CONICET | Buscador de Institutos y Recursos Humanos

The striatum is particularly vulnerable to perinatal asphyxia (PA). The main cells of this structure are the median spiny neurons, which are GABAergic calbindin (CB) positive neurons. At the time of delivery GABA has excitatory properties and the excitotoxicity process could be mediated via GABA-GABA synapsis. In previews works we found that the loss of calbindin neurons was compensated by an increase in other populations of GABAergic cells.The present work aims to analyze the effect of the loss of calbindin neurons over other subpulation of neurons in the striatum of the rat and to assess the therapeutic effect of deep hypothermia.The uterus was removed by caesarean section and the fetuses were exposed to hypoxia (19 min at 37 C˚) by immersion in water and exposed to a temperature of 10 C˚ for 30 min in case of hypothermic group. Four experimental groups of 3-4 rats each were formed. The labeling of CB, calrretinin, neuN, DAPI and reelin was measured in adult rats by an skilled observer blind to the treatment. Reelin+ cells that usually co-express claretinin, showed no stain in the striatum besides subventricular zone. The PA group shows a significant decrease in CB+ neurons, this group shows also a paradoxical increase in neuronas estimated in the Neun stain. Specific subpopulations of GABaergic cells as calretinin also showed an increase caused by PA. Deep hypothermia reversed most of this alterations probably by protecting calbindin neurons.The mechanism involved in this compensation is not clear yet. It is possible that the cells just ocupate the space left by calbindin neuron. Also is possible the existence of an active mechanism to quip the homeostasis in the excitation-inhibition balance. Deep hypothermia could be a superlative option to reduce severe disability generated by the PA.