Cold Suppresses Agonist-induced Activation of TRPV1

Cold therapy is frequently used to reduce pain and edema following acute injury or surgery such as tooth extraction. However, the neurobiological mechanisms of cold therapy are not completely understood. Transient receptor potential vanilloid 1 (TRPV1) is a capsaicin- and heat-gated nociceptive ion...

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Bibliographic Details
Published in:Journal of dental research 2011-09, Vol.90 (9), p.1098-1102
Main Authors: Chung, M.-K., Wang, S.
Format: Article
Language:English
Subjects:
Agonists
Animals
Biological and medical sciences
Capsaicin
Capsaicin - pharmacology
Capsaicin receptors
Cold
Cold Temperature
Dentistry
Edema
Ganglia
Heat
HEK293 Cells
Humans
Male
Medical sciences
Miscellaneous
Nociceptors - drug effects
Pain
Pain perception
Pain, Postoperative - therapy
Potentiation
Pulpitis - physiopathology
Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects)
Rats
Rats, Sprague-Dawley
Recombinant Proteins
Research Reports
Surgery
Tooth Extraction
Trigeminal ganglion
Trigeminal Ganglion - cytology
Trigeminal Ganglion - drug effects
TRPV Cation Channels - agonists
TRPV Cation Channels - antagonists & inhibitors
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Summary:Cold therapy is frequently used to reduce pain and edema following acute injury or surgery such as tooth extraction. However, the neurobiological mechanisms of cold therapy are not completely understood. Transient receptor potential vanilloid 1 (TRPV1) is a capsaicin- and heat-gated nociceptive ion channel implicated in thermosensation and pathological pain under conditions of inflammation or injury. Although capsaicin-induced nociception, neuropeptide release, and ionic currents are suppressed by cold, it is not known if cold suppresses agonist-induced activation of recombinant TRPV1. We demonstrate that cold strongly suppressed the activation of recombinant TRPV1 by multiple agonists and capsaicin-evoked currents in trigeminal ganglia neurons under normal and phosphorylated conditions. Cold-induced suppression was partially impaired in a TRPV1 mutant that lacked heat-mediated activation and potentiation. These results suggest that cold-induced suppression of TRPV1 may share a common molecular basis with heat-induced potentiation, and that allosteric inhibition may contribute, in part, to the cold-induced suppression. We also show that combination of cold and a specific antagonist of TRPV1 can produce an additive suppression. Our results provide a mechanistic basis for cold therapy and may enhance anti-nociceptive approaches that target TRPV1 for managing pain under inflammation and tissue injury, including that from tooth extraction.
ISSN:0022-0345
1544-0591
DOI:10.1177/0022034511412074