Life-altering anxiety disorders, such as posttraumatic stress disorder (PTSD), can co-occur at high rates with substance use disorders. Alcoholism, compared with other substance use disorders, is particularly common. Rodent studies of acute stress effects on alcohol consumption show that stress can alter ethanol (EtOH) consumption. This study examined voluntary EtOH consumption in male Long–Evans rats that had undergone a stress-enhanced fear learning (SEFL) procedure.
Adult Long–Evans rats were exposed to a stress that consisted of 15 inescapable foot-shocks (1 mA, 1 second) known to cause a long-lasting nonassociative enhancement of subsequent fear learning. Control animals received no shock. One day later, animals were placed in a novel and very different context and received a single foot-shock. On day 3, animals were returned to the single shock context and freezing was used as a measure of learned fear. The intermittent access 2-bottle choice (2BC) regimen consisted of 1 bottle of water and 1 bottle of experimental solution, either 19% EtOH or 28.4% sucrose–0.08% quinine, for a 24-hour period, 3 days a week, and all other times 2 water bottles. This regimen lasted until stable levels of experimental solution drinking were reached, at which point the experimental solution was removed for 40 days and then returned to measure the resumption of consumption.
Rats that received stress prior to EtOH consumed significantly more EtOH than control rats before and after reinstatement. Rats that received stress after drinking was established did not consume significantly more EtOH when the drug was returned. Stress had no significant effect on sucrose–quinine drinking, our calorie and taste control for EtOH.
A single traumatic event sufficient to produce long-lasting enhancement of fear learning increases voluntary EtOH consumption, but does not alter previously acquired EtOH drinking habits or alter the consumption of a calorically equivalent sweet-bitter-tasting solution.