Cell- and state-specific plasticity of striatal glutamatergic synapses is critical to the expression of levodopa-induced dyskinesia
Open Access
Abstract
No abstract availableKeywords
All Related Versions
Funding Information
- LabEx BRAIN
- JPB Foundation
- National Institute of Neurological Disorders and Stroke (NS 34696)
- Brain Research Foundation
- National Institutes of Health
- Vetenskapsrådet (2016-01307)
- Vetenskapsrådet (2020-02696)
This publication has 98 references indexed in Scilit:
- Upregulation of Src Family Tyrosine Kinases in the Rat Striatum by Adenosine A2A ReceptorsJournal of Molecular Neuroscience, 2022
- Dyskinesia MattersMovement Disorders, 2019
- Aberrant Striatal Activity in Parkinsonism and Levodopa-Induced DyskinesiaCell Reports, 2018
- The Kinase Fyn As a Novel Intermediate in l-DOPA-Induced Dyskinesia in Parkinson’s DiseaseMolecular Neurobiology, 2017
- L-DOPA Treatment Selectively Restores Spine Density in Dopamine Receptor D2–Expressing Projection Neurons in Dyskinetic MiceBiological Psychiatry, 2014
- An Optimized microRNA Backbone for Effective Single-Copy RNAiCell Reports, 2013
- Neuromodulatory control of striatal plasticity and behaviorCurrent Opinion in Neurobiology, 2011
- Nondopaminergic mechanisms in levodopa‐induced dyskinesiaMovement Disorders, 2005
- Upregulation of striatal adenosine A2A receptor mRNA in 6‐hydroxydopamine‐lesioned rats intermittently treated with L‐DOPASynapse, 2004
- Glutamate-mediated striatal dysregulation and the pathogenesis of motor response complications in Parkinson's diseaseAmino Acids, 2002