Title |
Anoctamin 1 Contributes to Inflammatory and Nerve-Injury Induced Hypersensitivity
|
---|---|
Published in |
Molecular Pain, January 2014
|
DOI | 10.1186/1744-8069-10-5 |
Pubmed ID | |
Authors |
Byeongjun Lee, Hawon Cho, Jooyoung Jung, Young Duk Yang, Dong-Jin Yang, Uhtaek Oh |
Abstract |
Various pathological conditions such as inflammation or injury can evoke pain hypersensitivity. That represents the response to innocuous stimuli or exaggerated response to noxious stimuli. The molecular mechanism based on the pain hypersensitivity is associated with changes in many of ion channels in dorsal-root ganglion (DRG) neurons. Anoctamin 1 (ANO1/TMEM16A), a Ca2+ activated chloride channel is highly visible in small DRG neurons and responds to heat. Mice with an abolished function of ANO1 in DRG neurons demonstrated attenuated pain-like behaviors when exposed to noxious heat, suggesting a role in acute thermal nociception. In this study, we further examined the function of ANO1 in mediating inflammation- or injury-induced hyperalgesia or allodynia. |
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