ArticleThe European journal of neuroscience2012
Anti-dyskinetic mechanisms of amantadine and dextromethorphan in the 6-OHDA rat model of Parkinson's disease: role of NMDA vs. 5-HT1A receptors.
Article in The European journal of neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 45 citations in OpenAlex.
- Effects of genetic knockdown of the serotonin transporter on established L-DOPA-induced dyskinesia and gene expression in hemiparkinsonian rats.Neuropharmacology · 2025Article
- Prediction of dyskinesia in Parkinson's disease patients using machine learning algorithms.Scientific reports · 2023Article
- Possible involvement of NO-cGMP signaling in the antidepressant like Effect of Amantadine in mice.Metabolic brain disease · 2022Article
- Serotonergic system modulation holds promise for L-DOPA-induced dyskinesias in hemiparkinsonian rats: A systematic review.EXCLI journal · 2020Review
- Hinokitiol Offers Neuroprotection Against 6-OHDA-Induced Toxicity in SH-SY5Y Neuroblastoma Cells by Downregulating mRNA Expression of MAO/α-Synuclein/LRRK2/PARK7/PINK1/PTEN Genes.Neurotoxicity research · 2019Article
- The combination of the opioid glycopeptide MMP-2200 and a NMDA receptor antagonist reduced l-DOPA-induced dyskinesia and MMP-2200 by itself reduced dopamine receptor 2-like agonist-induced dyskinesia.Neuropharmacology · 2018Article
- Efficacy and safety of amantadine for the treatment of L-DOPA-induced dyskinesia.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Animal models of L-DOPA-induced dyskinesia: the 6-OHDA-lesioned rat and mouse.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Current Experimental Studies of Gene Therapy in Parkinson's Disease.Frontiers in aging neuroscience · 2017Review
- Nondopaminergic treatments for Parkinson's disease: current and future prospects.Neurodegenerative disease management · 2016Review
- Review
- 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
- Ranitidine reduced levodopa-induced dyskinesia in a rat model of Parkinson's disease.Neuropsychiatric disease and treatment · 2014Article
- Treatment of Parkinson's disease: what's in the non-dopaminergic pipeline?Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2014Review
- Metabotropic glutamate receptors for Parkinson's disease therapy.Parkinson's disease · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Amantadine and dextromethorphan suppress levodopa (L-DOPA)-induced dyskinesia (LID) in patients with Parkinson's disease (PD) and abnormal involuntary movements (AIMs) in the unilateral 6-hydroxydopamine (6-OHDA) rat model. These effects have been attributed to N-methyl-d-aspartate (NMDA) antagonism. However, amantadine and dextromethorphan are also thought to block serotonin (5-HT) uptake and cause 5-HT overflow, leading to stimulation of 5-HT(1A) receptors, which has been shown to reduce LID. We undertook a study in 6-OHDA rats to determine whether the anti-dyskinetic effects of these two compounds are mediated by NMDA antagonism and/or 5-HT(1A) agonism. In addition, we assessed the sensorimotor effects of these drugs using the Vibrissae-Stimulated Forelimb Placement and Cylinder tests. Our data show that the AIM-suppressing effect of amantadine was not affected by the 5-HT(1A) antagonist WAY-100635, but was partially reversed by the NMDA agonist d-cycloserine. Conversely, the AIM-suppressing effect of dextromethorphan was prevented by WAY-100635 but not by d-cycloserine. Neither amantadine nor dextromethorphan affected the therapeutic effects of L-DOPA in sensorimotor tests. We conclude that the anti-dyskinetic effect of amantadine is partially dependent on NMDA antagonism, while dextromethorphan suppresses AIMs via indirect 5-HT(1A) agonism. Combined with previous work from our group, our results support the investigation of 5-HT(1A) agonists as pharmacotherapies for LID in PD patients.
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