The effect of the palmitoylethanolamide analogue, palmitoylallylamide (L-29) on pain behaviour in rodent models of neuropathy
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BACKGROUND AND PURPOSE: Cannabinoids are associated with analgesia in acute and chronic pain states. A spectrum of central cannabinoid (CB(1)) receptor-mediated motor and psychotropic side effects limit their therapeutic potential. Here, we investigate the analgesic effect of the palmitoylethanolamide (PEA) analogue, palmitoylallylamide (L-29), which via inhibition of fatty acid amide hydrolase (FAAH) may potentiate endocannabinoids thereby avoiding psychotropic side effects. EXPERIMENTAL APPROACH: The in vivo analysis of the effect of L-29 on measures of pain behaviour in three rat models of neuropathic pain. KEY RESULTS: Systemically administered L-29 (10 mg kg(-1)) reduced hypersensitivity to mechanical and thermal stimuli in the partial sciatic nerve injury (PSNI) model of neuropathic pain; and mechanical hypersensitivity in a model of antiretroviral (ddC)-associated hypersensitivity and a model of varicella zoster virus (VZV)-associated hypersensitivity. The effects of L-29 were comparable to those of gabapentin (50 mg kg(-1)). The CB(1) receptor antagonist SR141716a (1 mg kg(-1)) and the CB(2) receptor antagonist SR144528 (1 mg kg(-1)) reduced the effect of L-29 on hypersensitivity in the PSNI and ddC models, but not in the VZV model. The peroxisome proliferator-activated receptor-alpha antagonist, MK-886 (1 mg kg(-1)), partially attenuated the effect of L-29 on hypersensitivity in the PSNI model. L-29 (10 mg kg(-1)) significantly attenuated thigmotactic behaviour in the open field arena without effect on locomotor activity. CONCLUSIONS AND IMPLICATIONS: L-29 produces analgesia in a range of neuropathic pain models. This presents L-29 as a novel analgesic compound that may target the endogenous cannabinoid system while avoiding undesirable side effects associated with direct cannabinoid receptor activation.
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L29-induced suppression of thermal hyperalgesia was mediated by both the CB1 receptor and PPAR-α, whereas suppression of mechanical allodynia was mediated by CB1/CB2 and PPAR-α receptors.
“The L29-induced suppression of thermal hyperalgesia was mediated by both the CB1 receptor and PPAR-α, whereas suppression of mechanical allodynia was mediated by CB1/CB2 and PPAR-α receptors.64”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [64]
L-29 suppressed thermal hyperalgesia and mechanical allodynia in the Seltzer model.
“The fatty-acid analogue of PEA, L-29, also suppressed thermal hyperalgesia and mechanical allodynia in the Seltzer model.”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [64]
Approximately 50% of rats exposed to varicella-zoster virus developed mechanical allodynia in the ipsilateral paw by 14 days post-infection; no thermal hyperalgesia or cold allodynia was observed.
“Approximately 50% of rats exposed to the varicella-zoster virus (VZV) developed mechanical allodynia in the ipsilateral paw by 14 days post-infection; no thermal hyperalgesia or cold allodynia was observed.64”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [64]
Neither a CB1- nor a CB2-specific antagonist suppressed L-29 mediated suppression of varicella-zoster virus-induced mechanical allodynia.
“However, neither a CB1- nor CB2-specific antagonist suppressed L-29 mediated suppression of VZV-induced mechanical allodynia.64”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [64]
The PEA analogue L-29 suppressed mechanical allodynia in the varicella-zoster virus model with an earlier onset relative to gabapentin.
“The PEA analogue L-29 suppressed mechanical allodynia in this model with an earlier onset relative to gabapentin.”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [64]
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- Rice ASC, Lever I, Zarnegar R (2007). Cannabinoids and Analgesia, with Special Reference to Neuropathic Pain In: McQuay HJ and Moore RA (eds). IASP Press: Seattle, (in press).
Cited by
Sorted by citations
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BindingDB Entry 50038737: Discovery and development of fatty acid amide hydrolase (FAAH) inhibitors.
BindingDB (2012) · UC San Diego · doi:10.7270/q2j67ht8
- Authors
- Wallace, V. C. J., Segerdahl, A. R., Lambert, D. M., Vandevoorde, S., Blackbeard, J., Pheby, T., Hasnie, F., & Rice, A. S. C.
- Affiliations
- Chelsea and Westminster Hospital (GB)
- UCLouvain (BE)
- Corresponding author
- Rice, A S C
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2007-08
- Volume
- 151
- Issue
- 7
- Pages
- 1117-1128
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC2042941
- OpenAlex
- W2165127221
- Cited by
- 66
- References
- 85
- Citations by year
- 2024: 3 · 2023: 4 · 2022: 1 · 2021: 4 · 2020: 4 · 2019: 3 · 2017: 3 · 2016: 4 · 2015: 3 · 2014: 5 · 2013: 4 · 2012: 6
- FWCI
- 3.58
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DIAL (Catholic University of Leuven) (submittedVersion, other-oa)
- Funders
- Fonds De La Recherche Scientifique - FNRS
- Fondation Charcot
- 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
- neuropathic pain, analgesia, endocannabinoid system, fatty acid amide hydrolase inhibition, CB1 receptor, CB2 receptor, PPARα, varicella-zoster virus, thigmotaxis, gabapentin
- MeSH terms
- Gabapentin, Rimonabant, Amides, Amines, Animals, Behavior, Animal, Camphanes, Chlorobenzenes, Cyclohexanecarboxylic Acids, Dose-Response Relationship, Drug, Ethanolamines, gamma-Aminobutyric Acid, Hindlimb, Indoles, Injections, Intraperitoneal, Male, Pain, Pain Measurement, Palmitic Acids, Physical Stimulation, Piperidines, Pyrazoles, Temperature, Zalcitabine, Rats, Wistar, Pain Threshold, Sciatic Neuropathy, Receptor, Cannabinoid, CB1, Receptor, Cannabinoid, CB2, PPAR alpha, Rats, Endocannabinoids
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