The Effects of Single Prolonged Stress and Ethanol Consumption on Neuronal Activity in Corticolimbic Reward Circuitry

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Jonathan Kim James Herman


By Jonathan Kim, Neuroscience

Advisor: James Herman

Presentation ID: PM_A28

Abstract: About 10% of post-traumatic stress disorder (PTSD) cases also reported comorbid alcohol abuse. We employed single-prolonged stress (SPS), a well-established rodent model of PTSD symptomatology, with a voluntary drinking paradigm to assess the impact of traumatic stress on alcohol consumption and brain circuitry. We utilize c-fos, a molecular marker, to quantify neuronal activity in brain nuclei. We hypothesize that SPS would increase voluntary consumption of ethanol and lead to subsequent changes in neuronal activity in the brain regions: infralimbic cortex (IL), prelimbic cortex (PL), nucleus accumbens (NAc), paraventricular nucleus (PVN), bed nucleus of the stria terminalis (BST), basolateral (BLA) and medial amygdala (MeA). Adult male rats were randomly assigned to either the SPS group or non-stress control group. 7 days post-stress, rats began a modified "drinking in the dark" procedure utilizing "gelatin shots". All rats underwent an acquisition, abstinence and relapse regimen, an intraperitoneal ethanol injection, and euthanization. Collected brains were processed for immunohistochemical analysis of c-fos expression in regions of interests (ROI) and counted using ImageJ software. There was a significant interaction of SPS history and SPS-treated rats consuming significantly more ethanol gelatin on days 7, 8, and 17. These results indicate that a prior history of traumatic stress can lead to increased alcohol consumption. Moreover, our c-fos analysis will allow us to map neuronal activation patterns in brain areas known to mediate both stress and reward phenotypes. These data will inform future studies aimed at identifying potential biomarkers and therapeutic targets for PTSD with comorbid substance abuse.

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