Year: 2025
Type: conference-paper
Abstract: BACKGROUND Psychological stress can induce gastrointestinal symptoms and exacerbate existing gastrointestinal disorders, indicating an interaction between the central and enteric nervous systems. Central nervous system activation of opioid receptors stimulates sympathetic outflow to the enteric nervous system, delaying motility and reducing gastrointestinal secretions, producing a similar clinical presentation to IBS. HYPOTHESIS We hypothesize that social isolation induces anxiety states, disrupting homeostatic noradrenergic activity in the brain and gut, leading to neurophysiological changes in the cecum characterized by altered expression of opioid receptors. METHODS Sprague-Dawley rats were housed in either group (control) or socially isolated conditions. Affective behavior was assessed using the Open Field, Elevated Plus Maze, Three-Chamber Social Isolation, and Defensive Shock Probe Burial tests. Cecal tissue was collected, cleaned, and processed for mRNA extraction and purification. RT-qPCR was used to quantify δ, κ, and μ opioid receptor expression. RESULTS Socially isolated rats exhibited decreased social behavior, increased neophobia, and more passive coping strategies compared to controls. μ opioid receptor (MOR) expression was significantly elevated in the socially isolated cohort compared to the control. δ and κ opioid receptor expression was undetectable by qPCR, suggesting low expression in the cecum and minimal involvement in gut opioid signaling. CONCLUSIONS Behavioral changes associated with social isolation stress correspond with increased MOR expression in the cecum. This upregulation may mediate stress-induced gastrointestinal dysfunction and represents a potential target for therapeutic intervention in stress-related GI disorders.
Authors: Jordan Riser, John Tkaczynski, Nicole Shellenbarger, Maya Patel, Daniel Chandler, Daniel Manvich
Language: English
Subfield: Gastroenterology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
OpenAlex ID: W7084073092
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