ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
The adenosine A1 receptor agonist adenosine amine congener exerts a neuroprotective effect against the development of striatal lesions and motor impairments in the 3-nitropropionic acid model of neurotoxicity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 70 citations in OpenAlex.
- Neuroprotective effects of candesartan in 3-nitropropionic acid-induced Huntington's disease: modulation of angiotensin and CREB/BDNF/PGC1-α signaling.Inflammopharmacology · 2025Article
- Article
- Metabolic Aspects of Adenosine Functions in the Brain.Frontiers in pharmacology · 2021Review
- Adenosine: a partially discovered medicinal agent.Future journal of pharmaceutical sciences · 2021Review
- Purinergic Signaling in the Pathophysiology and Treatment of Huntington's Disease.Frontiers in neuroscience · 2021Review
- Purinergic Receptors in Basal Ganglia Diseases: Shared Molecular Mechanisms between Huntington's and Parkinson's Disease.Neuroscience bulletin · 2020Review
- Adenosine Augmentation Evoked by an ENT1 Inhibitor Improves Memory Impairment and Neuronal Plasticity in the APP/PS1 Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2018Article
- The Role of Adenosine Tone and Adenosine Receptors in Huntington's Disease.Journal of caffeine and adenosine research · 2018Review
- Purinergic Receptors in Neurological Diseases With Motor Symptoms: Targets for Therapy.Frontiers in pharmacology · 2018Review
- L-theanine, a Component of Green Tea Prevents 3-Nitropropionic Acid (3-NP)-Induced Striatal Toxicity by Modulating Nitric Oxide Pathway.Molecular neurobiology · 2017Article
- Pharmacokinetic Properties of Adenosine Amine Congener in Cochlear Perilymph after Systemic Administration.BioMed research international · 2017Article
- Equilibrative nucleoside transporter ENT1 as a biomarker of Huntington disease.Neurobiology of disease · 2016Article
- Protective Effect of Spermidine Against Excitotoxic Neuronal Death Induced by Quinolinic Acid in Rats: Possible Neurotransmitters and Neuroinflammatory Mechanism.Neurotoxicity research · 2015Article
- Adenosine amine congener as a cochlear rescue agent.BioMed research international · 2014Article
- Article
- Adenosine amine congener mitigates noise-induced cochlear injury.Purinergic signalling · 2010Article
- Adenosine, ketogenic diet and epilepsy: the emerging therapeutic relationship between metabolism and brain activity.Current neuropharmacology · 2009Article
- Co-localization and functional cross-talk between A1 and P2Y1 purine receptors in rat hippocampus.The European journal of neuroscience · 2007Article
- The corticostriatal pathway in Huntington's disease.Progress in neurobiology · 2007Review
- Neuroprotection by adenosine in the brain: From A(1) receptor activation to A (2A) receptor blockade.Purinergic signalling · 2005Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease is a genetic neurodegenerative disorder characterized clinically by both motor and cognitive impairments and striatal lesions. At present, there are no pharmacological treatments able to prevent or slow its development. In the present study, we report the neuroprotective effect of adenosine amine congener (ADAC), a specific A1 receptor agonist known to be devoid of any of the side effects that usually impair the clinical use of such compounds. Remarkably, in a rat model of Huntington's disease generated by subcutaneous infusion of the mitochondrial inhibitor 3-nitropropionic acid (3NP), we have observed that an acute treatment with ADAC (100 microg x kg(-1) x d(-1)) not only strongly reduces the size of the striatal lesion (-40%) and the remaining ongoing striatal degeneration (-30%), but also prevents the development of severe dystonia of hindlimbs. Electrophysiological recording on corticostriatal brain slices demonstrated that ADAC strongly decreases the field EPSP amplitude by 70%, whereas it has no protective effect up to 1 microm against the 3NP-induced neuronal death in primary striatal cultures. This suggests that ADAC protective effects may be mediated presynaptically by the modulation of the energetic impairment-induced striatal excitotoxicity. Altogether, our results indicate that A1 receptor agonists deserve further experimental evaluation in animal models of Huntington's disease.
Indexed as
Identifiers
12388620PMC6757706W1653077694What OpenQuestion holds
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.