ArticleThe European journal of neuroscience2010
Impact of dendritic spine preservation in medium spiny neurons on dopamine graft efficacy and the expression of dyskinesias in parkinsonian rats.
Article in The European journal of neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 66 citations in OpenAlex.
- Disease-modifying, multidimensional efficacy of putaminal CaMolecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Advancing age and sex modulate antidyskinetic efficacy of striatal CaNeurobiology of aging · 2025Article
- Advancing age and the rs6265 BDNF SNP are permissive to graft-induced dyskinesias in parkinsonian rats.NPJ Parkinson's disease · 2024Article
- Control of Dopamine Signal in High-Order Receptor Complex on Striatal Astrocytes.International journal of molecular sciences · 2024Article
- Quinpirole inhibits levodopa-induced dyskinesias at structural and behavioral levels: Efficacy negated by co-administration of isradipine.Experimental neurology · 2023Article
- Therapeutic Potential of Heterocyclic Compounds Targeting Mitochondrial Calcium Homeostasis and Signaling in Alzheimer's Disease and Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Downregulation of striatal CaNeurobiology of disease · 2023Article
- The Role of Striatal Cav1.3 Calcium Channels in Therapeutics for Parkinson's Disease.Handbook of experimental pharmacology · 2023Review
- Spontaneous Graft-Induced Dyskinesias Are Independent of 5-HT Neurons and Levodopa Priming in a Model of Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2022Article
- The BDNF Val66Met polymorphism (rs6265) enhances dopamine neuron graft efficacy and side-effect liability in rs6265 knock-in rats.Neurobiology of disease · 2021Article
- Striatal Nurr1 Facilitates the Dyskinetic State and Exacerbates Levodopa-Induced Dyskinesia in a Rat Model of Parkinson's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Dopaminergic Progenitors Derived From Epiblast Stem Cells Function Similarly to Primary VM-Derived Progenitors When Transplanted Into a Parkinson's Disease Model.Frontiers in neuroscience · 2020Article
- Cell therapy for Parkinson's disease: Why it doesn't work every time.Movement disorders : official journal of the Movement Disorder Society · 2019Article
- Genetic silencing of striatal CaV1.3 prevents and ameliorates levodopa dyskinesia.Movement disorders : official journal of the Movement Disorder Society · 2019Article
- The Rodent Models of Dyskinesia and Their Behavioral Assessment.Frontiers in neurology · 2019Review
- Levodopa treatment and dendritic spine pathology.Movement disorders : official journal of the Movement Disorder Society · 2018Review
- Loss and remodeling of striatal dendritic spines in Parkinson's disease: from homeostasis to maladaptive plasticity?Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- The role of nonhuman primate models in the development of cell-based therapies for Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- BDNF in the Aged Brain: Translational Implications for Parkinson's Disease.Austin neurology & neurosciences · 2017Article
- Repairing the Aged Parkinsonian Striatum: Lessons from the Lab and Clinic.Journal of clinical & cellular immunology · 2016Article
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6 authors at 2 institutions in 1 country.
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Abstract
Dopamine deficiency associated with Parkinson's disease (PD) results in numerous changes in striatal transmitter function and neuron morphology. Specifically, there is marked atrophy of dendrites and dendritic spines on striatal medium spiny neurons (MSN), primary targets of inputs from nigral dopamine and cortical glutamate neurons, in advanced PD and rodent models of severe dopamine depletion. Dendritic spine loss occurs via dysregulation of intraspine Cav1.3 L-type Ca(2+)channels and can be prevented, in animal models, by administration of the calcium channel antagonist, nimodipine. The impact of MSN dendritic spine loss in the parkinsonian striatum on dopamine neuron graft therapy remains unexamined. Using unilaterally parkinsonian Sprague-Dawley rats, we tested the hypothesis that MSN dendritic spine preservation through administration of nimodipine would result in improved therapeutic benefit and diminished graft-induced behavioral abnormalities in rats grafted with embryonic ventral midbrain cells. Analysis of rotational asymmetry and spontaneous forelimb use in the cylinder task found no significant effect of dendritic spine preservation in grafted rats. However, analyses of vibrissae-induced forelimb use, levodopa-induced dyskinesias and graft-induced dyskinesias showed significant improvement in rats with dopamine grafts associated with preserved striatal dendritic spine density. Nimodipine treatment in this model did not impact dopamine graft survival but allowed for increased graft reinnervation of striatum. Taken together, these results demonstrate that even with grafting suboptimal numbers of cells, maintaining normal spine density on target MSNs results in overall superior behavioral efficacy of dopamine grafts.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.