Calretinin+ neurons partially compensate the loss of calbindin+ neurons caused by perinatal asphyxia in the rat's striatum

LUCILA KARGIEMAN; ANDRES ACUÑA; MANUEL SOLIÑO ; JUAN JOSE LOPEZ; MAURO ORTIZ ; FRANCISCO URBANO; CÉSAR FABIÁN LOIDL; PABLO VAZQUEZ

Córdoba

Congreso; XXXIII REUNIÓN ANUAL DE LA SAN (SOCIEDAD ARGENTINA DE INVESTIGACIÓN EN NEUROCIENCIAS); 2018

SAN (SOCIEDAD ARGENTINA DE INVESTIGACIÓN EN NEUROCIENCIAS)

The striatum is particularly vulnerable to perinatal asphyxia (PA). The main neuronal populations of the striatum are GABAergic median spiny neurons. A high portion of them also co-express calbindin (CB).At delivery time GABA has excitatory properties and excitotoxicity process could be mediated via GABAergic networks in case of pathological events. In previews works we found that PA generate a loss of calbindin neurons (around 50%) followed by an increase in other GABAergic subpopulations. The aim of the present work is to analyze the effect of PA over subpopulations of GABAergic neurons 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 by immersion 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 besides subventricular zone. The PA group showed a significant decrease in CB+ neurons and a paradoxical increase in neurons estimated by Neun stain. Moreover, a specific subpopulation of GABaergic Calretinin + cells showed an increase caused by PA. Deep hypothermia reversed most of these alterations 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 the homeostasis at excitation-inhibition balance is also plausible. Deep hypothermia could be a superlative option to reduce severe disability generated by the PA.