Inhibitory role of diazepam on autoimmune inflammation in rats with experimental autoimmune encephalomyelitis.

BIBOLINI MJ ; CHANADAY NL; BÁEZ NS; DEGANO AL; MONFERRAN CG ; ROTH GA

PERGAMON-ELSEVIER SCIENCE LTD

Lugar: Amsterdam; Año: 2011 vol. 199 p. 421 - 421

Glutamate and GABA are the main excitatory and inhibitory neurotransmitters in the CNS, and both may be involved in the neuronal dysfunction in neurodegenerative conditions. We have recently found that glutamate release was decreased in isolated synaptosomes from the rat cerebral cortex during the development of experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis. In contrast to control animals where GABA induced a decrease in the evoked glutamate release, which was abolished by picrotoxin (a GABA(A) antagonist), synaptosomes from EAE rats showed a loss in the inhibition of the glutamate release mediated by GABA with a concomitant diminution of the flunitrazepam-sensitive GABA(A) receptor density. We have presently further evaluated the relevance of the GABAergic system in EAE by treating rats challenged for the disease with the GABA agonist diazepam. Administration of diazepam during 6 days starting at day 6 or