Impaired striatal D2 receptor function leads to enhanced GABA transmission in a mouse model of DYT1 dystonia

DYT1 dystonia is caused by a deletion in a glutamic acid residue in the C-terminus of the protein torsinA, whose function is still largely unknown. Alterations in GABAergic signaling have been involved in the pathogenesis of dystonia. We recorded GABA- and glutamate-mediated synaptic currents from a...

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Autors principals: Sciamanna, Giuseppe, Bonsi, Paola, Tassone, Annalisa, Cuomo, Dario, Tscherter, Anne, Viscomi, Maria Teresa, Martella, Giuseppina, Sharma, Nutan, Bernardi, Giorgio, Standaert, David G., Pisani, Antonio
Format: Artigo
Idioma:Inglês
Publicat: 2009
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Article
Accés en línia:https://ncbi.nlm.nih.gov/pmc/articles/PMC3786200/
https://ncbi.nlm.nih.gov/pubmed/19187797
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.nbd.2009.01.001
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