in hypothalamic and plasma AVP levels correspond to the degree of withdrawal severity. Furthermore, these studies will also assess whether ethanol-exposed, taurine-treated groups display AVP levels different from those ethanol groups without taurine treatment. As a result, data collected from these studies could provide evidence that supports the therapeutic use of taurine in alcoholism.
