Akademik Veri Yönetim Sistemi
FENS Forum 2024, Vienna, Avusturya, 25 - 29 Haziran 2024, ss.711, (Özet Bildiri)
Early Life Stress (ELS) can result in enduring health consequences, highlighting the need for exploring timely intervention approaches. Our study aims to investigate whether metformin, a long-recognized diabetes medication with neuroprotective and neurotrophic potential, can mitigate ELS-induced disruptions in hippocampal neurogenesis and dendritic growth. To test this hypothesis, both male and female neonatal Wistar rats were allocated into four distinct groups: control, metformin treatment, ELS model, and ELS model with metformin treatment (ELS+M). During the initial two weeks, ELS model was induced by subjecting neonates to daily 180-minute maternal separation and isolation. Simultaneously, intraperitoneal metformin was administered at 50 mg/kg/day, and weight measurements were recorded. At postnatal day 15, blood samples were collected for basal and post-stress corticosterone measurements, and subsequent brain processing was carried out for histological analysis. Serial thick coronal sections collected through the hippocampus were immunolabeled with proliferation (Ki67), newborn neuron (Doublecortin; DCX), mature neuron (NeuN), and apoptosis (cleaved-caspase-3) markers and stained with hematoxylin and eosin for stereological volume estimates. Golgi-Cox impregnated granule neurons underwent quantitative analysis to evaluate dendritic architecture and spine density. Preliminary findings suggest that metformin administration in the ELS model ameliorates developmental neurogenesis in the dentate gyrus for both genders by improving impaired proliferation, forming new neurons, enhancing dendritic growth, and increasing survival. Nevertheless, it notably slows down body weight gain in stressed newborn males, starting from postnatal day 8 (p<0.05). Further research is warranted to explore the lasting effects of the intervention into adulthood.