Participation of the GABAergic system on the glutamate release of frontal cortex synaptosomes from rats with Experimental autoimmune encephalomyelitis

CID MARIANA P.; VILCAES A. ALEJANDRO; RUPIL LUCÍA L.; SALVATIERRA NANCY A.; ROTH GERMAN A.

PERGAMON-ELSEVIER SCIENCE LTD

Año: 2011 vol. 189 p. 337 - 337

e previously found that the glutamate release was decreased in synaptosomes from rat cerebral cortex during the development of experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis. Various other reports have shown a deficit in the expression of proteins associated with GABAergic neurotransmission in the neocortex of patients with multiple sclerosis and it was also demonstrated that the activation of GABAA receptors leads to an inhibition of glutamate release. Now, in order to evaluate the events that may affect the neuronal function in EAE synaptosomes, we analyzed the participation of the GABAergic system in glutamate release and in the flunitrazepam-sensitive GABAA receptor density. This revealed alterations in the GABAergic system of the frontal cortex synaptosomes from EAE animals. GABA induced a decrease in the 4-aminopyridine-evoked glutamate release in control synaptosomes which was abolished by picrotoxin, a GABAA receptor antagonist. In con