GABAergic agonists modulate the glutamate release from frontal cortex synaptosomes of rats with experimental autoimmune encephalomyelitis

FERNÁNDEZ HURST, NICOLÁS; CHANADAY, NATALÍ L.; ROTH, GERMAN A.

Inflammation & Allergy. Drug Targets

Bentham Science

Lugar: Dubai; Año: 2015 vol. 14 p. 105 - 105

1871-5281

bstract: Experimental autoimmune encephalomyelitis (EAE) is a model that mimics many of the clinical and pathological features of multiple sclerosis. We have previously found a significant reduction in the GABAergic regulation of glutamate release from synaptosomes of EAE rats during the acute stage of the disease. In order to deepen into the possible metabolic pathways responsible for this alteration, in this work we evaluate the direct effect of different GABAergic agonists on the glutamate release and synapsin I phosphorylation in synaptosomes from the frontal cortex of control and EAE animals. The results show that all tested GABA agonists negatively modulate control synaptosomes, downregulating glutamate release and synapsin I phosphorylation on P-site 3, while synaptosomes from EAE group are less responsive to GABAergic agonists, with no change in their sensitivity to allosteric modulators. GABA and the GABA receptor agonists Muscimol (GABAA agonist) and Baclofen (GABAB agonist)