{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,2]],"date-time":"2026-11-02T22:59:05Z","timestamp":1793660345107,"version":"4.5.1"},"reference-count":51,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2014,1,1]],"date-time":"2014-01-01T00:00:00Z","timestamp":1388534400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Mol Pain"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>\n                      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 Ca\n                      <jats:sup>2+<\/jats:sup>\n                      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.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec sec-type=\"results\">\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      Using\n                      <jats:italic toggle=\"yes\">\n                        Advillin\/Ano1\n                        <jats:sup>fl\/fl<\/jats:sup>\n                      <\/jats:italic>\n                      (\n                      <jats:italic toggle=\"yes\">Adv\/Ano1<\/jats:italic>\n                      <jats:sup>fl\/fl<\/jats:sup>\n                      ) mice that have a functional ablation of\n                      <jats:italic toggle=\"yes\">Ano1<\/jats:italic>\n                      mainly in DRG neurons, we were able to determine its role in mediating thermal hyperalgesia and mechanical allodynia induced by inflammation or nerve injury. The thermal hyperalgesia and mechanical allodynia induced by carrageenan injection and spared-nerve injury were significantly reduced in\n                      <jats:italic toggle=\"yes\">\n                        Adv\/Ano1\n                        <jats:sup>fl\/fl<\/jats:sup>\n                      <\/jats:italic>\n                      mice. In addition, flinching or licking behavior after bradykinin or formalin injection was also significantly reduced in\n                      <jats:italic toggle=\"yes\">\n                        Adv\/Ano1\n                        <jats:sup>fl\/fl<\/jats:sup>\n                      <\/jats:italic>\n                      mice. Since pathological conditions augment nociceptive behaviors, we expected ANO1's contribution to the excitability of DRG neurons. Indeed, the application of inflammatory mediators reduced the threshold for action potential (rheobase) or time for induction of the first action potential in DRG neurons isolated from control (\n                      <jats:italic toggle=\"yes\">\n                        Ano1\n                        <jats:sup>fl\/fl<\/jats:sup>\n                      <\/jats:italic>\n                      ) mice. These parameters for neuronal excitability induced by inflammatory mediators were not changed in\n                      <jats:italic toggle=\"yes\">\n                        Adv\/Ano1\n                        <jats:sup>fl\/fl<\/jats:sup>\n                      <\/jats:italic>\n                      mice, suggesting an active contribution of ANO1 in augmenting the neuronal excitability.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec sec-type=\"conclusions\">\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>In addition to ANO1's role in mediating acute thermal pain as a heat sensor, ANO1 is also capable of augmenting the excitability of DRG neurons under inflammatory or neuropathic conditions and thereby aggravates inflammation- or tissue injury-induced pathological pain.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/1744-8069-10-5","type":"journal-article","created":{"date-parts":[[2014,1,22]],"date-time":"2014-01-22T23:02:01Z","timestamp":1390431721000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":95,"title":["Anoctamin 1 Contributes to Inflammatory and Nerve-Injury Induced Hypersensitivity"],"prefix":"10.1177","volume":"10","author":[{"given":"Byeongjun","family":"Lee","sequence":"first","affiliation":[{"name":"Sensory Research Center, CRI, College of Pharmacy, Seoul National University, Gwanak, Daehak-Ro 1, Seoul 151-742, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hawon","family":"Cho","sequence":"additional","affiliation":[{"name":"Sensory Research Center, CRI, College of Pharmacy, Seoul National University, Gwanak, Daehak-Ro 1, Seoul 151-742, Republic of 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