Focal lysolecithin-induced demyelination of peripheral afferents results in neuropathic pain behavior that is attenuated by cannabinoids
Open accessAbstract
Demyelinating diseases can be associated with painful sensory phenomena such as tactile allodynia and hyperalgesia. To study the mechanisms underlying demyelination-induced pain, we have characterized a novel model of demyelination of the sciatic or saphenous nerve. Topical lysolecithin application causes focal demyelination of afferent nerve A-fibers without axonal loss, as assessed either by electron and light microscopy or by immunohistochemical analysis of dorsal root ganglia (DRG) for a neuronal injury marker, activating transcription factor 3. Focal demyelination is accompanied by spontaneous action potentials in afferents and increased expression of neuropeptide Y and Na(v)1.3 sodium channels specifically in DRG neurons that coexpress a specific marker of myelinated afferents. In contrast, expression of tetrodotoxin-resistant, Na(v)1.8 sodium channels is specifically decreased in the same subgroup of DRG cells. Central sensitization of somatosensory processing is also induced, with increased behavioral reflex responsiveness to thermal and mechanical stimuli. These changes are reversed by intrathecal administration of an NMDA receptor antagonist or cannabinoid (CB) receptor agonist, but not by a mu-opioid receptor agonist. Recovery of behavioral reflexes occurred approximately 3 weeks after lysolecithin treatment. This is the first time that demyelination of afferent A-fibers has been shown to specifically induce neuropathic pain and indicates that axonal damage is not a prerequisite for development of the pain state. The profile of phenotypic changes in DRG is distinct from other pain models and displays a sensitivity to NMDA and CB receptor agents that may be exploitable therapeutically.
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In the lysolecithin-induced demyelination model, heightened sensitivity to non-noxious and noxious mechanical stimulation emerged 5 days post-exposure and peaked between 9-15 days, with recovery to baseline by day 23.
“Heightened sensitivity to both non-noxious and noxious mechanical stimulation is observed in lysolecithin-treated rats; this hypersensitivity emerged 5 days post-exposure and peaked between 9-15 days post-exposure.125 Recovery to baseline levels was observed by day 23 post-lysolecithin.”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [125]
The anti-hyperalgesic and anti-allodynic effects of WIN55,212-2 were reversed by a CB1-specific antagonist in both tests.
“Notably, the anti-hyperalgesic and anti-allodynic effects of WIN55,212-2 were reversed by a CB1-specific antagonist in both tests.”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [125]
DAMGO failed to produce an effect in the lysolecithin-induced demyelination model.
“By contrast, DAMGO failed to produce an effect.”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [125]
WIN55,212-2 attenuated mechanical allodynia and thermal hyperalgesia in the lysolecithin model and remained efficacious for up to one hour post injection.
“WIN55,212-2 attenuated mechanical allodynia and thermal hyperalgesia in this model and remained efficacious for up to one hour post injection.125”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [125]
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Mizuno, Y., & Yanagisawa, N. (2008) · European Neurology · doi:10.1159/000113461 · Cited by 9 · see citing works
Rittenhouse, P. (1996) · Peptides · doi:10.1016/s0196-9781(96)00129-5 · Cited by 2 · see citing works
Flagged first, then by citations
Research works printed but not linked: 1
- Wilcox GL (1991) Excitatory neurotransmitters and pain. In: Proceedings of the 6th World Congress of Pain (Bond MR, Charlton JE, Woolf CJ, eds), pp 97-117. Amsterdam: Elsevier.
Cited by
Sorted by citations
The biopsychosocial approach to chronic pain: Scientific advances and future directions.
Gatchel, R. J., Peng, Y. B., Peters, M. L., Fuchs, P. N., & Turk, D. C. (2007) · Psychological Bulletin · doi:10.1037/0033-2909.133.4.581 · Cited by 3,392 · see citing works
Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside
Rahn, E. J., & Hohmann, A. G. (2009) · Neurotherapeutics · doi:10.1016/j.nurt.2009.08.002 · Cited by 305 · see citing works
Changes in spinal and supraspinal endocannabinoid levels in neuropathic rats
Petrosino, S., Palazzo, E., de Novellis, V., Bisogno, T., Rossi, F., Maione, S., & Di Marzo, V. (2007) · Neuropharmacology · doi:10.1016/j.neuropharm.2006.08.011 · Cited by 227 · see citing works
Characterization of rodent models of HIV-gp120 and anti-retroviral-associated neuropathic pain
Wallace, V. C. J., Blackbeard, J., Segerdahl, A. R., Hasnie, F., Pheby, T., McMahon, S. B., & Rice, A. S. C. (2007) · Brain · doi:10.1093/brain/awm195 · Cited by 176 · see citing works
Self-citationWalczak, J.-S., Pichette, V., Leblond, F., Desbiens, K., & Beaulieu, P. (2005) · Neuroscience · doi:10.1016/j.neuroscience.2005.02.010 · Cited by 133 · see citing works
Ninkina, N., Papachroni, K., Robertson, D. C., Schmidt, O., Delaney, L., O'Neill, F., Court, F., Rosenthal, A., Fleetwood-Walker, S. M., Davies, A. M., et al. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.22.8233-8245.2003 · Cited by 75 · see citing works
Self-citationWallace, V. C. J., Segerdahl, A. R., Lambert, D. M., Vandevoorde, S., Blackbeard, J., Pheby, T., Hasnie, F., & Rice, A. S. C. (2007) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0707326 · Cited by 66 · see citing works
Self-citationWalczak, J., Pichette, V., Leblond, F., Desbiens, K., & Beaulieu, P. (2006) · Journal of Neuroscience Research · doi:10.1002/jnr.20821 · Cited by 62 · see citing works
Effects of a cannabinoid agonist on spinal nociceptive neurons in a rodent model of neuropathic pain
Liu, C., & Walker, J. M. (2006) · Journal of Neurophysiology · doi:10.1152/jn.00498.2006 · Cited by 37 · see citing works
- Authors
- Wallace, V. C. J., Cottrell, D. F., Brophy, P. J., & Fleetwood-Walker, S. M.
- Affiliations
- University of Edinburgh (GB)
- ORCID
- Brophy, Peter J.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2003-04-15
- Volume
- 23
- Issue
- 8
- Pages
- 3221-3233
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6742302
- OpenAlex
- W2103425524
- Cited by
- 134
- References
- 105
- Citations by year
- 2025: 1 · 2024: 5 · 2023: 2 · 2022: 5 · 2021: 6 · 2020: 2 · 2019: 6 · 2018: 2 · 2017: 4 · 2016: 5 · 2015: 5 · 2014: 1 · 2013: 8 · 2012: 9
- FWCI
- 4.60
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Funders
- Wellcome Trust
- Medical Research Council
- 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
- peripheral neuropathic pain, sciatic nerve, saphenous nerve, dorsal root ganglia, neuropeptide Y, Nav1.8 sodium channel, central sensitization, NMDA receptor antagonists, cannabinoid receptor agonists, mu-opioid receptor, mechanical allodynia, hyperalgesia
- MeSH terms
- Action Potentials, Animals, Behavior, Animal, Cannabinoids, Demyelinating Diseases, Disease Models, Animal, Drug Administration Routes, Ganglia, Spinal, Immunohistochemistry, Lysophosphatidylcholines, Mice, Inbred C57BL, Nerve Fibers, Myelinated, Neurons, Afferent, Neuropeptide Y, Pain, Peripheral Nerves, Reflex, Sciatic Nerve, Sodium Channels, Receptors, N-Methyl-D-Aspartate, Receptors, Opioid, mu, Excitatory Amino Acid Antagonists, Mononeuropathies, Mice
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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