ArticleBritish journal of pharmacology2010
Neuroprotective potential of CB1 receptor agonists in an in vitro model of Huntington's disease.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 66 citations in OpenAlex.
- Canonical Cannabinoid Receptors.Current topics in behavioral neurosciences · 2026Review
- Cannabinoid Receptor 1: The Neural Gatekeeper of Health and Disease.Current neurovascular research · 2025Review
- Cannabinoids' Role in Modulating Central and Peripheral Immunity in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Neuroprotection of retinal ganglion cellsNeuronal signaling · 2022Article
- Evaluation of the profiles of CBBritish journal of pharmacology · 2020Article
- Differential activation of G protein-mediated signaling by synthetic cannabinoid receptor agonists.Pharmacology research & perspectives · 2020Article
- Cannabinoid CB1 receptor agonist ACEA alleviates brain ischemia/reperfusion injury via CB1-Drp1 pathway.Cell death discovery · 2020Article
- Druggable targets of the endocannabinoid system: Implications for the treatment of HIV-associated neurocognitive disorder.Brain research · 2019Review
- Intracerebroventricular Administration of L-arginine Improves Spatial Memory Acquisition in Triple Transgenic Mice Via Reduction of Oxidative Stress and Apoptosis.Translational neuroscience · 2018Article
- GαBritish journal of pharmacology · 2017Article
- Protective Effect of Quercetin against Oxidative Stress-Induced Cytotoxicity in Rat Pheochromocytoma (PC-12) Cells.Molecules (Basel, Switzerland) · 2017Article
- RTP801 Is Involved in Mutant Huntingtin-Induced Cell Death.Molecular neurobiology · 2016Article
- CB2 and GPR55 Receptors as Therapeutic Targets for Systemic Immune Dysregulation.Frontiers in pharmacology · 2016Review
- Application of xCELLigence RTCA Biosensor Technology for Revealing the Profile and Window of Drug Responsiveness in Real Time.Biosensors · 2015Article
- Promising cannabinoid-based therapies for Parkinson's disease: motor symptoms to neuroprotection.Molecular neurodegeneration · 2015Review
- The therapeutic potential of cannabinoids for movement disorders.Movement disorders : official journal of the Movement Disorder Society · 2015Review
- Cannabinoids: new promising agents in the treatment of neurological diseases.Molecules (Basel, Switzerland) · 2014Review
- Functionally Optimized Neuritogenic Farinosone C Analogs: SAR-Study and Investigations on Their Mode of Action.ACS medicinal chemistry letters · 2014Article
- Real-time characterization of cannabinoid receptor 1 (CB1 ) allosteric modulators reveals novel mechanism of action.British journal of pharmacology · 2013Article
- MAP kinase phosphatase 1 (MKP-1/DUSP1) is neuroprotective in Huntington's disease via additive effects of JNK and p38 inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe therapeutic potential of cannabinoids in Huntington's disease (HD) has been investigated by several groups with complex and sometimes contrasting results. We sought to examine key points of intersection between cannabinoid receptor 1 (CB(1)) signalling, survival and the formation of mutant huntingtin aggregates in HD. EXPERIMENTAL APPROACH: Using a simplified pheochromocytoma (PC12) cell model of HD expressing exon 1 of wild-type or mutant huntingtin, we assayed cell death and aggregate formation using high-throughput cytotoxicity and image-based assays respectively. KEY
resultsCB(1) activation by HU210 conferred a small but significant level of protection against mutant huntingtin-induced cell death. Pertussis toxin uncoupled HU210 from the inhibition of cAMP, preventing rescue of cell death. Phosphorylation of extracellular signal-regulated kinase (ERK) was also critical to CB(1)-mediated rescue. Conversely, treatments that elevated cAMP exacerbated mutant huntingtin-induced cell death. Despite opposing effects on HD cell survival, both HU210 and compounds that elevated cAMP increased the formation of mutant huntingtin aggregates. The increase in aggregation by HU210 was insensitive to Pertussis toxin and UO126, suggesting a G-protein alpha subtype s (G(s))-linked mechanism. CONCLUSIONS AND IMPLICATIONS: We suggest that the CB(1) receptor, through G-protein alpha subtype i/o (G(i/o))-linked, ERK-dependent signal transduction, is a therapeutic target in HD. However the protective potential of CB(1) may be limited by promiscuous coupling to G(s), the stimulation of cAMP formation and increased aggregate formation. This may underpin the poor therapeutic efficacy of cannabinoids in more complex model systems and suggest that therapies that are selective for the G(i/o), ERK pathway may be of most benefit in HD.
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Registered trials
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