Rapamycin, by Inhibiting mTORC1 Signaling, Prevents the Loss of Striatal Bidirectional Synaptic Plasticity in a Rat Model of L-DOPA-Induced Dyskinesia.
Parkinson’s disease
depotentiation
dorsolateral striatum
functional plasticity
levodopa-induced dyskinesia
Journal
Frontiers in aging neuroscience
ISSN: 1663-4365
Titre abrégé: Front Aging Neurosci
Pays: Switzerland
ID NLM: 101525824
Informations de publication
Date de publication:
2020
2020
Historique:
received:
10
12
2019
accepted:
30
06
2020
entrez:
28
8
2020
pubmed:
28
8
2020
medline:
28
8
2020
Statut:
epublish
Résumé
Levodopa (L-DOPA) treatment is the main gold-standard therapy for Parkinson disease (PD). Besides good antiparkinsonian effects, prolonged use of this drug is associated to the development of involuntary movements known as L-DOPA-induced dyskinesia (LID). L-DOPA-induced dyskinesia is linked to a sensitization of dopamine (DA) D1 receptors located on spiny projection neurons (SPNs) of the dorsal striatum. Several evidences have shown that the emergence of LID can be related to striatal D1/cAMP/PKA/DARPP-32 and extracellular signal-regulated kinases (ERK1/2) pathway overactivation associated to aberrant
Identifiants
pubmed: 32848709
doi: 10.3389/fnagi.2020.00230
pmc: PMC7431470
doi:
Types de publication
Journal Article
Langues
eng
Pagination
230Informations de copyright
Copyright © 2020 Calabrese, Di Maio, Marino, Cardinale, Natale, De Rosa, Campanelli, Mancini, Napolitano, Avallone, Calabresi, Usiello, Ghiglieri and Picconi.
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