ArticleNeuroscience2015
Alterations in primary motor cortex neurotransmission and gene expression in hemi-parkinsonian rats with drug-induced dyskinesia.
Article in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Widespread and Heterologous Effects of L-DOPA on Monoaminergic Tissue Metabolism in Newborn Rats Expressing Air-Stepping.International journal of molecular sciences · 2025Article
- Transcranial Magnetic Stimulation Attenuates Dyskinesias and FosB and c-Fos Expression in a Parkinson's Disease Model.Brain sciences · 2024Article
- Cerebellar stimulation prevents Levodopa-induced dyskinesia in mice and normalizes activity in a motor network.Nature communications · 2022Article
- Single-cell transcriptomics of human iPSC differentiation dynamics reveal a core molecular network of Parkinson's disease.Communications biology · 2022Article
- Current Knowledge on the Background, Pathophysiology and Treatment of Levodopa-Induced Dyskinesia-Literature Review.Journal of clinical medicine · 2021Review
- Article
- Reciprocal cross-sensitization of D1 and D3 receptors following pharmacological stimulation in the hemiparkinsonian rat.Psychopharmacology · 2020Article
- Prior stress followed by a novel stress challenge results in sex-specific deficits in behavioral flexibility and changes in gene expression in rat medial prefrontal cortex.Hormones and behavior · 2020Article
- Altered Recruitment of Motor Cortex Neuronal Activity During the Grasping Phase of Skilled Reaching in a Chronic Rat Model of Unilateral Parkinsonism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Late aging-associated increases in L-DOPA-induced dyskinesia are accompanied by heightened neuroinflammation in the hemi-parkinsonian rat.Neurobiology of aging · 2019Article
- Regulation of dopamine neurotransmission from serotonergic neurons by ectopic expression of the dopamine D2 autoreceptor blocks levodopa-induced dyskinesia.Acta neuropathologica communications · 2019Article
- Effect of Intrastriatal 6-OHDA Lesions on Extrastriatal Brain Structures in the Mouse.Molecular neurobiology · 2018Article
- D-512, a novel dopamine DBritish journal of pharmacology · 2017Article
- Loss of dopamine D1 receptors and diminished D1/5 receptor-mediated ERK phosphorylation in the periaqueductal gray after spinal cord lesion.Neuroscience · 2017Article
- The Role of Primary Motor Cortex (M1) Glutamate and GABA Signaling in l-DOPA-Induced Dyskinesia in Parkinsonian Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Treatment of Parkinson's disease (PD) with dopamine replacement relieves symptoms of poverty of movement, but often causes drug-induced dyskinesias. Accumulating clinical and pre-clinical evidence suggests that the primary motor cortex (M1) is involved in the pathophysiology of PD and that modulating cortical activity may be a therapeutic target in PD and dyskinesia. However, surprisingly little is known about how M1 neurotransmitter tone or gene expression is altered in PD, dyskinesia or associated animal models. The present study utilized the rat unilateral 6-hydroxydopamine (6-OHDA) model of PD/dyskinesia to characterize structural and functional changes taking place in M1 monoamine innervation and gene expression. 6-OHDA caused dopamine pathology in M1, although the lesion was less severe than in the striatum. Rats with 6-OHDA lesions showed a PD motor impairment and developed dyskinesia when given L-DOPA or the D1 receptor agonist, SKF81297. M1 expression of two immediate-early genes (c-Fos and ARC) was strongly enhanced by either L-DOPA or SKF81297. At the same time, expression of genes specifically involved in glutamate and GABA signaling were either modestly affected or unchanged by lesion and/or treatment. We conclude that M1 neurotransmission and signal transduction in the rat 6-OHDA model of PD/dyskinesia mirror features of human PD, supporting the utility of the model to study M1 dysfunction in PD and the elucidation of novel pathophysiological mechanisms and therapeutic targets.
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Registered trials
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.