| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 322775 | Hormones and Behavior | 2013 | 8 Pages |
Chronic exposure to stress has many deleterious effects on behavior, which can often lead to self-medication with anxiolytics, antidepressants, or alcohol. We determined the effects of alcohol administration following a stressor on established behavioral, physiological, and neural responses to stress. Male Sprague–Dawley rats received: No alcohol/No stress (CON), Alcohol alone (ALC), Stress alone (STR), or Stress plus Alcohol (STR + ALC). For seven consecutive days, two cohorts received an oral dose of 2.0 g/kg of either 20% ethanol or saline. In Cohort 1, behavioral testing began after the final treatment (day-8). Memory was tested using the object recognition (OR) and Y-maze, anxiety on the plus maze, and depression on the forced swim task. Memory on OR and Y-maze tasks was impaired in the ALC and STR groups. This deficit was reversed in the STR + ALC group, which performed not differently from the CON group. Stress alone was associated with increased anxiety, which was alleviated with alcohol treatment. No treatment effects were found in the forced swim task. In Cohort 2, hippocampal GABAα4 was upregulated in the STR + ALC group and GluN2B was upregulated in the ALC and STR + ALC groups. The STR + ALC group in Cohort 1 showed enhanced corticosterone levels after forced swim. The STR + ALC group in Cohort 2 showed increased corticosterone levels on day-1 of treatment and a habituation by day-7. In conclusion, this study found a reversal of stress-induced deficits in cognition and anxiety when alcohol was given post-stress, and changes in neurotransmitter receptor expression may contribute to these behavioral effects.
► Memory was impaired by stress or alcohol, but alleviated when combined. ► Stress-induced anxiety was blocked by alcohol. ► Corticosterone response to stress was altered by alcohol. ► Neurotransmitter receptor expression was upregulated by stress and alcohol.
