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Neurochem Int. 2019 Jun;126:1-10. doi: 10.1016/j.neuint.2019.02.019. Epub 2019 Feb 27.

Contribution of cholinergic interneurons to striatal pathophysiology in Parkinson's disease.

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Aix Marseille Univ, CNRS, LNC, FR3C, Marseille, France; Department of Molecular Therapeutics, New York State Psychiatric Institute, New York, NY 10032, USA; Department of Psychiatry, Columbia University, New York, NY, 10032, USA.
Aix Marseille Univ, CNRS, LNC, FR3C, Marseille, France. Electronic address:


Parkinson's disease (PD) is a neurodegenerative disorder caused by the loss of nigral dopaminergic neurons innervating the striatum, the main input structure of the basal ganglia. This creates an imbalance between dopaminergic inputs and cholinergic interneurons (ChIs) within the striatum. The efficacy of anticholinergic drugs, one of the earliest therapy for PD before the discovery of L-3,4-dihydroxyphenylalanine (L-DOPA) suggests an increased cholinergic tone in this disease. The dopamine (DA)-acetylcholine (ACh) balance hypothesis is now revisited with the use of novel cutting-edge techniques (optogenetics, pharmacogenetics, new electrophysiological recordings). This review will provide the background of the specific contribution of ChIs to striatal microcircuit organization in physiological and pathological conditions. The second goal of this review is to delve into the respective contributions of nicotinic and muscarinic receptor cholinergic subunits to the control of striatal afferent and efferent neuronal systems. Special attention will be given to the role played by muscarinic acetylcholine receptors (mAChRs) in the regulation of striatal network which may have important implications in the development of novel therapeutic strategies for motor and cognitive impairment in PD.


Acetylcholine; Cholinergic interneurons; Dopamine; Parkinson's disease; Striatum

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