Inhibitory effect of anandamide on resiniferatoxin-induced sensory neuropeptide release in vivo and neuropathic hyperalgesia in the rat
Abstract
Anandamide (AEA) is an endogenous cannabinoid ligand acting predominantly on the cannabinoid 1 (CB(1)) receptor, but it is also an agonist on the capsaicin VR(1)/TRPV(1) receptor. In the present study we examined the effects of AEA and the naturally occurring cannabinoid 2 (CB(2)) receptor agonist palmitylethanolamide (PEA) on basal and resiniferatoxin (RTX)-induced release of calcitonin gene-related peptide (CGRP) and somatostatin in vivo. Since these sensory neuropeptides play important role in the development of neuropathic hyperalgesia, the effect of AEA and PEA was also examined on mechanonociceptive threshold changes after partial ligation of the sciatic nerve. Neither AEA nor PEA affected basal plasma peptide concentrations, but both of them inhibited RTX-induced release. The inhibitory effect of AEA was prevented by the CB(1) receptor antagonist SR141716A. AEA abolished and PEA significantly decreased neuropathic mechanical hyperalgesia 7 days after unilateral sciatic nerve ligation, which was antagonized by SR141716A and the CB(2) receptor antagonist SR144528, respectively. Both SR141716A and SR144528 increased hyperalgesia, indicating that endogenous cannabinoids acting on CB(1) and peripheral CB(2)-like receptors play substantial role in neuropathic conditions to diminish hyperalgesia. AEA and PEA exert inhibitory effect on mechanonociceptive hyperalgesia and sensory neuropeptide release in vivo suggesting their potential therapeutical use to treat chronic neuropathic pain.
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AEA and PEA exert effects at least in part through a peripheral mechanism, suppressing release of calcitonin gene-related peptide and somatostatin evoked by resiniferotoxin without altering peptide release under basal conditions.
“Anandamide and PEA exerts effects, at least in part, through a peripheral mechanism; both fatty-acid amides suppressed release of calcitonin gene-related peptide and somatostatin evoked by the irritant resiniferotoxin without altering peptide release under basal conditions.65”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [65]
Pro-hyperalgesic effects of SR141716 and SR144528 have been reported in the Seltzer model, indicating a potential alteration in endocannabinoid tone following nerve injury.
“Pro-hyperalgesic effects of SR141716 and SR144528 have been reported in the Seltzer model,65 indicating a potential alteration in endocannabinoid tone following nerve injury.”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [65]
Anti-hyperalgesic effects of AEA and PEA were blocked by a CB1 and CB2 antagonist, respectively.
“Anti-hyperalgesic effects of AEA and PEA were blocked by a CB1 and CB2 antagonist, respectively.65”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [65]
Anandamide produces anti-hyperalgesic and anti-allodynic effects through a CB1 mechanism.
“Interestingly, anandamide produced anti-hyperalgesic and anti-allodynic effects through a CB1 mechanism,65, 66”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [65]
PEA abolished mechanical hyperalgesia following partial sciatic nerve ligation through a mechanism that was blocked by a CB2 antagonist.
“PEA abolished mechanical hyperalgesia following partial sciatic nerve ligation through a mechanism that was blocked by a CB2 antagonist.65”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [65]
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References 32 · Cited by 85
- Authors
- Helyes, Z., Németh, J., Thán, M., Bölcskei, K., Pintér, E., & Szolcsányi, J.
- Affiliations
- University of Pecs (HU)
- Hungarian Academy of Sciences (HU)
- Corresponding author
- Helyes, Zsuzsanna
- Venue
- Life Sciences
- Publisher
- Elsevier BV
- Published
- 2003-09
- Volume
- 73
- Issue
- 18
- Pages
- 2345-2353
- ISSN
- 0024-3205 (ISSN-L)
- OpenAlex
- W2046872480
- Cited by
- 85
- References
- 32
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 1 · 2022: 4 · 2021: 5 · 2020: 4 · 2018: 3 · 2017: 6 · 2016: 3 · 2015: 3 · 2014: 3 · 2013: 9 · 2012: 5
- FWCI
- 3.83
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Life Sciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Keywords
- anandamide, resiniferatoxin, CB1 receptor, CB2 receptor, calcitonin gene-related peptide, somatostatin, mechanical hyperalgesia, sciatic nerve ligation, endocannabinoids, chronic neuropathic pain, TRPV1 receptor
- MeSH terms
- Rimonabant, Amides, Animals, Arachidonic Acids, Camphanes, Cannabinoids, Diterpenes, Dose-Response Relationship, Drug, Ethanolamines, Hyperalgesia, Injections, Intravenous, Male, Neuropeptides, Neurotoxins, Palmitic Acids, Piperidines, Pyrazoles, Sciatic Nerve, Somatostatin, Calcitonin Gene-Related Peptide, Rats, Wistar, Sciatic Neuropathy, Rats, Polyunsaturated Alkamides, Endocannabinoids
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