👤 Kalyani Soren

Vicarious trauma, the psychological distress from witnessing others' suffering, is an increasingly recognized precursor to depression and anxiety. However, the underlying neurobiological mechanisms remain poorly understood and appear to be sex-dependent. This study investigated the behavioral, physiological, and molecular consequences of purely psychological stress using a novel rodent model of vicarious learned helplessness (VLH). Male and female C57BL/6J mice were used to establish VLH paradigm. Observer mice witnessed conspecifics receiving inescapable foot shocks through a partitioned chamber allowing multisensory interaction. Following 7 days of conditioning, behavioral assays assessed anxiety and depressive symptoms. Prefrontal cortex tissue was analyzed using RT-qPCR and immunoblotting to identify molecular alterations. Vicarious stress induced depression phenotype in both sexes, characterized by active avoidance deficits, anhedonia and anxiety, comparable to direct physical trauma. Physiological assessments revealed hypothalamic-pituitary-adrenal (HPA) axis hyperactivity with elevated plasma corticosterone in both sexes. While molecular analysis showed shared downregulation of metabotropic glutamate receptor 2 (mGluR2) and elevated Il6 mRNA in the prefrontal cortex, distinct sexual dimorphism emerged. Males displayed specific deficits in neurotrophic support ( Vicarious trauma is sufficient to drive depression-like pathology through distinct molecular trajectories in males and females. These findings are suggestive of the critical necessity for sex-specific therapeutic strategies when treating trauma-related psychiatric disorders. Show less

This study characterizes the expression of fibroblast growth factors (FGFs) and their receptors in the porcine corpus luteum (CL) across distinct stages of the oestrous cycle, and evaluates the regulatory role of FGF2 on angiogenesis, steroidogenesis, and cell survival in vitro. The CL was classified morphologically into four phases: Phase I (days 1-8; corpus haemorrhagicum; ELP), Phase II (days 9-14; highly vascularized CL; MLP), Phase III (day 15 onward; ischemic regression; LLP), and Phase IV (corpus albicans; avascular and regressed; RR). Each phase included 10 biological replicates (n = 10). Quantitative RT-PCR revealed significant upregulation (p < 0.001) of FGF1, FGF2, FGF7, FGFR1, FGFR2, and FGFR4 during early and mid-luteal stages. FGFR3 and FGFR2IIIC showed no significant variation, while FGFR2IIIB was downregulated (p < 0.001) during early/mid-luteal stages and upregulated during luteal regression. FGF10 expression declined significantly (p < 0.001) during regression. Western blotting Densitometry confirmed trends mRNA expression. In-vitro supplementation of FGF2 (1, 10, and 100 ng/ml) during the mid-luteal stage enhanced mRNA expression of angiogenic (vWF), steroidogenic (StAR, CYP11A1, 3β-HSD), and cell survival (PCNA, BAX) markers. StAR, CYP11A1, and 3β-HSD were significantly upregulated (p < 0.001) from 24 to 72 h in a dose-dependent manner. vWF and PCNA showed significant increases at 48 and 72 h, while BAX expression progressively declined (p > 0.001). The 100 ng/ml dose elicited the most pronounced effects. These findings suggest that FGF family members exert autocrine/paracrine effects that support luteal cell proliferation, differentiation, angiogenesis, steroidogenesis, and survival, underscoring their critical role in porcine ovarian physiology. Show less