Subject(s)
Adrenergic Agents/pharmacology , Cardiovascular Agents/pharmacology , Clonidine/pharmacology , Myocardial Ischemia/drug therapy , Propranolol/pharmacology , Stress Disorders, Post-Traumatic/physiopathology , Animals , Anxiety/drug therapy , Anxiety/pathology , Anxiety/physiopathology , Disease Models, Animal , Disease Susceptibility , Heart/drug effects , Heart/physiopathology , Male , Myocardial Ischemia/pathology , Myocardial Ischemia/physiopathology , Myocardium , Random Allocation , Rats, Sprague-Dawley , Stress Disorders, Post-Traumatic/drug therapy , Stress Disorders, Post-Traumatic/pathology , Sympathetic Nervous System/drug effects , Sympathetic Nervous System/physiopathology , Treatment FailureABSTRACT
Post-traumatic stress disorder (PTSD) is a debilitating psychological disorder typified by diagnostic symptom clusters including hyperarousal, avoidance, negative cognitions and mood, and intrusive re-experiencing of the traumatic event. Patients with PTSD have been reported to self-medicate with alcohol to ameliorate hyperarousal symptoms associated with the disorder. Research utilizing rodent models of PTSD to emulate this behavioral phenomenon has thus far yielded inconsistent results. In the present study, we examined the effects of a predator-based psychosocial stress model of PTSD on voluntary ethanol consumption. In the first of two experiments, following exposure to a 31-day stress or control paradigm, rats were singly housed during the dark cycle with free access to 1% sucrose solution or 10% ethanol, which was also sweetened with 1% sucrose. Over the course of a 20-day period of ethanol access, stressed rats consumed significantly less ethanol than non-stressed rats. These counterintuitive results prompted the completion of a second experiment which was identical to the first, except rats were also exposed to the two-bottle paradigm for 20 days before the stress or control paradigm. In the second experiment, after the stress manipulation, stressed rats exhibited significantly greater ethanol preference than non-stressed rats. These findings suggest that prior exposure to ethanol influences the subsequent effect of stress on ethanol intake. They also validate the use of the present model of PTSD to examine potential mechanisms underlying stress-related changes in ethanol-seeking behavior.