The Blockade of the Transient Receptor Potential Vanilloid Type 1 and Fatty Acid Amide Hydrolase Decreases Symptoms and Central Sequelae in the Medial Prefrontal Cortex of Neuropathic Rats
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Background: Neuropathic pain is a chronic disease resulting from dysfunction within the “pain matrix”. The basolateral amygdala (BLA) can modulate cortical functions and interactions between this structure and the medial prefrontal cortex (mPFC) are important for integrating emotionally salient information. In this study, we have investigated the involvement of the transient receptor potential vanilloid type 1 (TRPV1) and the catabolic enzyme fatty acid amide hydrolase (FAAH) in the morphofunctional changes occurring in the pre-limbic/infra-limbic (PL/IL) cortex in neuropathic rats. Results: The effect of N-arachidonoyl-serotonin (AA-5-HT), a hybrid FAAH inhibitor and TPRV1 channel antagonist, was tested on nociceptive behaviour associated with neuropathic pain as well as on some phenotypic changes occurring on PL/IL cortex pyramidal neurons. Those neurons were identified as belonging to the BLA-mPFC pathway by electrical stimulation of the BLA followed by hind-paw pressoceptive stimulus application. Changes in their spontaneous and evoked activity were studied in sham or spared nerve injury (SNI) rats before or after repeated treatment with AA-5-HT. Consistently with the SNI-induced changes in PL/IL cortex neurons which underwent profound phenotypic reorganization, suggesting a profound imbalance between excitatory and inhibitory responses in the mPFC neurons, we found an increase in extracellular glutamate levels, as well as the upregulation of FAAH and TRPV1 in the PL/IL cortex of SNI rats. Daily treatment with AA-5-HT restored cortical neuronal activity, normalizing the electrophysiological changes associated with the peripheral injury of the sciatic nerve. Finally, a single acute intra-PL/IL cortex microinjection of AA-5-HT transiently decreased allodynia more effectively than URB597 or I-RTX, a selective FAAH inhibitor or a TRPV1 blocker, respectively. Conclusion: These data suggest a possible involvement of endovanilloids in the cortical plastic changes associated with peripheral nerve injury and indicate that therapies able to normalize endovanilloid transmission may prove useful in ameliorating the symptoms and central sequelae associated with neuropathic pain.
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In both SNL and pSNL models, the FAAH inhibitor URB597 evoked anti-allodynic as well as anti-hyperalgesic effects.
“In both SNL and pSNL models, the FAAH inhibitor URB597 evoked anti-allodynic (de Novellis et al, 2011), as well as anti-hyperalgesic effects (Desroches et al, 2008(Desroches et al, , 2014b)).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as de Novellis et al, 2011
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Flagged first, then by citations
Research works printed but not linked: 1
- Millecamps M Centeno MV Berra HH Rudick CN Lavarello S Tkatch T Apkarian AV D-cycloserine reduces neuropathic pain behavior through limbic NMDA-mediated circuitry Pain 2007 132 108 23 10.1016/j.pain.2007.03.003 17449176 PMC3224847 · DOI
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Donvito, G., Nass, S. R., Wilkerson, J. L., Curry, Z. A., Schurman, L. D., Kinsey, S. G., & Lichtman, A. H. (2018) · Neuropsychopharmacology · doi:10.1038/npp.2017.204 · Cited by 301 · see citing works
Guindon, J., Lai, Y., Takacs, S. M., Bradshaw, H. B., & Hohmann, A. G. (2013) · Pharmacological Research · doi:10.1016/j.phrs.2012.10.013 · Cited by 160 · see citing works
Modulation of defensive behavior by transient receptor potential vanilloid type-1 (TRPV1) channels
Aguiar, D. C., Moreira, F. A., Terzian, A. L., Fogaça, M. V., Lisboa, S. F., Wotjak, C. T., & Guimaraes, F. S. (2014) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2014.03.026 · Cited by 57 · see citing works
- Authors
- de Novellis, V., Vita, D., Gatta, L., Luongo, L., Bellini, G., De Chiaro, M., Marabese, I., Siniscalco, D., Boccella, S., Piscitelli, F., Di Marzo, V., Palazzo, E., Rossi, F., & Maione, S.
- Affiliations
- Department of Experimental Medicine, Division of Pharmacology, Second university of Naples, via Costantinopoli 16, 80138 Naples, Italy
- University of Campania "Luigi Vanvitelli" (IT)
- Istituto di Chimica Biomolecolare (IT)
- Institute of Biomolecular Chemistry, Consiglio Nazionale delle Ricerche, Via Campi Flegrei 34, Pozzuoli (NA), Italy
- Corresponding author
- Maione, Sabatino
- ORCID
- Venue
- Molecular Pain
- Publisher
- SAGE Publications
- Published
- 2011-01-01
- Volume
- 7
- Pages
- 7-7
- ISSN
- 1744-8069 (ISSN-L)
- PMC
- PMC3031241
- OpenAlex
- W2155933772
- Cited by
- 90
- References
- 98
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 2 · 2023: 2 · 2021: 9 · 2020: 9 · 2019: 2 · 2018: 5 · 2017: 11 · 2016: 10 · 2015: 7 · 2014: 8 · 2013: 8 · 2012: 9
- FWCI
- 6.33
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Molecular Pain (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Archivio Istituzionale della Ricerca - Università degli Studi della Campania "Luigi Vanvitelli" (submittedVersion)
- 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
- neuropathic pain, TRPV1, fatty acid amide hydrolase, endovanilloids, medial prefrontal cortex, basolateral amygdala, spared nerve injury, allodynia, glutamate, cortical plasticity, pyramidal neurons, endocannabinoids
- MeSH terms
- Fatty Acid Amide Hydrolases, Amidohydrolases, Amygdala, Animals, Arachidonic Acids, Benzamides, Carbamates, Electric Stimulation, Electrodes, Male, Microinjections, Neurons, Nociceptors, Piperidines, Pyrazoles, RNA, Messenger, Serotonin, Rats, Wistar, Prefrontal Cortex, Microdialysis, Mononeuropathies, TRPV Cation Channels, Rats, Electrophysiological Phenomena
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