The Effects of Chronic Ethanol Consumption and Severe Stress on Dorsal Hippocampal Interleukin-1β, Tumor Necrosis Factor-α, and Glial Fibrillary Acidic Protein (2024)

Undergraduate: Sidney Steinsberger

Faculty Advisor: Shveta Parekh
Department: Psychology and Neuroscience

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Alcohol use disorder (AUD) is often found to be comorbid with post-traumatic stress disorder, yet there remains a lack of preclinical evidence on how prior alcohol dependence can exacerbate the development of post-traumatic stress disorder (PTSD). Astrocytes and the cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) have been suggested to play a key role in the neural mechanisms behind this comorbidity. To address this gap in literature, a rodent model was created that combined a fifteen day ethanol exposure with a severe footshock stressor to mimic comorbid AUD and PTSD in rodents. Immunohistochemistry was performed to visualize GFAP, a marker for astrocytes, IL-1β, and TNF-α. The tissue was then imaged and analyzed using widefield microscopy and ImageJ software. Following ethanol exposure, TNF-α levels were found to decrease while GFAP and IL-1β levels remained unaltered. Following a severe stressor, IL-1β and TNF-α levels were found to decrease while GFAP protein levels remained unaltered. These results suggest that decreased expression of proinflammatory cytokines in the dentate gyrus of the dorsal hippocampus could be a mechanism underlying the comorbidity of AUD and PTSD.