"Nerve terminal alterations in frontal cortex from rats with experimental autoinmune encephalomyelitis (EAE)"

CHANADAY NL; DEGANO AL; ROTH GA

Huerta Grande, Córdoba

Congreso; XXVI Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias; 2011

Multiple sclerosis (MS) is a human inflammatory demyelinating disease of the central nervous system that leads to motor, sensory, and cognitive deficits. Although it has been classically considered a white matter pathology, cortical lesions has increasingly received attention as they may contribute to disease progression and emergence of cognitive deficits. EAE is the classical model that mimics many of the clinical and pathological features of MS. While EAE research has been mostly focused on spinal cord inflammation/demyelination, the extent of cortical alterations are still not completely known. Besides corroborating the previously found diminution in Ca2+-dependent glutamate release from frontal cortex synaptosomes of EAE rats, herein we show that this alteration is accompanied by increased levels of the GABA synthesizing enzyme GAD65/67, without changes in the content of glutamatergic and GABAergic terminals. Concomitantly, differential activation upon stimulation of kinases was observed. Moreover, these changes are reversed when the animals are completely recovered from the clinical signs of the disease. These data indicate that the machinery of neurotransmitter release is affected in EAE, and shed light into the mechanism of neuronal dysfunction in the frontal cortex.