Glutamate release machinery is altered in the frontal cortex of rats with experimental autoimmune encephalomyelitis

CHANADAY, NATALÍ L.; VILCAES A. ALEJANDRO; DE PAUL ANA L.; TORRES ALICIA I.; DEGANO ALICIA L.; ROTH GERMAN A.

MOLECULAR NEUROBIOLOGY

HUMANA PRESS INC

Lugar: New York; Año: 2015 vol. 51 p. 1353 - 1353

0893-7648

xperimental autoimmune encephalomyelitis (EAE) is an animal model that mimics many of the clinical and pathological features of the human disease multiple sclerosis (MS). Both are inflammatory demyelinating and neurodegenerative pathologies of the central nervous system associated with motor, sensory, and cognitive deficits. In MS, gray matter atrophy is related to the emergence of cognitive deficits and contributes to clinical progression. In particular, prefrontal cortex injury and dysfunction have been correlated to the development of fatigue, one of the most common and disabling symptoms in MS. However, the molecular bases of these changes remain unknown. Taking advantage of EAE similitude, we herein analyze functional and morphological changes in isolated cortical presynaptic terminals (synaptosomes) from an acute rat model. We found impaired glutamate release in the frontal cortex from EAE rats. This defect appeared along with the onset of the disease, reversing when clinical si