ArticleFrontiers in pharmacology2017
Antiparkinsonian Efficacy of Guanosine in Rodent Models of Movement Disorder.
Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Signaling Mechanisms Underlying the Glioprotective Effects of Guanosine Against Glucose Deprivation-Induced Glial Dysfunction.Neurochemical research · 2025Article
- Lessons from the physiological role of guanosine in neurodegeneration and cancer: Toward a multimodal mechanism of action?Purinergic signalling · 2025Review
- Neuroprotective Effects of Guanosine in Ischemic Stroke-Small Steps towards Effective Therapy.International journal of molecular sciences · 2021Review
- Adenosine APurinergic signalling · 2021Article
- Guanosine Mechanisms of Action: Toward Molecular Targets.Frontiers in pharmacology · 2021Article
- Guanosine Neuroprotection of Presynaptic Mitochondrial Calcium Homeostasis in a Mouse Study with Amyloid-β Oligomers.Molecular neurobiology · 2020Article
- Involvement of adenosine APurinergic signalling · 2020Article
- Striatal Dopamine DFrontiers in pharmacology · 2020Article
- Guanosine Protects Striatal Slices Against 6-OHDA-Induced Oxidative Damage, Mitochondrial Dysfunction, and ATP Depletion.Neurotoxicity research · 2019Article
- Neuromodulatory Effects of Guanine-Based Purines in Health and Disease.Frontiers in cellular neuroscience · 2018Review
- Novel Targets for Fast Antidepressant Responses: Possible Role of Endogenous Neuromodulators.Chronic stress (Thousand Oaks, Calif.)Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Guanosine (GUO) is a guanine-based purine nucleoside with important trophic functions and promising neuroprotective properties. Although the neuroprotective effects of GUO have been corroborated in cellular models of Parkinson's disease (PD), its efficacy as an antiparkinsonian agent has not been fully explored in PD animal models. Accordingly, we evaluated the effectiveness of GUO in reversing motor impairments in several rodent movement disorder models, including catalepsy, tremor, and hemiparkinsonism. Our results showed that orally administered GUO antagonized reserpine-mediated catalepsy, reduced reserpine-induced tremulous jaw movements, and potentiated the number of contralateral rotations induced by L-3,4-dihydroxyphenylalanine in unilaterally 6-hydroxidopamine-lesioned rats. In addition, at 5 and 7.5 mg/kg, GUO inhibited L-DOPA-induced dyskinesia in rats chronically treated with a pro-dopaminergic agent. Overall, we describe the therapeutic potential of GUO, which may be effective not only for reversing parkinsonian motor impairments but also for reducing dyskinesia induced by treatment for PD.
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