INHIBITORY ROLE OF DIAZEPAM ON AUTOIMMUNE INFLAMMATION IN RATS WITH EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS

MARIO J. BIBOLINI; NATALÍ L. CHANADAY; NATALIA S. BAEZ; ALICIA L. DEGANO; CLARA G. MONFERRAN; GERMÁN A. ROTH

NEUROSCIENCE

PERGAMON-ELSEVIER SCIENCE LTD

Año: 2011

0306-4522

lutamate and GABA are the main excitatory and inhibitory neurotransmitters in the central nervous system 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 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 six days starting at day 6 or 11 after EAE active in