Interneurônios inibitórios do neocórtex e sua relação com a epileptogênese frente à exposição pré-natal ao álcool

Abstract

Prenatal alcohol exposure (PAE) is considered a risk factor that can lead to alterations in the development of the central nervous system, such as structural and functional changes, including epileptogenesis. This study aimed to investigate the effects of PAE on cortical excitability and inhibitory interneurons in the neocortex of mice, focusing on the Parvalbumin+, Somatostatin+, and Vasoactive Intestinal Peptide (VIP)+ subtypes. Pregnant Swiss mice were subjected to oral administration of ethanol (3.0 g/kg, 30% v/v) from gestational day 14 to 19. On postnatal day 16 (PND16), the offspring were evaluated for susceptibility to febrile and pentylenetetrazol (PTZ)-induced seizures, as well as for brain morphology and immunofluorescence analysis to identify interneurons. The results showed that PAE did not cause significant changes in cortical thickness or length. However, an increased duration of stage 6 of the PTZ-induced seizure was observed in ethanolexposed animals, as well as a longer latency to febrile seizures. Immunolabeling revealed an increased density of Parvalbumin+ interneurons in the supragranular layers of the cortex, with no significant changes in the Somatostatin+ and VIP+ populations. These findings suggest that PAE alters the distribution of interneurons, impacting the regulation of cortical excitability and possibly contributing to the increased susceptibility to epileptogenesis observed in fetal alcohol spectrum disorder.