Breathing alterations against hypoxia as a function of early ethanol exposure

Abstract

Maternal ethanol (EtOH) intake during pregnancy and lactation is a highly frequent “social” behavior in Argentine, exposing fetus or neonates to moderate EtOH intoxication through the amniotic fluid and placenta. Early EtOH exposure triggers a spectrum of neurobehavioral dysfunctions affecting, also, the breathing response. In an animal model equivalent to the 3rd trimester of the human gestation we explore the early ethanol exposure effects on the ventilatory responses in normoxic and hypoxic-air conditions. We also study central areas involved in breathing modulation as the solitary tract nucleus and the medullary raphe system. Our results show that a brief and early ethanol exposure alters both basal and hypoxia-induced breathing frequencies and apneas through modifications in the activation patterns of central areas of study. Actually, early ethanol exposure induces a basal breathing depression in normoxic conditions but, against a hypoxic challenge, ethanol triggers two consecutive altered events: first a lower hyperventilation rate during the hypoxic event itself and then, during the post-hypoxic period, ethanol elicit the emergency of an adaptive phenomenon, the ventilatory long-term facilitation. Alterations in the activation patterns in the NTS and raphe obscurus, and an increase in the 5HT levels in the medullary raphe nuclei (magnus, obscurus y pallidus) were observed as a function of different ways of early ethanol exposure. Funding by MINCyT-Cba; FONCyT and SECyT-UNC.