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- Cenci Nilsson, Angela
(författare)
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Post- Versus Pre-Synaptic Plasticity
- 2010
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Ingår i: Movement Disorders. - : Wiley. - 0885-3185. ; 25, s. 582-583
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Konferensbidrag (refereegranskat)
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| 3. |
- Fieblinger, Tim, et al.
(författare)
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Zooming in on the small: The plasticity of striatal dendritic spines in l-DOPA-Induced dyskinesia.
- 2015
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Ingår i: Movement Disorders. - : Wiley. - 0885-3185. ; 30:4, s. 484-493
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Tidskriftsartikel (refereegranskat)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.
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- Stefanova, Nadia, et al.
(författare)
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High dose levodopa therapy is not toxic in multiple system atrophy: Experimental evidence
- 2007
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Ingår i: Movement Disorders. - : Wiley. - 0885-3185. ; 27:7, s. 969-973
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Tidskriftsartikel (refereegranskat)abstract
- Levodopa is generally regarded the first choice therapy for parkinsonism associated with multiple system atrophy (MSA-P). However, MSA-P patients often show a poor or unsustained levodopa response which inflicts high dose therapy. This is generally attributed to progressive striatal degeneration with loss of dopamine receptors. Experimental evidence suggests that dopaminergic stimulation may accelerate the striatal disease process in MSA, possibly by pro-oxidative mechanisms. Intact nigrostriatal dopamine release augments striatal lesion size in the unilateral nigral and striatal double lesion rat model of MSA-P. Further, neuronal vulnerability to exogenous oxidative stress is increased in a transgenic MSA mouse model with oligodendroglial alpha-synuclein inclusions. The aim of the present study was to analyze whether high dose levodopa delivery in the transgenic MSA model is associated with neurotoxicity exacerbated by the presence of oligodendroglial alpha-synuclein inclusion pathology. Control and transgenic MSA mice underwent pulsatile treatment with either vehicle, low or high dose levodopa for a period of 1 month. Behavioral and neuropathological indices failed to show evidence for neurotoxic effects of high-dose levodopa in this alpha-synuclein transgenic MSA model. These findings support the idea that high dose levodopa therapy in MSA is not detrimental to the underlying neuropathological process. (C) 2007 Movement Disorder Society.
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