Derangement of Ras-guanine nucleotide-releasing factor 1 (Ras-GRF1) and extracellular signal-regulated kinase (ERK) dependent striatal plasticity in L-DOPA-induced dyskinesia.

Carmela Giampa', Milica Cerovic, Vincenza Bagetta, Valentina Pendolino, Veronica Ghiglieri, Stefania Fasano, Ilaria Morella, Neil Hardingham, Andreas Heuer, Alessandro Papale, Francesca Marchisella, Carmela Giampà, Paolo Calabresi, Barbara Picconi, Riccardo Brambilla

Risultato della ricerca: Contributo in rivistaArticolo in rivista

46 Citazioni (Scopus)

Abstract

BACKGROUND: Bidirectional long-term plasticity at the corticostriatal synapse has been proposed as a central cellular mechanism governing dopamine-mediated behavioral adaptations in the basal ganglia system. Balanced activity of medium spiny neurons (MSNs) in the direct and the indirect pathways is essential for normal striatal function. This balance is disrupted in Parkinson's disease and in l-3,4-dihydroxyphenylalanine (l-DOPA)-induced dyskinesia (LID), a common motor complication of current pharmacotherapy of Parkinson's disease.
Lingua originaleEnglish
pagine (da-a)106-115
Numero di pagine10
RivistaBiological Psychiatry
Stato di pubblicazionePubblicato - 2015

Keywords

  • Depotentiation

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