Cannabinoids mediate analgesia largely via peripheral type 1 cannabinoid receptors in nociceptors
Open accessAbstract
Although endocannabinoids constitute one of the first lines of defense against pain, the anatomical locus and the precise receptor mechanisms underlying cannabinergic modulation of pain are uncertain. Clinical exploitation of the system is severely hindered by the cognitive deficits, memory impairment, motor disturbances and psychotropic effects resulting from the central actions of cannabinoids. We deleted the type 1 cannabinoid receptor (CB1) specifically in nociceptive neurons localized in the peripheral nervous system of mice, preserving its expression in the CNS, and analyzed these genetically modified mice in preclinical models of inflammatory and neuropathic pain. The nociceptor-specific loss of CB1 substantially reduced the analgesia produced by local and systemic, but not intrathecal, delivery of cannabinoids. We conclude that the contribution of CB1-type receptors expressed on the peripheral terminals of nociceptors to cannabinoid-induced analgesia is paramount, which should enable the development of peripherally acting CB1 analgesic agonists without any central side effects.
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Selective CB1 receptor deletion in peripheral nociceptors leads to enhanced pain behavior as well as diminished antinociceptive effects of cannabinoid receptor agonists.
“Strikingly, selective CB 1 receptor deletion in peripheral nociceptors leads to enhanced pain behavior as well as diminished antinociceptive effects of cannabinoid receptor agonists, suggesting an important role of peripheral CB 1 receptors in neuropathic pain (Agarwal et al, 2007).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Agarwal et al, 2007
Peripheral CB1 receptors play an important role in neuropathic pain.
“suggesting an important role of peripheral CB 1 receptors in neuropathic pain (Agarwal et al, 2007).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Agarwal et al, 2007
CB1 receptors on nociceptors in the periphery account for much of the antinociceptive effects of cannabinoids.
“Thus, CB1 receptors on nociceptors in the periphery account for much of the antinociceptive effects of cannabinoids.7”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [7]
SNS-CB1- mice showed exaggerated sensitivity to noxious levels of mechanical stimulation and a cold plate relative to their wild-type counterparts, whereas differential sensitivity was not observed between genotypes with non-noxious levels of mechanical stimulation and noxious levels of thermal stimulation.
“SNS-CB1- mice showed exaggerated sensitivity to noxious levels of mechanical stimulation and a cold plate relative to their wild-type counterparts, whereas differential sensitivity was not observed between genotypes with non-noxious levels of mechanical stimulation and noxious levels of thermal stimulation.7”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [7]
Acute WIN55,212-2 suppressed thermal hyperalgesia and mechanical allodynia in both SNS-CB1- mice and their wild-type controls; differences in antinociceptive effects were observed between genotypes, and these effects were greater with mechanical than thermal sensitivity.
“Acute WIN55,212-2 suppressed thermal hyperalgesia and mechanical allodynia in both mice lacking CB1 receptors in primary nociceptors (SNS-CB1-) and their wild-type controls; however differences in the antinociceptive effects of WIN55,212-2 were observed between genotypes, and these effects were greater with mechanical than thermal sensitivity.”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [7]
Comparable responses to WIN55,212-2 were only observed at doses high enough to induce sedation and rigidity in all mice.
“Comparable responses to WIN55,212-2 were only observed at doses high enough to induce sedation and rigidity in all mice.”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [7]
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- Authors
- Agarwal, N., Pacher, P., Tegeder, I., Amaya, F., Constantin, C. E., Brenner, G. J., Rubino, T., Michalski, C. W., Marsicano, G., Monory, K., Mackie, K., Marian, C., Batkai, S., Parolaro, D., Fischer, M. J., Reeh, P., Kunos, G., Kress, M., Lutz, B., Woolf, C. J., & Kuner, R.
- Affiliations
- Heidelberg University (DE)
- Goethe University Frankfurt (DE)
- Harvard University (US)
- Innsbruck Medical University (AT)
- University of Insubria (IT)
- Johannes Gutenberg University Mainz (DE)
- University of Washington (US)
- Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
- National Institutes of Health (US)
- Corresponding author
- Kuner, Rohini
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2007-06-10
- Volume
- 10
- Issue
- 7
- Pages
- 870-879
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC2234438
- OpenAlex
- W1991319303
- Cited by
- 571
- References
- 47
- Citations by year
- 2026: 16 · 2025: 11 · 2024: 20 · 2023: 21 · 2022: 25 · 2021: 18 · 2020: 25 · 2019: 29 · 2018: 31 · 2017: 23 · 2016: 21 · 2015: 22 · 2014: 32 · 2013: 48 · 2012: 51
- FWCI
- 33.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- IrInSubria (University of Insubria) (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Austrian Science Fund
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (Z01AA000375)
- National Institute on Drug Abuse (DA00286, DA11322, R01DA011322, K02DA000286)
- National Institute of Neurological Disorders and Stroke (NS 038253, R01NS038253, R37NS039518, NS-039518, R01NS039518)
- Topics
- Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Keywords
- cannabinoids, CB1 receptor, nociceptors, peripheral analgesia, endocannabinoids, inflammatory pain, neuropathic pain
- MeSH terms
- Alleles, Analgesia, Animals, Cannabinoids, Central Nervous System, Electrophysiology, Ganglia, Spinal, Mice, Inbred C57BL, Neurons, Afferent, Nociceptors, Peripheral Nervous System Diseases, DNA Primers, Peripheral Nervous System, Mice, Knockout, Nerve Fibers, Unmyelinated, Receptor, Cannabinoid, CB1, Mice, Cannabinoid Receptor Modulators
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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