ArticleBrain research2011
Deletion of adenosine A₁ or A(₂A) receptors reduces L-3,4-dihydroxyphenylalanine-induced dyskinesia in a model of Parkinson's disease.
Article in Brain research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 47 citations in OpenAlex.
- Caffeine consumption and risk of dyskinesia in CALM-PD.Movement disorders : official journal of the Movement Disorder Society · 2013Trial
- Role of P11 through serotonergic and glutamatergic pathways in LID.Molecular biology reports · 2023Review
- Levodopa-Induced Dyskinesia in Parkinson's Disease: Pathogenesis and Emerging Treatment Strategies.Cells · 2022Review
- Caenorhabditis elegans provides an efficient drug screening platform for GNAO1-related disorders and highlights the potential role of caffeine in controlling dyskinesia.Human molecular genetics · 2022Article
- Molecular Mechanisms and Therapeutic Strategies for Levodopa-Induced Dyskinesia in Parkinson's Disease: A Perspective Through Preclinical and Clinical Evidence.Frontiers in pharmacology · 2022Review
- Current and Emerging MR Methods and Outcome in Rodent Models of Parkinson's Disease: A Review.Frontiers in neuroscience · 2021Review
- Caffeine: An Overview of Its Beneficial Effects in Experimental Models and Clinical Trials of Parkinson's Disease.International journal of molecular sciences · 2020Review
- The belated US FDA approval of the adenosine APurinergic signalling · 2020Review
- Caffeine Protects Dopaminergic Neurons From Dopamine-Induced Neurodegeneration via Synergistic Adenosine-Dopamine D2-Like Receptor Interactions in TransgenicFrontiers in neuroscience · 2018Article
- CK2 Oppositely Modulates l-DOPA-Induced Dyskinesia via Striatal Projection Neurons Expressing D1 or D2 Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Label-Free Neuroproteomics of the Hippocampal-Accumbal Circuit Reveals Deficits in Neurotransmitter and Neuropeptide Signaling in Mice Lacking Ethanol-Sensitive Adenosine Transporter.Journal of proteome research · 2017Article
- A Meta-Analysis of Adenosine A2A Receptor Antagonists on Levodopa-Induced DyskinesiaFrontiers in neurology · 2017Article
- Role of purinergic P2X4 receptors in regulating striatal dopamine homeostasis and dependent behaviors.Journal of neurochemistry · 2016Article
- Overexpression of GRK6 rescues L-DOPA-induced signaling abnormalities in the dopamine-depleted striatum of hemiparkinsonian rats.Experimental neurology · 2015Article
- Coffee, Genetic Variants, and Parkinson's Disease: Gene-Environment Interactions.Journal of caffeine research · 2015Review
- Caffeine: cognitive and physical performance enhancer or psychoactive drug?Current neuropharmacology · 2015Review
- Review
- Using caffeine and other adenosine receptor antagonists and agonists as therapeutic tools against neurodegenerative diseases: a review.Life sciences · 2014Review
- The emerging role of nutrition in Parkinson's disease.Frontiers in aging neuroscience · 2014Review
- Drug-induced dyskinesia in Parkinson's disease. Should success in clinical management be a function of improvement of motor repertoire rather than amplitude of dyskinesia?BMC medicine · 2013Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Adenosine A(₂A) receptor antagonism provides a promising approach to developing nondopaminergic therapy for Parkinson's disease (PD). Clinical trials of A(₂A) antagonists have targeted PD patients with L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in an effort to improve parkinsonian symptoms. The role of adenosine in the development of LID is little known, especially regarding its actions via A₁ receptors. We aimed to examine the effects of genetic deletion and pharmacological blockade of A₁ and/or A(₂A) receptors on the development of LID, on the induction of molecular markers of LID including striatal preprodynorphin and preproenkephalin (PPE), and on the integrity of dopaminergic nigrostriatal neurons in hemiparkinsonian mice. Following a unilateral 6-hydroxydopamine lesion A₁, A(₂A) and double A₁-A(₂A) knockout (KO) and wild-type littermate mice, and mice pretreated with caffeine (an antagonist of both A₁ and A(₂A) receptors) or saline were treated daily for 18-21 days with a low dose of L-DOPA. Total abnormal involuntary movements (AIMs, a measure of LID) were significantly attenuated (p<0.05) in A₁ and A(₂A) KOs, but not in A₁-A(₂A) KOs and caffeine-pretreated mice. An elevation of PPE mRNA ipsilateral to the lesion in WT mice was reduced in all KO mice. In addition, neuronal integrity assessed by striatal dopamine content was similar in all KOs and caffeine-pretreated mice following 6-hydroxydopamine lesioning. Our findings raise the possibility that A₁ or A(₂A) receptors blockade might also confer a disease-modifying benefit of reduced risk of disabling LID, whereas the effect of their combined inactivation is less clear.
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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.