{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T00:41:15Z","timestamp":1790383275393,"version":"4.1.0"},"reference-count":66,"publisher":"American Society for Clinical Investigation","issue":"5","funder":[{"name":"NIH","award":["R01 HL122228"],"award-info":[{"award-number":["R01 HL122228"]}]},{"name":"NIH","award":["U01 AI123832"],"award-info":[{"award-number":["U01 AI123832"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,3,7]]},"abstract":"<jats:p>\n                    Increased airway vagal sensory C-fiber activity contributes to the symptoms of inflammatory airway diseases. The KCNQ\/K\n                    <jats:sub>v<\/jats:sub>\n                    7\/M-channel is a well-known determinant of neuronal excitability, yet whether it regulates the activity of vagal bronchopulmonary C-fibers and airway reflex sensitivity remains unknown. Here we addressed this issue using single-cell RT-PCR, patch clamp technique, extracellular recording of single vagal nerve fibers innervating the mouse lungs, and telemetric recording of cough in free-moving mice. Single-cell mRNA analysis and biophysical properties of M-current (I\n                    <jats:sub>M<\/jats:sub>\n                    ) suggest that KCNQ3\/K\n                    <jats:sub>v<\/jats:sub>\n                    7.3 is the major M-channel subunit in mouse nodose neurons. The M-channel opener retigabine negatively shifted the voltage-dependent activation of I\n                    <jats:sub>M<\/jats:sub>\n                    , leading to membrane hyperpolarization, increased rheobase, and suppression of both evoked and spontaneous action potential (AP) firing in nodose neurons in an M-channel inhibitor XE991\u2013sensitive manner. Retigabine also markedly suppressed the \u03b1,\u03b2-methylene ATP\u2013induced AP firing in nodose C-fiber terminals innervating the mouse lungs, and coughing evoked by irritant gases in awake mice. In conclusion, KCNQ\/M-channels play a role in regulating the excitability of vagal airway C-fibers at both the cell soma and nerve terminals. Drugs that open M-channels in airway sensory afferents may relieve the sufferings associated with pulmonary inflammatory diseases such as chronic coughing.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.124467","type":"journal-article","created":{"date-parts":[[2019,2,5]],"date-time":"2019-02-05T12:02:22Z","timestamp":1549368142000},"source":"Crossref","is-referenced-by-count":30,"title":["KCNQ\/M-channels regulate mouse vagal bronchopulmonary C-fiber excitability and cough sensitivity"],"prefix":"10.1172","volume":"4","author":[{"given":"Hui","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8545-2222","authenticated-orcid":true,"given":"An-Hsuan","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Kentucky, Lexington, 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