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Reversal of neurobehavioral social deficits in dystrophic mice using inhibitors of phosphodiesterases PDE5A and PDE9A.

Translational psychiatry (2016-09-28)
M S Alexander, M J Gasperini, P T Tsai, D E Gibbs, J M Spinazzola, J L Marshall, M J Feyder, M T Pletcher, E L P Chekler, C A Morris, M Sahin, J F Harms, C J Schmidt, R J Kleiman, L M Kunkel
RÉSUMÉ

Duchenne muscular dystrophy is caused by mutations in the DYSTROPHIN gene. Although primarily associated with muscle wasting, a significant portion of patients (approximately 25%) are also diagnosed with autism spectrum disorder. We describe social behavioral deficits in dystrophin-deficient mice and present evidence of cerebellar deficits in cGMP production. We demonstrate therapeutic potential for selective inhibitors of the cGMP-specific PDE5A and PDE9A enzymes to restore social behaviors in dystrophin-deficient mice.

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Sérum de chèvre
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Monoclonal Anti-Calbindin-D-28K antibody produced in mouse, clone CB-955, ascites fluid