ArticleJournal of neurochemistry2009
Inactivation of neuronal forebrain A receptors protects dopaminergic neurons in a mouse model of Parkinson's disease.
Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 64 citations in OpenAlex.
- SCH58261 effectively prevents the reduction in excitability of striatal MSNs in mice following 20 h of sleep deprivation.Purinergic signalling · 2025Article
- Adenosine AInternational journal of molecular sciences · 2024Article
- The Pharmacological Potential of Adenosine AMolecules (Basel, Switzerland) · 2022Review
- Neuroprotective Effects of Coffee Bioactive Compounds: A Review.International journal of molecular sciences · 2020Review
- Pathological overproduction: the bad side of adenosine.British journal of pharmacology · 2017Review
- Prokineticin-2 upregulation during neuronal injury mediates a compensatory protective response against dopaminergic neuronal degeneration.Nature communications · 2016Article
- Neuroprotection by caffeine in the MPTP model of parkinson's disease and its dependence on adenosine A2A receptors.Neuroscience · 2016Article
- Article
- Adenosine A2A receptor antagonism reverses inflammation-induced impairment of microglial process extension in a model of Parkinson's disease.Neurobiology of disease · 2014Article
- The angiotensin converting enzyme inhibitor captopril protects nigrostriatal dopamine neurons in animal models of parkinsonism.Experimental neurology · 2013Article
- Delayed caffeine treatment prevents nigral dopamine neuron loss in a progressive rat model of Parkinson's disease.Experimental neurology · 2012Article
- Adenosine A2A receptor gene disruption protects in an α-synuclein model of Parkinson's disease.Annals of neurology · 2012Article
- Past, present and future of A(2A) adenosine receptor antagonists in the therapy of Parkinson's disease.Pharmacology & therapeutics · 2011Review
- Deletion of adenosine A₁ or A(₂A) receptors reduces L-3,4-dihydroxyphenylalanine-induced dyskinesia in a model of Parkinson's disease.Brain research · 2011Article
- Heteromerization of G protein-coupled receptors: relevance to neurological disorders and neurotherapeutics.CNS & neurological disorders drug targets · 2010Review
- Caffeine attenuates lipopolysaccharide-induced neuroinflammation.Neuroscience letters · 2010Article
- Caffeine protects against combined paraquat and maneb-induced dopaminergic neuron degeneration.Experimental neurology · 2010Article
- Adenosine-dopamine interactions in the pathophysiology and treatment of CNS disorders.CNS neuroscience & therapeutics · 2010Review
- Neuroprotection by caffeine: time course and role of its metabolites in the MPTP model of Parkinson's disease.Neuroscience · 2010Article
- Pathophysiological roles for purines: adenosine, caffeine and urate.Progress in brain research · 2010Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Adenosine A(2A) receptors antagonists produce neuroprotective effects in animal models of Parkinson's disease (PD). As neuroinflammation is involved in PD pathogenesis, both neuronal and glial A(2A) receptors might participate to neuroprotection. We employed complementary pharmacologic and genetic approaches to A(2A) receptor inactivation, in a multiple MPTP mouse model of PD, to investigate the cellular basis of neuroprotection by A(2A) antagonism. MPTP.HCl (20 mg/kg daily for 4 days) was administered in mice treated with the A(2A) antagonist SCH58261, or in conditional knockout mice lacking A(2A) receptors on forebrain neurons (fbnA(2A)KO mice). MPTP-induced partial loss of dopamine neurons in substantia nigra pars compacta (SNc) and striatum (Str), associated with increased astroglial and microglial immunoreactivity in these areas. Astroglia was similarly activated 1, 3, and 7 days after MPTP administration, whereas maximal microglial reactivity was detected on day 1, returning to baseline 7 days after MPTP administration. SCH58261 attenuated dopamine cell loss and gliosis in SNc and Str. Selective depletion of A(2A) receptors in fbnA(2A)KO mice completely prevented MPTP-induced dopamine neuron degeneration and gliosis in SNc, and partially counteracted gliosis in Str. Results provide evidence of a primary role played by neuronal A(2A) receptors in neuroprotective effects of A(2A) antagonists in a multiple MPTP injections model of PD. With the symptomatic antiparkinsonian potential of several A(2A) receptor antagonists being pursued in clinical trials, this study adds to the rationale for broader clinical benefit and use of these drugs early in the treatment of PD.
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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.