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TRPV4 is necessary for trigeminal irritant pain and functions as a cellular formalin receptor.

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Date
2014-12
Authors
Chen, Yong
Kanju, Patrick
Fang, Quan
Lee, Suk Hee
Parekh, Puja K
Lee, Whasil
Moore, Carlene
Brenner, Daniel
Gereau, Robert W
Wang, Fan
Liedtke, Wolfgang
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(11 total)
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Abstract
Detection of external irritants by head nociceptor neurons has deep evolutionary roots. Irritant-induced aversive behavior is a popular pain model in laboratory animals. It is used widely in the formalin model, where formaldehyde is injected into the rodent paw, eliciting quantifiable nocifensive behavior that has a direct, tissue-injury-evoked phase, and a subsequent tonic phase caused by neural maladaptation. The formalin model has elucidated many antipain compounds and pain-modulating signaling pathways. We have adopted this model to trigeminally innervated territories in mice. In addition, we examined the involvement of TRPV4 channels in formalin-evoked trigeminal pain behavior because TRPV4 is abundantly expressed in trigeminal ganglion (TG) sensory neurons, and because we have recently defined TRPV4's role in response to airborne irritants and in a model for temporomandibular joint pain. We found TRPV4 to be important for trigeminal nocifensive behavior evoked by formalin whisker pad injections. This conclusion is supported by studies with Trpv4(-/-) mice and TRPV4-specific antagonists. Our results imply TRPV4 in MEK-ERK activation in TG sensory neurons. Furthermore, cellular studies in primary TG neurons and in heterologous TRPV4-expressing cells suggest that TRPV4 can be activated directly by formalin to gate Ca(2+). Using TRPA1-blocker and Trpa1(-/-) mice, we found that both TRP channels co-contribute to the formalin trigeminal pain response. These results imply TRPV4 as an important signaling molecule in irritation-evoked trigeminal pain. TRPV4-antagonistic therapies can therefore be envisioned as novel analgesics, possibly for specific targeting of trigeminal pain disorders, such as migraine, headaches, temporomandibular joint, facial, and dental pain, and irritation of trigeminally innervated surface epithelia.
Type
Journal article
Subject
ERK
Formalin model
Formalin receptor
Irritant
MEK
TRPV4
Trigeminal ganglion
Trigeminal pain
Whisker pad
Animals
Butadienes
Cells, Cultured
Disease Models, Animal
Enzyme Inhibitors
Extracellular Signal-Regulated MAP Kinases
Fixatives
Formaldehyde
Keratinocytes
Membrane Potentials
Mice
Mice, Inbred C57BL
Mice, Transgenic
Morpholines
Neurons
Nitriles
Pain
Pyrroles
TRPV Cation Channels
Trigeminal Ganglion
Ubiquitin Thiolesterase
Vibrissae
Permalink
https://hdl.handle.net/10161/12970
Published Version (Please cite this version)
10.1016/j.pain.2014.09.033
Publication Info
Chen, Yong; Kanju, Patrick; Fang, Quan; Lee, Suk Hee; Parekh, Puja K; Lee, Whasil; ... Liedtke, Wolfgang (2014). TRPV4 is necessary for trigeminal irritant pain and functions as a cellular formalin receptor. Pain, 155(12). pp. 2662-2672. 10.1016/j.pain.2014.09.033. Retrieved from https://hdl.handle.net/10161/12970.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Chen

Yong Chen

Associate Professor in Neurology
Liedtke

Wolfgang Bernhard Liedtke

Adjunct Professor in the Department of Neurology
Research Interests in the Liedtke-Lab: Pain/ nociception Sensory transduction and -transmission TRP ion channels Water and salt equilibrium regulated by the central nervous system Visit the lab's website, download papers and read Dr. Liedtke's CV here.
Moore

Carlene D Moore

Assistant Professor in Neurology
Wang

Fan Wang

Adjunct Professor in the Department of Neurobiology
My lab studies neural circuit basis of sensory perception. Specifically we are interested in determining neural circuits underlying (1) active touch sensation including tactile processing stream and motor control of touch sensors on the face; (2) pain sensation including both sensory-discriminative and affective aspects of pain; and (3) general anesthesia including the active pain-suppression process. We use a combination of genetic, viral, electrophysiology, and in vivo imaging (in f
Alphabetical list of authors with Scholars@Duke profiles.
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