The neurobehavioral impact of stress and the therapeutic role of valproic acid in a PTSD animal model.

This study examines the impact of stress on cognitive and behavioral functions and evaluates Valproic Acid (VPA) as a potential therapy in a mouse model of Post-Traumatic Stress Disorder (PTSD). Sixty-three male mice were assigned to control, PTSD, VPA, and PTSD + VPA groups, with behavioral assessments including anxiety, social interaction, memory, and depression-like tests. Histological analyses assessed neuronal integrity in the hippocampus, amygdala, cingulate cortex, and insula cortex. Stress significantly impaired cognitive performance, indicated by a lower Preference Index (PI%) in the novel object recognition task. Social interaction tests revealed decreased engagement in the PTSD group, reflecting social withdrawal. Behavioral assessments indicated increased immobility time in the tail suspension and forced swimming tests among PTSD mice, suggesting depression-like behaviors. In contrast, VPA treatment reduced immobility time, with the PTSD + VPA group showing improvements comparable to controls. Histological evaluations showed a higher percentage of degenerated cells in the hippocampus, amygdala, cingulate cortex, and insula cortex of the PTSD group versus controls. VPA administration significantly lowered the percentage of degenerated cells in the PTSD + VPA group, indicating neuroprotective effects, which were also noted in the hippocampus, amygdala, cingulate cortex, and insula cortex. These findings suggest VPA's potential as a therapeutic agent for PTSD, warranting further pharmacological investigation.