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Vanilloid receptor 1-positive neurons mediate thermal hyperalgesia and tactile allodynia.
Spine J. 2008 Mar-Apr; 8(2):351-8.SJ

Abstract

BACKGROUND CONTEXT

The vanilloid receptor 1 (VR1) is expressed by the type II A-delta and C-fiber neurons, functioning as a molecular integrator for nociception. VR1 can be selectively ablated by resiniferatoxin (RTX), an ultra-potent excitotoxic agonist, when injected into sensory ganglia.

PURPOSE

To evaluate the role of the VR1-positive neurons in neuropathic pain.

STUDY DESIGN

Photochemical injury to rat sciatic nerve (Gazelius model).

METHODS

Two groups of rats underwent the photochemical injury and RTX treatment. RTX was injected in the dorsal root ganglia (DRGs) of the L3, L4, L5, and L6 nerve roots, either after or before the nerve injury. The animals were tested for thermal hyperalgesia (noxious heat stimuli) and mechanical allodynia (von Frey filaments). Immunohistochemical analysis of the DRGs was performed after euthanasia.

RESULTS

In the tactile allodynic rats, RTX injection in the DRGs improved the average withdrawal threshold from 1.62 g to 5.68 g. Immunohistochemical labeling showed that almost all VR1-positive neurons were eliminated. When RTX was administrated into the ipsilateral DRGs before the nerve injury, this treatment prevented the development of tactile allodynia in 12 out of 14 rats. Immunohistochemical staining revealed that the VR1-positive neurons were eliminated in the rats that did not develop tactile allodynia, whereas they were still present in the allodynic rats.

CONCLUSIONS

VR1-positive neurons are essential for the development of mechanical allodynia. In rats already exhibiting neuropathic pain, the VR1-positive neurons mediate the most sensitive part of mechanical allodynia. RTX injection in sensory ganglia may represent a novel treatment for neuropathic pain.

Authors+Show Affiliations

Department of Neurosurgery, Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18029293

Citation

Tender, Gabriel C., et al. "Vanilloid Receptor 1-positive Neurons Mediate Thermal Hyperalgesia and Tactile Allodynia." The Spine Journal : Official Journal of the North American Spine Society, vol. 8, no. 2, 2008, pp. 351-8.
Tender GC, Li YY, Cui JG. Vanilloid receptor 1-positive neurons mediate thermal hyperalgesia and tactile allodynia. Spine J. 2008;8(2):351-8.
Tender, G. C., Li, Y. Y., & Cui, J. G. (2008). Vanilloid receptor 1-positive neurons mediate thermal hyperalgesia and tactile allodynia. The Spine Journal : Official Journal of the North American Spine Society, 8(2), 351-8.
Tender GC, Li YY, Cui JG. Vanilloid Receptor 1-positive Neurons Mediate Thermal Hyperalgesia and Tactile Allodynia. Spine J. 2008 Mar-Apr;8(2):351-8. PubMed PMID: 18029293.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vanilloid receptor 1-positive neurons mediate thermal hyperalgesia and tactile allodynia. AU - Tender,Gabriel C, AU - Li,Yuan-Yuan, AU - Cui,Jian-Guo, Y1 - 2007/11/26/ PY - 2006/12/18/received PY - 2007/04/11/revised PY - 2007/08/27/accepted PY - 2007/11/22/pubmed PY - 2008/5/21/medline PY - 2007/11/22/entrez SP - 351 EP - 8 JF - The spine journal : official journal of the North American Spine Society JO - Spine J VL - 8 IS - 2 N2 - BACKGROUND CONTEXT: The vanilloid receptor 1 (VR1) is expressed by the type II A-delta and C-fiber neurons, functioning as a molecular integrator for nociception. VR1 can be selectively ablated by resiniferatoxin (RTX), an ultra-potent excitotoxic agonist, when injected into sensory ganglia. PURPOSE: To evaluate the role of the VR1-positive neurons in neuropathic pain. STUDY DESIGN: Photochemical injury to rat sciatic nerve (Gazelius model). METHODS: Two groups of rats underwent the photochemical injury and RTX treatment. RTX was injected in the dorsal root ganglia (DRGs) of the L3, L4, L5, and L6 nerve roots, either after or before the nerve injury. The animals were tested for thermal hyperalgesia (noxious heat stimuli) and mechanical allodynia (von Frey filaments). Immunohistochemical analysis of the DRGs was performed after euthanasia. RESULTS: In the tactile allodynic rats, RTX injection in the DRGs improved the average withdrawal threshold from 1.62 g to 5.68 g. Immunohistochemical labeling showed that almost all VR1-positive neurons were eliminated. When RTX was administrated into the ipsilateral DRGs before the nerve injury, this treatment prevented the development of tactile allodynia in 12 out of 14 rats. Immunohistochemical staining revealed that the VR1-positive neurons were eliminated in the rats that did not develop tactile allodynia, whereas they were still present in the allodynic rats. CONCLUSIONS: VR1-positive neurons are essential for the development of mechanical allodynia. In rats already exhibiting neuropathic pain, the VR1-positive neurons mediate the most sensitive part of mechanical allodynia. RTX injection in sensory ganglia may represent a novel treatment for neuropathic pain. SN - 1529-9430 UR - https://www.unboundmedicine.com/medline/citation/18029293/Vanilloid_receptor_1_positive_neurons_mediate_thermal_hyperalgesia_and_tactile_allodynia_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1529-9430(07)00780-2 DB - PRIME DP - Unbound Medicine ER -