Abnormal striatal plasticity in a DYT11/SGCE myoclonus dystonia mouse model is reversed by adenosine A2A receptor inhibition

Abnormal striatal plasticity in a DYT11/SGCE myoclonus dystonia mouse model is reversed by adenosine A2A receptor inhibition

Striatal dysfunction is implicated in many movement disorders. However, the precise nature of defects often remains uncharacterized, which hinders therapy development. Here we examined striatal function in a mouse model of the incurable movement disorder, myoclonus dystonia, caused by SGCE mutations...

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Bibliographic Details
Main Authors: M. Maltese, G. Martella, P. Imbriani, Jeroen Schuermans, Karolien Billion, G. Sciamanna, Febin Farook, G. Ponterio, A. Tassone, M. Santoro, P. Bonsi, A. Pisani, Rose E. Goodchild
Format: Article
Language:English
Published: Elsevier 2017-12-01
Series:Neurobiology of Disease
Subjects:
Dystonia
Sarcoglycan
Striatum
Adenosine 2A receptor
Plasticity
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996117301845

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http://www.sciencedirect.com/science/article/pii/S0969996117301845

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