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

The consequences of perinatal asphyxia (PA) 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 study is to assess if a deep and...

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Bibliographic Details
Published in:Journal of comparative neurology (1911) 2019-02, Vol.527 (2), p.362-371
Main Authors: Vázquez‐Borsetti, Pablo, Peña, Elena, Rojo, Yanina, Acuña, Andrés, Loidl, Fabián C.
Format: Article
Language:English
Subjects:
Air temperature
Asphyxia
Body temperature
Calbindin
Cortex (insular)
Hypothermia
Mental disorders
Neurons
perinatal hypoxia
Reelin protein
RRID:AB_2336821
RRID:AB_563448
Schizophrenia
Social interaction
social interaction RRID:AB_1603148
Uterus
γ-Aminobutyric acid
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Summary:The consequences of perinatal asphyxia (PA) 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 study is to assess if a deep and short‐hypothermic treatment can ameliorate this damage in a model of PA. Rats offsprings were exposed to 19 min of asphyxia by immersing the uterus horns in water at 37 °C followed by 30 min in air at 10 °C that resulted in 15 °C body temperature. At postnatal day 36–38, the rats were tested in the 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 PA in play soliciting. PA 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 PA and this increase was reversed by hypothermia. This suggests a compensatory mechanism, where reelin neurons trend to compensate for the loss of calbindin neurons, at least within Anterior Insular Cortex. Finally, the deep hypothermic shock might represent a valuable therapeutic alternative to treat PA. At birth, there are calbindin+ cells in the cortex but no reelin+ cells besides cajal retzius neurons. Perinatal asphyxia (PA) seems to decrease the density of calbindin+ neurons while therapeutic hypothermia (Hyp) prevents this damage. GABAergic‐reelin+ neurons that appear in the cortex after birth seem to compensate the loss of calbindin+ neurons in the AIC.
ISSN:0021-9967
1096-9861
DOI:10.1002/cne.24539