Zooming in on the small: The plasticity of striatal dendritic spines in l-DOPA-Induced dyskinesia.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/5264749
- author
- Fieblinger, Tim LU and Cenci Nilsson, Angela LU
- organization
- publishing date
- 2015
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Movement Disorders
- volume
- 30
- issue
- 4
- pages
- 484 - 493
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- pmid:25759263
- wos:000352614200005
- scopus:84926170709
- pmid:25759263
- 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
- 2016-04-01 10:48:37
- date last changed
- 2022-03-27 19:47:18
@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 Inc.}}, 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}}, doi = {{10.1002/mds.26139}}, volume = {{30}}, year = {{2015}}, }