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

BIBOLINI, M. J.; CHANADAY RICAGNI NATALÍ L.; BÁEZ, NATALIA S.; DEGANO ALICIA L.; MONFERRAN, CLARA G.; ROTH GERMAN A.

PERGAMON-ELSEVIER SCIENCE LTD

Año: 2011 vol. 199 p. 421 - 421

lutamate and GABA are the main excitatory and inhibitory neurotransmitters in the CNS, and both may be involved in the neuronal dysfunction in neurodegenerativeconditions. 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 GABAA 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 GABAA 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 11 after EAE active induction led to a mar