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This article is part of the Research Topic Basal Ganglia Circuits

Review ARTICLE

Front. Neuroanat., 07 February 2011 | http://dx.doi.org/10.3389/fnana.2011.00006

Centrality of striatal cholinergic transmission in basal ganglia function

  • 1 Laboratory of Neurophysiology and Plasticity, Fondazione Santa Lucia IRCCS, Rome, Italy
  • 2 Department of Neuroscience, University Tor Vergata, Rome, Italy

Work over the past two decades revealed a previously unexpected role for striatal cholinergic interneurons in the context of basal ganglia function. The recognition that these interneurons are essential in synaptic plasticity and motor learning represents a significant step ahead in deciphering how the striatum processes cortical inputs, and why pathological circumstances cause motor dysfunction. Loss of the reciprocal modulation between dopaminergic inputs and the intrinsic cholinergic innervation within the striatum appears to be the trigger for pathophysiological changes occurring in basal ganglia disorders. Accordingly, there is now compelling evidence showing profound changes in cholinergic markers in these disorders, in particular Parkinson’s disease and dystonia. Based on converging experimental and clinical evidence, we provide an overview of the role of striatal cholinergic transmission in physiological and pathological conditions, in the context of the pathogenesis of movement disorders.

Keywords: acetylcholine, striatum, interneuron, Parkinson’s disease, dystonia, movement disorders

Citation: Bonsi P, Cuomo D, Martella G, Madeo G, Schirinzi T, Puglisi F, Ponterio G and Pisani A (2011) Centrality of striatal cholinergic transmission in basal ganglia function. Front. Neuroanat. 5:6. doi: 10.3389/fnana.2011.00006

Received: 17 December 2010; Accepted: 21 January 2011;
Published online: 07 February 2011.

Edited by:

Jose L. Lanciego, University of Navarra, Spain

Reviewed by:

James M. Tepper, Rutgers, The State University of New Jersey, USA
Enrico Bracci, University of Manchester, UK

Copyright: © 2011 Bonsi, Cuomo, Martella, Madeo, Schirinzi, Puglisi, Ponterio and Pisani. This is an open-access article subject to an exclusive license agreement between the authors and Frontiers Media SA, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.

*Correspondence: Antonio Pisani, Department of Neuroscience, University Tor Vergata, Via Montpellier 1, 00133 Rome, Italy. e-mail: pisani@uniroma2.it