Alterations in frontal cortex synaptosomes from rats with experimental autoimmune encephalomyelitis

CHANADAY NL; VILCAES AA; DE PAUL A; TORRES A; DEGANO AL; ROTH GA

Huerta Grande, Córdoba

Congreso; XXVIII Congreso de la Sociedad Argentina de Investigación en Neurociencias & Reunión Satélite ?Bases Neurales de la Conducta: Neuroetología y Neurobiologia de la Memoria en el Cono Sur?; 2013

Sociedad Argentina de Investigación en Neurociencias

Experimental autoimmune encephalomyelitis (EAE) is an animal model of the human disease multiple sclerosis. Both are inflammatory demyelinating pathologies of the central nervous system associated with motor, sensory, and cognitive deficits. In the last years gray matter damage has increasingly received attention as they may contribute to disease progression and emergence of cognitive deficits. Herein we analyze functional and morphological changes in isolated presynaptic terminals (synaptosomes) from frontal cortex of rats with acute EAE. We show impairment in Ca2+-dependent L-glutamate release concomitant with alterations in the levels and phosphorylation state of synapsin I and kinases of the release machinery (Erk1/2 and CaMKII). These changes rapidly reverse when the animals begin to recover from the clinical signs of the disease. Our results indicate the release machinery is altered in the frontal cortex of rats with EAE. Furthermore, electron microscopy studies revealed differences in synaptic vesicles distribution and PSD size in EAE group. These are the first evidences unraveling the molecular mechanism of presynaptic dysfunction in frontal cortex during the course of EAE.