PRENATAL CLIMATE-RELATED STRESS DISRUPTS SUPRACHIASMATIC CLOCK INTEGRITY AND TRIGGERS ADAPTIVE NEUROBEHAVIORAL PROGRAMMING IN LONG-EVANS RATS

Escalating climate change and displacement crises increasingly expose pregnant populations to compounded stressors, such as extreme heatwaves and overcrowded internally displaced persons (IDP) camp conditions, with potential disruption of foetal neurodevelopment. This study modelled gestational exposure to climate-simulated stressors to investigate their impact on the suprachiasmatic nucleus (SCN), circadian gene expression, hormonal regulation, growth metrics, and behavioural outcomes in Long‑Evans rat offspring. Timed‑pregnant dams were exposed during late gestation (E15–E20) to control conditions or one of three paradigms: heat stress (38-40°C, 2h/day), displacement adversity (overnight crowding with restricted food/water), or combined stress. Male offspring were assessed at postnatal days (PND) 10 and 30. Histological analysis revealed significant SCN degeneration across all stress groups (p<0.001). Neuroendocrine assays showed reduced plasma corticosterone and melatonin, indicating disruption of circadian hormonal regulation. Clock gene analysis revealed stress-specific modulation: IDP exposure paradoxically upregulated Bmal1 and Per1, suggesting compensatory plasticity, whereas HS and HS+IDP groups exhibited maladaptive expression patterns. Immunofluorescence demonstrated distinct neuroglial responses: HS enhanced NeuN and GFAP expression, consistent with accelerated neuronal maturation and astrocytic support; IDP induced robust activation of both markers, reflecting adaptation; HS+IDP elicited exaggerated gliosis and neuronal activation, suggesting destabilised SCN circuitry. Behaviourally, combined stress exposure paradoxically reduced anxiety-like behaviour, preserved recognition memory, and enhanced sociability (p<0.05). Growth analysis revealed somatic restriction but relative brain sparing, evidenced by elevated brain‑to‑body weight ratios (p<0.001). These findings demonstrate that gestational stress paradigms exert stage-specific effects, with combined exposures overwhelming adaptive systems and producing maladaptive overcompensation.