ArticleBiochemical pharmacology2013
Multiple CNS nicotinic receptors mediate L-dopa-induced dyskinesias: studies with parkinsonian nicotinic receptor knockout mice.
Article in Biochemical pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Effect of nicotine on L-dopa-induced dyskinesia in animal models of Parkinson's disease: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014Pooled it
- Genome-wide association analyses reveal susceptibility variants linked to Parkinson's disease in the South African population using inferred global and local ancestry.medRxiv : the preprint server for health sciences · 2025Article
- Levodopa-Induced Dyskinesias in Parkinson's Disease: An Overview on Pathophysiology, Clinical Manifestations, Therapy Management Strategies and Future Directions.Journal of clinical medicine · 2023Review
- Nicotine-mediated effects in neuronal and mouse models of synucleinopathy.Frontiers in neuroscience · 2023Article
- Striatal synaptic adaptations in Parkinson's disease.Neurobiology of disease · 2022Review
- Cholinergic Receptor Modulation as a Target for Preventing Dementia in Parkinson's Disease.Frontiers in neuroscience · 2021Review
- Targeting the cholinergic system in Parkinson's disease.Acta pharmacologica Sinica · 2020Review
- Protective Effect of the α7 Nicotinic Receptor Agonist PNU-282987 on Dopaminergic Neurons Against 6-Hydroxydopamine, Regulating Anti-neuroinflammatory and the Immune Balance Pathways in Rat.Frontiers in aging neuroscience · 2020Article
- Dystonia and levodopa-induced dyskinesias in Parkinson's disease: Is there a connection?Neurobiology of disease · 2019Review
- Genetic Knockdown of mGluR5 in Striatal D1R-Containing Neurons Attenuates L-DOPA-Induced Dyskinesia in Aphakia Mice.Molecular neurobiology · 2019Article
- Receptor Ligands as Helping Hands to L-DOPA in the Treatment of Parkinson's Disease.Biomolecules · 2019Review
- Potential Therapeutic Application for Nicotinic Receptor Drugs in Movement Disorders.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2019Review
- Dyskinesia and brain-derived neurotrophic factor levels after long-term levodopa and nicotinic receptor agonist treatments in female mice with near-total unilateral dopaminergic denervation.BMC neuroscience · 2018Article
- The striatal cholinergic system in L-dopa-induced dyskinesias.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Striatal cholinergic interneurons and Parkinson's disease.The European journal of neuroscience · 2018Review
- Striatal D1 medium spiny neuron activation induces dyskinesias in parkinsonian mice.Movement disorders : official journal of the Movement Disorder Society · 2017Article
- Non-dopamine receptor ligands for the treatment of Parkinson's disease. Insight into the related chemical/property space.Molecular diversity · 2016Review
- Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson's disease.NPJ Parkinson's disease · 2016Review
- α7 nicotinic receptor agonists reduce levodopa-induced dyskinesias with severe nigrostriatal damage.Movement disorders : official journal of the Movement Disorder Society · 2015Article
- Preclinical Evidence for a Role of the Nicotinic Cholinergic System in Parkinson's Disease.Neuropsychology review · 2015Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Accumulating evidence supports the idea that drugs acting at nicotinic acetylcholine receptors (nAChRs) may be beneficial for Parkinson's disease, a neurodegenerative movement disorder characterized by a loss of nigrostriatal dopaminergic neurons. Nicotine administration to parkinsonian animals protects against nigrostriatal damage. In addition, nicotine and nAChR drugs improve L-dopa-induced dyskinesias, a debilitating side effect of L-dopa therapy which remains the gold-standard treatment for Parkinson's disease. Nicotine exerts its antidyskinetic effect by interacting with multiple nAChRs. One approach to identify the subtypes specifically involved in L-dopa-induced dyskinesias is through the use of nAChR subunit null mutant mice. Previous work with β2 and α6 nAChR knockout mice has shown that α6β2* nAChRs were necessary for the development/maintenance of L-dopa-induced abnormal involuntary movements (AIMs). The present results in parkinsonian α4 nAChR knockout mice indicate that α4β2* nAChRs also play an essential role since nicotine did not reduce L-dopa-induced AIMs in such mice. Combined analyses of the data from α4 and α6 knockout mice suggest that the α6α4β2β3 subtype may be critical. In contrast to the studies with α4 and α6 knockout mice, nicotine treatment did reduce L-dopa-induced AIMs in parkinsonian α7 nAChR knockout mice. However, α7 nAChR subunit deletion alone increased baseline AIMs, suggesting that α7 receptors exert an inhibitory influence on L-dopa-induced AIMs. In conclusion, α6β2*, α4β2* and α7 nAChRs all modulate L-dopa-induced AIMs, although their mode of regulation varies. Thus drugs targeting one or multiple nAChRs may be optimal for reducing L-dopa-induced dyskinesias in Parkinson's disease.
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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.