"ASSOCIATION BETWEEN CORTICAL EXCITABILITY AND NEUROPLASTICITY AFTER PRENATAL ALCOHOL EXPOSURE IN MICE"

Prenatal alcohol exposure poses a significant public health concern due to its teratogenic effects in humans. Alcohol's impact on central nervous system development disrupts cerebral organogenesis, affecting various cellular and molecular mechanisms. Babies exposed to alcohol in utero are more likely to develop seizures and epilepsy postnatally due to alterations in NMDA receptors and GABAergic inhibitory transmission, resulting in an imbalance between excitation and inhibition in the developing brain, affecting synaptogenesis and synaptic function. To investigate potential synaptic alterations, we utilized pregnant Swiss mice on gestational day 14, receiving daily oral doses of 3.0 g/kg ethanol (ETA) or vehicle (VEH) until gestational day 19. Seizure predisposition was assessed through hyperthermia and pentylenetetrazol (PTZ) administration, while synaptic changes were analyzed via immunohistochemistry and transmission electron microscopy. Our results revealed a significant increase in latency to generalized tonic-clonic seizures induced by hyperthermia in the ETA group compared to VEH (VEH 200.4 ± 9.06, ETA 292.6 ± 11.87). Through PTZ administration, we observed a significant increase in tonic seizure occurrences in the ETA group (319.8 ± 31.46) compared to VEH (106.2 ± 32.93). Macroscopic evaluation of brains showed a reduction in cortical width in the ETA group compared to VEH. From our findings, we conclude that prenatal alcohol exposure induces structural alterations and contributes to an imbalance in excitation/inhibition equilibrium.