Striatal spine plasticity in Parkinson’s disease
- 1 Yerkes National Primate Research Center, Emory University, Atlanta, GA, USA
- 2 Department of Neurology, Emory University, Atlanta, GA, USA
Striatal dopamine (DA) denervation results in a significant loss of dendritic spines on medium spiny projection neurons in Parkinson’s disease. In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated parkinsonian monkeys, spines contacted either by cortical or thalamic glutamatergic terminals are severely affected on both direct and indirect striatofugal neurons. In rodents, indirect pathway neurons appear to be more sensitive, at least in early stages of acute dopamine denervation. The remaining corticostriatal and thalamostriatal axo-spinous synapses undergo complex ultrastructural remodeling consistent with increased synaptic activity in the DA-denervated primate striatum, which may explain the pathophysiological overactivity of the corticostriatal system reported in various animal models of parkinsonism. The calcium-mediated regulation of the transcription factor myocyte enhancer factor 2 was recognized as a possible underlying mechanism for striatal spine plasticity. Future studies to determine how alterations in striatal spine plasticity contribute to the symptomatology of parkinsonism are warranted.
Keywords: dendritic spine, plasticity, dopamine, glutamate, Parkinson’s disease
Citation: Villalba RM and Smith Y (2010) Striatal spine plasticity in Parkinson’s disease. Front. Neuroanat. 4:133. doi: 10.3389/fnana.2010.00133
Received: 26 July 2010;
Paper pending published: 17 August 2010;
Accepted: 29 August 2010; Published online: 10 December 2010
Edited by:Jose L. Lanciego, University of Navarra, Spain
Reviewed by:Jose L. Lanciego, University of Navarra, Spain
José A. Armengol, University Pablo de Olavide, Spain
Copyright: © 2010 Villalba and Smith. This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.
*Correspondence: Rosa M. Villalba, Yerkes National Primate Research Center, Emory University, 954 Gatewood Rd. NE, Atlanta, GA 30329, USA. e-mail: firstname.lastname@example.org