ArticleThe European journal of neuroscience2010
Cannabinoid CB1 receptor facilitation of substance P release in the rat spinal cord, measured as neurokinin 1 receptor internalization.
Article in The European journal of neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
- Delta-9-tetrahydrocannabinol and Cannabidiol for Pain: Preclinical and Clinical Models.Current topics in behavioral neurosciences · 2026Review
- Dual Role of the Spinal Endocannabinoid System in Response to Noxious Stimuli: Antinociceptive Pathways and Neuropathic Pain Mechanisms.International journal of molecular sciences · 2025Review
- Acetaminophen inhibits diacylglycerol lipase synthesis of 2-arachidonoyl glycerol: Implications for nociception.Cell reports. Medicine · 2025Article
- Endocannabinoid signaling in stress, nausea, and vomiting.Neurogastroenterology and motility · 2025Review
- Treatment of Migraine With Phytocannabinoids, the Involvement of Endocannabinoids in Migraine, and Potential Mechanisms of Action.Pain research & management · 2025Review
- Cannabinoid Therapeutics in Chronic Neuropathic Pain: From Animal Research to Human Treatment.Frontiers in physiology · 2021Review
- Cannabinoid 1 receptor knockout mice display cold allodynia, but enhanced recovery from spared-nerve injury-induced mechanical hypersensitivity.Molecular pain · 2016Article
- Stress and pain response after oligofructose induced-lameness in dairy heifers.Journal of veterinary science · 2015Article
- μ-Opioid receptor inhibition of substance P release from primary afferents disappears in neuropathic pain but not inflammatory pain.Neuroscience · 2014Article
- Inflammation enhances Y1 receptor signaling, neuropeptide Y-mediated inhibition of hyperalgesia, and substance P release from primary afferent neurons.Neuroscience · 2014Article
- Cannabinoids suppress inflammatory and neuropathic pain by targeting α3 glycine receptors.The Journal of experimental medicine · 2012Article
- The interaction between intrathecal administration of low doses of palmitoylethanolamide and AM251 in formalin-induced pain related behavior and spinal cord IL1-β expression in rats.Neurochemical research · 2012Article
- CB1 receptors mediate rimonabant-induced pruritic responses in mice: investigation of locus of action.Psychopharmacology · 2011Article
- Cannabinoid potentiation of glycine receptors contributes to cannabis-induced analgesia.Nature chemical biology · 2011Article
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4 authors at 2 institutions in 2 countries.
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Abstract
The contribution of CB1 receptors in the spinal cord to cannabinoid analgesia is still unclear. The objective of this study was to investigate the effect of CB1 receptors on substance P release from primary afferent terminals in the spinal cord. Substance P release was measured as neurokinin 1 (NK1) receptor internalization in lamina I neurons. It was induced in spinal cord slices by dorsal root stimulation and in live rats by a noxious stimulus. In spinal cord slices, the CB1 receptor antagonists AM251, AM281 and rimonabant partially but potently inhibited NK1 receptor internalization induced by electrical stimulation of the dorsal root. This was due to an inhibition of substance P release and not of NK1 receptor internalization itself, because AM251 and AM281 did not inhibit NK1 receptor internalization induced by exogenous substance P. The CB1 receptor agonist ACEA increased NK1 receptor internalization evoked by dorsal root stimulation. The effects of AM251 and ACEA cancelled each other. In vivo, AM251 injected intrathecally decreased NK1 receptor internalization in spinal segments L5 and L6 induced by noxious hind paw clamp. Intrathecal AM251 also produced analgesia to radiant heat stimulation of the paw. The inhibition by AM251 of NK1 receptor internalization was reversed by antagonists of mu-opioid and GABA(B) receptors. This indicates that CB1 receptors facilitate substance P release by inhibiting the release of GABA and opioids next to primary afferent terminals, producing disinhibition. This results in a pronociceptive effect of CB1 receptors in the spinal cord.
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