CONICET | Buscador de Institutos y Recursos Humanos

The consequences of perinatal asphyxia include alterations which may manifest asschizophrenia. Characteristic features of this disease include a decrease in specificsubpopulations of GABAergic cells and deterioration of social interaction. Thepurpose of this work is to assess if a deep and short hypothermic treatment canameliorate this damage in a model of perinatal asphyxia.Rats offsprings were exposed to 19 min of asphyxia by immersing the uterus hornsin water at 37° followed by 30min in air at 10°C that resulted in 15° bodytemperature. At PND 36-38 the rats were tested in open field and social interactionparadigms and processed for immunostaining of calbindin and reelin.A brief exposure to deep hypothermia reversed the deterioration produced byperinatal asphyxia in play soliciting. Perinatal asphyxia decreased the density of calbindin neurons in layer II of the Anterior Insular Cortex, while deep hypothermiareversed this effect. Paradoxically, in AIC there was a significant increase in thenumber of reelin secreting neurons in layers II and III generated by perinatalasphyxia and this increase was reversed by hypothermia. This suggests acompensatory mechanism, where reelin neurons trend to compensate the loss ofcalbindin neurons, at least within Anterior Insular Cortex. Finally, deep hypothermicshock might represent a valuable therapeutic alternative to treat perinatal asphyxia.