Crucial Role of CB2Cannabinoid Receptor in the Regulation of Central Immune Responses during Neuropathic Pain
Open accessAbstract
Neuropathic pain is a clinical manifestation of nerve injury difficult to treat even with potent analgesic compounds. Here, we used different lines of genetically modified mice to clarify the role played by CB 2 cannabinoid receptors in the regulation of the central immune responses leading to the development of neuropathic pain. CB 2 knock-out mice and wild-type littermates were exposed to sciatic nerve injury, and both genotypes developed a similar hyperalgesia and allodynia in the ipsilateral paw. Most strikingly, knock-outs also developed a contralateral mirror image pain, associated with an enhanced microglial and astrocytic expression in the contralateral spinal horn. In agreement, hyperalgesia, allodynia, and microglial and astrocytic activation induced by sciatic nerve injury were attenuated in transgenic mice overexpressing CB 2 receptors. These results demonstrate the crucial role of CB 2 cannabinoid receptor in modulating glial activation in response to nerve injury. The enhanced manifestations of neuropathic pain were replicated in irradiated wild-type mice reconstituted with bone marrow cells from CB 2 knock-outs, thus demonstrating the implication of the CB 2 receptor expressed in hematopoietic cells in the development of neuropathic pain at the spinal cord.
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Ectopic genetic overexpression of CB2R in mice may mitigate behavioral reactions to chronic stress.
“ectopic genetic overexpression CB2R in mice (Racz et al., 2008) may mitigate behavioral reactions to chronic stress (Garcia-Gutierrez et al., 2010).”
From The endocannabinoid system as a target for novel anxiolytic drugs (2017) · cites this paper as Racz et al., 2008
A bilateral augmented allodynic response occurs in CB2-/- mice subjected to sciatic nerve injury.
“This bilateral augmented allodynic response has also been reported to occur in CB 2 ( -/ -) mice subjected to sciatic nerve injury, indicating the mirrored response is not MIA model specific (Racz et al, 2008).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Racz et al, 2008
The mirrored bilateral allodynic response in CB2-/- mice is not specific to the MIA model.
“indicating the mirrored response is not MIA model specific (Racz et al, 2008).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Racz et al, 2008
CB2-/- mice show exacerbated pain behavior, while CB2 overexpression in the CNS attenuates neuropathic pain.
“CB 2 ( -/ -) mice show exacerbated pain behavior, while CB 2 overexpression in the CNS attenuates neuropathic pain (Racz et al, 2008).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Racz et al, 2008
Overexpression of the CB2 receptor attenuated enhanced expression of microglia.
“Further support for this hypothesis is derived from the observation that overexpression of the CB2 receptor attenuated enhanced expression of microglia.63”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [63]
CB2-/- mice exhibit increased microglial and astrocyte expression in the contralateral spinal dorsal horn.
“However, CB2-/- mice notably exhibit increased microglial and astrocyte expression in the contralateral spinal dorsal horn – a mechanism which may help to explain differences in neuropathic nociception between wild-types and knockouts.63”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [63]
CB2-/- mice develop thermal hyperalgesia and mechanical allodynia in the contralateral paw following surgery, whereas CB2+/+ mice do not.
“CB2-/- mice reportedly develop thermal hyperalgesia and mechanical allodynia in the contralateral paw following surgery, whereas CB2+/+ do not.63”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [63]
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- Authors
- Racz, I., Nadal, X., Alferink, J., Baños, J. E., Rehnelt, J., Martín, M., Pintado, B., Gutierrez-Adan, A., Sanguino, E., Manzanares, J., Zimmer, A., & Maldonado, R.
- Affiliations
- Universitat Pompeu Fabra (ES)
- University of Bonn (DE)
- Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (ES)
- Consejo Superior de Investigaciones Científicas (ES)
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-11-12
- Volume
- 28
- Issue
- 46
- Pages
- 12125-12135
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3844839
- OpenAlex
- W2128022755
- Cited by
- 195
- References
- 52
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 7 · 2023: 15 · 2022: 5 · 2021: 7 · 2020: 12 · 2019: 10 · 2018: 8 · 2017: 11 · 2016: 8 · 2015: 11 · 2014: 18 · 2013: 14 · 2012: 17
- FWCI
- 8.12
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Repositori digital de la UPF (Universitat Pompeu Fabra) (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-sa)
- RECERCAT (Consorci de Serveis Universitaris de Catalunya) (submittedVersion, other-oa)
- Funders
- European Commission
- Deutsche Forschungsgemeinschaft (SFB 645, FOR926)
- Generalitat de Catalunya
- National Institute on Drug Abuse (1R01-DA01 6768-0111, R01DA016768)
- Topics
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
- Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
- Keywords
- CB2 receptor, neuropathic pain, sciatic nerve injury, microglial activation, astrocyte activation, hyperalgesia, allodynia, hematopoietic cells, bone marrow transplantation, spinal cord, glial activation
- MeSH terms
- Animals, Astrocytes, Disease Models, Animal, Female, Gliosis, Hematopoietic Stem Cells, Hyperalgesia, Male, Neuralgia, Peripheral Nervous System Diseases, Spinal Cord, Bone Marrow Transplantation, Microglia, Mice, Knockout, Sciatic Neuropathy, Posterior Horn Cells, Receptor, Cannabinoid, CB2, Mice
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