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Zooming in on the small: The plasticity of striatal dendritic spines in l-DOPA-Induced dyskinesia.

Fieblinger, Tim LU and Cenci Nilsson, Angela LU (2015) In Movement Disorders 30(4). p.484-493
Abstract
The spiny dendrites of striatal projection neurons integrate synaptic inputs of different origins to regulate movement. It has long been known that these dendrites lose spines and display atrophic features in Parkinson's disease (PD), but the significance of these morphological changes has remained unknown. Some recent studies reveal a remarkable structural plasticity of striatal spines in parkinsonian rodents treated with L-3,4-dihydroxyphenylalanine (L-DOPA), and they demonstrate an association between this plasticity and the development of dyskinesia. These studies used different approaches and animal models, which possibly explains why they emphasize different plastic changes as being most closely linked to dyskinesia (such as a growth... (More)
The spiny dendrites of striatal projection neurons integrate synaptic inputs of different origins to regulate movement. It has long been known that these dendrites lose spines and display atrophic features in Parkinson's disease (PD), but the significance of these morphological changes has remained unknown. Some recent studies reveal a remarkable structural plasticity of striatal spines in parkinsonian rodents treated with L-3,4-dihydroxyphenylalanine (L-DOPA), and they demonstrate an association between this plasticity and the development of dyskinesia. These studies used different approaches and animal models, which possibly explains why they emphasize different plastic changes as being most closely linked to dyskinesia (such as a growth of new spines in neurons of the indirect pathway, or a loss of spines in neurons of the direct pathway, or the appearance of spines with aberrant synaptic features). Clearly, further investigations are required to reconcile these intriguing findings and integrate them in a coherent pathophysiological model. Nevertheless, these studies may mark the beginning of a new era for dyskinesia research. In addition to addressing neurochemical and molecular events that trigger involuntary movements, there is a need to better understand the long-lasting structural reorganization of cells and circuits that maintain the brain in a "dyskinesia-prone" state. This may lead to the identification of new efficacious approaches to prevent the complications of dopaminergic therapies in PD. © 2015 International Parkinson and Movement Disorder Society. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Movement Disorders
volume
30
issue
4
pages
484 - 493
publisher
John Wiley & Sons
external identifiers
  • pmid:25759263
  • wos:000352614200005
  • scopus:84926170709
ISSN
0885-3185
DOI
10.1002/mds.26139
language
English
LU publication?
yes
id
e3249093-335b-4da1-90e9-9f5a223e5a3c (old id 5264749)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25759263?dopt=Abstract
date added to LUP
2015-04-02 18:54:07
date last changed
2017-11-19 03:16:49
@article{e3249093-335b-4da1-90e9-9f5a223e5a3c,
  abstract     = {The spiny dendrites of striatal projection neurons integrate synaptic inputs of different origins to regulate movement. It has long been known that these dendrites lose spines and display atrophic features in Parkinson's disease (PD), but the significance of these morphological changes has remained unknown. Some recent studies reveal a remarkable structural plasticity of striatal spines in parkinsonian rodents treated with L-3,4-dihydroxyphenylalanine (L-DOPA), and they demonstrate an association between this plasticity and the development of dyskinesia. These studies used different approaches and animal models, which possibly explains why they emphasize different plastic changes as being most closely linked to dyskinesia (such as a growth of new spines in neurons of the indirect pathway, or a loss of spines in neurons of the direct pathway, or the appearance of spines with aberrant synaptic features). Clearly, further investigations are required to reconcile these intriguing findings and integrate them in a coherent pathophysiological model. Nevertheless, these studies may mark the beginning of a new era for dyskinesia research. In addition to addressing neurochemical and molecular events that trigger involuntary movements, there is a need to better understand the long-lasting structural reorganization of cells and circuits that maintain the brain in a "dyskinesia-prone" state. This may lead to the identification of new efficacious approaches to prevent the complications of dopaminergic therapies in PD. © 2015 International Parkinson and Movement Disorder Society.},
  author       = {Fieblinger, Tim and Cenci Nilsson, Angela},
  issn         = {0885-3185},
  language     = {eng},
  number       = {4},
  pages        = {484--493},
  publisher    = {John Wiley & Sons},
  series       = {Movement Disorders},
  title        = {Zooming in on the small: The plasticity of striatal dendritic spines in l-DOPA-Induced dyskinesia.},
  url          = {http://dx.doi.org/10.1002/mds.26139},
  volume       = {30},
  year         = {2015},
}