Deep hypothermia reverses behavioral and histological alterations in a rat model of perinatal asphyxia.

The consequences of perinatal asphyxia include alterations which may manifest as schizophrenia. Characteristic features of this disease include a decrease in specific subpopulations of GABAergic cells and deterioration of social interaction. The purpose of this work is to assess if a deep and short hypothermic treatment can ameliorate this damage in a model of perinatal asphyxia. Rats offsprings were exposed to 19 min of asphyxia by immersing the uterus horns in water at 37° followed by 30min in air at 10°C that resulted in 15° body temperature. At PND 36-38 the rats were tested in open field and social interaction paradigms and processed for immunostaining of calbindin and reelin. A brief exposure to deep hypothermia reversed the deterioration produced by perinatal asphyxia in play soliciting. Perinatal asphyxia decreased the density of calbindin neurons in layer II of the Anterior Insular Cortex, while deep hypothermia reversed this effect. Paradoxically, in AIC there was a significant increase in the number of reelin secreting neurons in layers II and III generated by perinatal asphyxia and this increase was reversed by hypothermia. This suggests a compensatory mechanism, where reelin neurons trend to compensate the loss of calbindin neurons, at least within Anterior Insular Cortex. Finally, deep hypothermic shock might represent a valuable therapeutic alternative to treat perinatal asphyxia. This article is protected by copyright. All rights reserved.