Cannabinoid CB2receptor agonists protect the striatum against malonate toxicity: Relevance for Huntington's disease
Open accessAbstract
Cannabinoid agonists might serve as neuroprotective agents in neurodegenerative disorders. Here, we examined this hypothesis in a rat model of Huntington's disease (HD) generated by intrastriatal injection of the mitochondrial complex II inhibitor malonate. Our results showed that only compounds able to activate CB 2 receptors were capable of protecting striatal projection neurons from malonate‐induced death. That CB 2 receptor agonists are neuroprotective was confirmed by using the selective CB 2 receptor antagonist, SR144528, and by the observation that mice deficient in CB 2 receptor were more sensitive to malonate than wild‐type animals. CB 2 receptors are scarce in the striatum in healthy conditions, but they are markedly upregulated after the lesion with malonate. Studies of double immunostaining revealed a significant presence of CB 2 receptors in cells labeled with the marker of reactive microglia OX‐42, and also in cells labeled with GFAP (a marker of astrocytes). We further showed that the activation of CB 2 receptors significantly reduced the levels of tumor necrosis factor‐α (TNF‐α) that had been increased by the lesion with malonate. In summary, our results demonstrate that stimulation of CB 2 receptors protect the striatum against malonate toxicity, likely through a mechanism involving glial cells, in particular reactive microglial cells in which CB 2 receptors would be upregulated in response to the lesion. Activation of these receptors would reduce the generation of proinflammatory molecules like TNF‐α. Altogether, our results support the hypothesis that CB 2 receptors could constitute a therapeutic target to slowdown neurodegeneration in HD. © 2008 Wiley‐Liss, Inc.
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The selective CB2 receptor agonist SR144528 could protect the striatum against mitochondrial toxin malonate toxicity via effects on glial cells, especially reactive microglia.
“The selective CB2 receptor agonist, SR144528, could protect the striatum against mitochondrial toxin malonate toxicity via their effects on glial cells, especially reactive microglia.521”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [521]
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- Authors
- Sagredo, O., González, S., Aroyo, I., Pazos, M. R., Benito, C., Lastres‐Becker, I., Romero, J. P., Tolón, R. M., Mechoulam, R., Brouillet, E., Romero, J., & Fernández‐Ruiz, J.
- Affiliations
- Universidad Complutense de Madrid (ES)
- Biomedical Research Networking Center on Neurodegenerative Diseases (ES)
- Hebrew University of Jerusalem (IL)
- Centre National de la Recherche Scientifique (FR)
- ORCID
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2008-12-29
- Volume
- 57
- Issue
- 11
- Pages
- 1154-1167
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC2706932
- OpenAlex
- W2044784707
- Cited by
- 201
- References
- 68
- Citations by year
- 2026: 3 · 2025: 11 · 2024: 12 · 2023: 9 · 2022: 12 · 2021: 16 · 2020: 12 · 2019: 10 · 2018: 9 · 2017: 21 · 2016: 13 · 2015: 15 · 2014: 12 · 2013: 11 · 2012: 8
- FWCI
- 6.07
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Sanofi
- National Institute on Drug Abuse (P01DA009789)
- Topics
- Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Keywords
- CB2 receptor agonist, Huntington's disease, striatum, neuroprotection, mitochondrial complex II inhibition, reactive microglia, astrocytes, TNF-α, neuroinflammation, SR144528, neurodegeneration
- MeSH terms
- Animals, Arachidonic Acids, Camphanes, Cannabinoids, Central Nervous System Agents, Corpus Striatum, Disease Models, Animal, Huntington Disease, Male, Malonates, Neuroglia, Neurons, Pyrazoles, Tumor Necrosis Factor-alpha, Cell Death, Rats, Sprague-Dawley, Mice, Knockout, Neuroprotective Agents, Receptor, Cannabinoid, CB2, Mice, Rats
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