Peripheral hyperpolarization-activated cyclic nucleotide-gated channels contribute to inflammation-induced hypersensitivity of the rat temporomandibular joint

Background Hyperpolarization‐activated cyclic nucleotide‐gated (HCN) channels conduct an inward cation current (Ih) that contributes to the maintenance of neuronal membrane potential and have been implicated in a number of animal models of neuropathic and inflammatory pain. In the current study, we...

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Bibliographic Details
Published in:European journal of pain 2013-08, Vol.17 (7), p.972-982
Main Authors: Hatch, R.J., Jennings, E.A., Ivanusic, J.J.
Format: Article
Language:English
Subjects:
Animals
Disease Models, Animal
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - metabolism
Hypersensitivity - metabolism
Hypersensitivity - physiopathology
Inflammation - metabolism
Male
Membrane Potentials - physiology
Pain - metabolism
Rats
Rats, Sprague-Dawley
Temporomandibular Joint - metabolism
Trigeminal Ganglion - metabolism
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Summary:Background Hyperpolarization‐activated cyclic nucleotide‐gated (HCN) channels conduct an inward cation current (Ih) that contributes to the maintenance of neuronal membrane potential and have been implicated in a number of animal models of neuropathic and inflammatory pain. In the current study, we investigated HCN channel involvement in inflammatory pain of the temporomandibular joint (TMJ). Methods The contribution of HCN channels to inflammation (complete Freund's adjuvant; CFA)‐induced mechanical hypersensitivity of the rat TMJ was tested with injections of the HCN channel blocker ZD7288. Retrograde labelling and immunohistochemistry was used to explore HCN channel expression in sensory neurons that innervate the TMJ. Results Injection of CFA into the TMJ (n = 7) resulted in a significantly increased mechanical sensitivity relative to vehicle injection (n = 7) (p 
ISSN:1090-3801
1532-2149
DOI:10.1002/j.1532-2149.2012.00261.x