Article
Postsynaptic alteration of NR2A subunit and defective autophosphorylation of alphaCaMKII at threonine-286 contribute to abnormal plasticity and morphology of upper motor neurons in presymptomatic SOD1G93A mice, a murine model for amyotrophic lateral sclerosis.
Cerebral cortex (New York, N.Y. : 1991) - 1 Apr 2011
Spalloni A, Origlia N, Sgobio C, Trabalza A, Nutini M, Berretta N, Bernardi G, Domenici L, Ammassari-Teule M, Longone P
Abstract excerpt
Although amyotrophic lateral sclerosis (ALS) has long been considered as a lower motor neuron (MN) disease, degeneration of upper MNs arising from a combination of mechanisms including insufficient growth factor signaling and enhanced extracellular glutamate levels is now well documented. The observation that these mechanisms are altered in presymptomatic superoxide dismutase (SOD1) mice, an ALS mouse model,...
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