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Chronic Intermittent Ethanol Exposure Increases Ethanol Consumption Following Traumatic Stress Exposure in Mice
Veronica M Piggott1,2,3, Scott C Lloyd1,2,3, Shane A Perrine1,3
1Research & Development Service, John D. Dingell VA Medical Center, Detroit, MI, United States.
Mice exposed to both traumatic stress and chronic alcohol developed greater alcohol withdrawal effects. Traumatic stress increased impulsivity, while chronic alcohol exposure worsened anhedonia, highlighting a mouse model for post-traumatic stress disorder-alcohol use disorder comorbidity.
Area of Science:
- Neuroscience
- Behavioral Science
- Pharmacology
Background:
- Post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) frequently co-occur.
- Comorbid PTSD-AUD leads to heightened alcohol cravings and relapse rates.
- Animal models are needed to mechanistically explore PTSD-AUD behavioral effects.
Purpose of the Study:
- To investigate the effects of comorbid traumatic stress and alcohol exposure on ethanol intake, impulsivity, and anhedonia in mice.
- To establish and validate a mouse model for PTSD-AUD comorbidity.
Main Methods:
- Mice were exposed to mouse single-prolonged stress (mSPS) or control conditions.
- Chronic intermittent ethanol (CIE) vapor exposure was used to induce alcohol dependence.
- Ethanol intake, novelty suppressed feeding (NSF), and hedonic-like behavior were assessed.
Main Results:
- mSPS alone did not alter baseline ethanol consumption.
- Mice exposed to both mSPS and CIE showed increased ethanol consumption post-withdrawal.
- mSPS exposure increased impulsivity (shorter latency to feed), while CIE increased anhedonia (reduced palatable food intake).
Conclusions:
- The mSPS-CIE mouse model effectively mimics key behavioral aspects of PTSD-AUD comorbidity.
- Combined traumatic stress and alcohol exposure exacerbate withdrawal vulnerability.
- Specific behavioral deficits, impulsivity and anhedonia, are differentially affected by traumatic stress and chronic alcohol exposure.
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