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We have developed the transgenic mouse line <jats:italic>Actin<\/jats:italic>-tTS::<jats:italic>Nkcc1<\/jats:italic><jats:sup>tetO\/tetO<\/jats:sup> for manipulatable expression of the cochlear K<jats:sup>+<\/jats:sup> circulation protein, NKCC1. <jats:italic>Nkcc1<\/jats:italic> transcription was blocked by the binding of a tetracycline-dependent transcriptional silencer to the tetracycline operator sequences inserted upstream of the <jats:italic>Nkcc1<\/jats:italic> translation initiation site. Administration of the tetracycline derivative doxycycline reversibly regulated <jats:italic>Nkcc1<\/jats:italic> knockdown. Progeny from pregnant\/lactating mothers fed doxycycline-free chow from embryonic day 0 showed strong suppression of <jats:italic>Nkcc1<\/jats:italic> expression (~90% downregulation) and <jats:italic>Nkcc1<\/jats:italic> null phenotypes at postnatal day 35 (P35). P35 transgenic mice from mothers fed doxycycline-free chow starting at P0 (delivery) showed weaker suppression of <jats:italic>Nkcc1<\/jats:italic> expression (~70% downregulation) and less hearing loss with mild cochlear structural changes. Treatment of these mice at P35 with doxycycline for 2 weeks reactivated <jats:italic>Nkcc1<\/jats:italic> transcription to control levels and improved hearing level at high frequency; i.e., these doxycycline-treated mice exhibited partially reversible hearing loss. Thus, development of the <jats:italic>Actin<\/jats:italic>-tTS::<jats:italic>Nkcc1<\/jats:italic><jats:sup>tetO\/tetO<\/jats:sup> transgenic mouse line provides a mouse model for the study of variable hearing loss through reversible knockdown of <jats:italic>Nkcc1<\/jats:italic>.<\/jats:p>","DOI":"10.1038\/s41598-017-13997-7","type":"journal-article","created":{"date-parts":[[2017,10,13]],"date-time":"2017-10-13T15:01:18Z","timestamp":1507906878000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Time-controllable Nkcc1 knockdown replicates reversible hearing loss in postnatal mice"],"prefix":"10.1038","volume":"7","author":[{"given":"Takahisa","family":"Watabe","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miho","family":"Watanabe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junichi","family":"Nabekura","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Taiga","family":"Higuchi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karin","family":"Hori","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mitsuo P.","family":"Sato","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fumiaki","family":"Nin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0688-1489","authenticated-orcid":false,"given":"Hiroshi","family":"Hibino","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaoru","family":"Ogawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masatsugu","family":"Masuda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenji F.","family":"Tanaka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2017,10,19]]},"reference":[{"key":"13997_CR1","doi-asserted-by":"publisher","first-page":"1142","DOI":"10.1097\/MAO.0b013e3182635417","volume":"33","author":"M Masuda","year":"2012","unstructured":"Masuda, M. et al. 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