ArticleMovement disorders : official journal of the Movement Disorder Society2010
Aberrant striatal plasticity is specifically associated with dyskinesia following levodopa treatment.
Article in Movement disorders : official journal of the Movement Disorder Society, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32 citing papers in PubMed, 51 citations in OpenAlex.
- Altered wakeful theta activity characterizes levodopa-induced dyskinesia in Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Exploring causal effects of sarcopenia on risk and progression of Parkinson disease by Mendelian randomization.NPJ Parkinson's disease · 2024Article
- Differential Activation States of Direct Pathway Striatal Output Neurons during l-DOPA-Induced Dyskinesia Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Pathological cell assembly dynamics in a striatal MSN network model.Frontiers in computational neuroscience · 2024Article
- Targeting Striatal Glutamate and Phosphodiesterases to Control L-DOPA-Induced Dyskinesia.Cells · 2023Review
- Downregulation of striatal CaNeurobiology of disease · 2023Article
- Article
- Insights into the Pathophysiology of Psychiatric Symptoms in Central Nervous System Disorders: Implications for Early and Differential Diagnosis.International journal of molecular sciences · 2021Review
- Histological Correlates of Neuroanatomical Changes in a Rat Model of Levodopa-Induced Dyskinesia Based on Voxel-Based Morphometry.Frontiers in aging neuroscience · 2021Article
- Preclinical evidence in support of repurposing sub-anesthetic ketamine as a treatment for L-DOPA-induced dyskinesia.Experimental neurology · 2020Article
- Functional Relevance of Endocannabinoid-Dependent Synaptic Plasticity in the Central Nervous System.ACS chemical neuroscience · 2018Review
- Synaptic plasticity and levodopa-induced dyskinesia: electrophysiological and structural abnormalities.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Dysregulation of BET proteins in levodopa-induced dyskinesia.Neurobiology of disease · 2017Article
- Opioid system in L-DOPA-induced dyskinesia.Translational neurodegeneration · 2017Review
- Maladaptive Synaptic Plasticity in L-DOPA-Induced Dyskinesia.Frontiers in neural circuits · 2016Review
- M4 Muscarinic Receptor Signaling Ameliorates Striatal Plasticity Deficits in Models of L-DOPA-Induced Dyskinesia.Neuron · 2015Article
- Levodopa-induced plasticity: a double-edged sword in Parkinson's disease?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Review
- Age-related alterations in the expression of genes and synaptic plasticity associated with nitric oxide signaling in the mouse dorsal striatum.Neural plasticity · 2015Article
- Differential effects of the NMDA receptor antagonist MK-801 on dopamine receptor D1- and D2-induced abnormal involuntary movements in a preclinical model.Neuroscience letters · 2014Article
- Chronic methylphenidate exposure during adolescence reduces striatal synaptic responses to ethanol.The European journal of neuroscience · 2014Article
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3 authors at 1 institution in 1 country.
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Abstract
Chronic levodopa treatment for Parkinson's disease often results in the development of abnormal involuntary movement, known as L-dopa-induced dyskinesia (LIDs). Studies suggest that LIDs may be associated with aberrant corticostriatal plasticity. Using in vivo extracellular recordings from identified Type I and Type II medium spiny striatal neurons, chronic L-dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic L-dopa treatment in dopamine-depleted rats, there was a transition from a cortically evoked long-term depression (LTD) to a complementary but opposing form of plasticity, long-term potentiation, in Type II "indirect" pathway neurons. In contrast, LTD could still be induced in Type I neurons. Interestingly, the one parameter that correlated best with dyskinesias was the inability to de-depress established LTD in Type I medium spiny striatal neurons. Taken as a whole, we propose that the induction of LIDs is due, at least in part, to an aberrant induction of plasticity within the Type II indirect pathway neurons combined with an inability to de-depress established plastic responses in Type I neurons. Such information is critical for understanding the cellular mechanisms underlying one of the major caveats to L-dopa therapy.
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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.