Restoration of Hippocampal Serotonergic Receptor Expression by Fluoxetine and Glutathione Following Chronic Stress in Wistar Rats

This dataset comprises gene expression measurements of serotonin receptors HTR1 and HTR2 in the hippocampus of Wistar rats subjected to four experimental conditions: control, chronic unpredictable mild stress (CUMS), CUMS treated with fluoxetine, and CUMS supplemented with glutathione. The CUMS protocol was applied for four weeks to induce a stress-related phenotype. Gene expression levels were assessed by polymerase chain reaction (PCR), followed by gel electrophoresis. Band intensities were quantified using integrated density (mean intensity volume), and expression levels were normalized to the housekeeping gene GAPDH.

Statistical analyses were performed separately for each gene using linear models to evaluate the effect of experimental group, followed by post hoc pairwise comparisons. Residual diagnostics were assessed using simulation-based approaches. Significant effects of experimental condition were observed for both genes, indicating that chronic stress and subsequent treatments modulate serotonergic receptor expression in the hippocampus.

For HTR1, CUMS exposure resulted in a marked reduction in expression relative to controls, whereas fluoxetine treatment restored and increased expression levels beyond baseline. Glutathione supplementation produced a partial recovery, with intermediate expression levels. For HTR2, a similar trend was observed: CUMS reduced expression, while both fluoxetine and glutathione treatments promoted recovery toward control levels, with differing magnitudes of effect.

Biologically, these findings support the sensitivity of hippocampal serotonergic receptors to chronic stress and their modulation by pharmacological and antioxidant interventions. The downregulation of HTR1 and HTR2 under CUMS conditions is consistent with impaired serotonergic signaling associated with stress-related disorders. The restoration observed with fluoxetine aligns with its role as a selective serotonin reuptake inhibitor, while the effects of glutathione suggest a contribution of oxidative stress mechanisms in regulating gene expression and neuroplasticity