CONICET | Buscador de Institutos y Recursos Humanos

The striatum is particularly vulnerable to perinatal asphyxia (PA). The main neuronal populationsof the striatum are GABAergic median spiny neurons. A high portion of them also co-expresscalbindin (CB).At delivery time GABA has excitatory properties and excitotoxicity process could be mediated viaGABAergic networks in case of pathological events.In previews works we found that PA generate a loss of calbindin neurons (around 50%) followedby an increase in other GABAergic subpopulations.The aim of the present work is to analyze the effect of PA over subpopulations of GABAergicneurons in the striatum and to assess the deep hypothermia therapeutic outcome.The uterus was removed by caesarean section and the fetuses were exposed to hypoxia byimmersion in water (19 min) at 37 C ̊ (PA). The hypothermic group was exposed to 10 C ̊ during 30min after PA. Four experimental groups of 3-4 rats were formed. The immunolabeling of CB,Calretinin, Neun, and reelin was measured in adult rats by a skilled observer blind to treatment.Reelin+ cells that usually co-express Calretinin, showed no stain in the striatum besidessubventricular zone. The PA group showed a significant decrease in CB+ neurons and a paradoxicalincrease in neurons estimated by Neun stain. Moreover, a specific subpopulation of GABaergicCalretinin + cells showed an increase caused by PA. Deep hypothermia reversed most of thesealterations most likely by protecting calbindin neurons.The mechanism involved in this compensation is not clear. It is possible that Neun and Calretinin +cells filled the space left by Calbindin neurons. As well, an active mechanism to keep thehomeostasis at excitation-inhibition balance is also plausible. Deep hypothermia could be asuperlative option to reduce severe disability generated by the PA.