{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,24]],"date-time":"2025-11-24T21:37:10Z","timestamp":1764020230537,"version":"3.37.3"},"reference-count":73,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2018,11,20]],"date-time":"2018-11-20T00:00:00Z","timestamp":1542672000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001663","name":"Volkswagen Foundation","doi-asserted-by":"publisher","award":["ZN3153"],"award-info":[{"award-number":["ZN3153"]}],"id":[{"id":"10.13039\/501100001663","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["Hu787\/7\u20101,8\u20101"],"award-info":[{"award-number":["Hu787\/7\u20101,8\u20101"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2019,1]]},"abstract":"<jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Newborn mice produce ultrasonic vocalization to communicate with their mother.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The neuronal glycine transporter (GlyT2) is required for efficient loading of synaptic vesicles in glycinergic neurons.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Mice lacking GlyT2 develop a phenotype that resembles human hyperekplexia and the mice die in the second postnatal week.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In the present study, we show that GlyT2\u2010knockout mice do not acquire adult ultrasonic vocalization\u2010associated breathing patterns.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Despite the strong impairment of glycinergic inhibition, they can produce sufficient expiratory airflow to produce ultrasonic vocalization.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Because mouse ultrasonic vocalization is a valuable read\u2010out in translational research, these data are highly relevant for a broad range of research fields.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec><jats:sec><jats:title>Abstract<\/jats:title><jats:p>Mouse models are instrumental with respect to determining the genetic basis and neural foundations of breathing regulation. To test the hypothesis that glycinergic synaptic inhibition is required for normal breathing and proper post\u2010inspiratory activity, we analysed breathing and ultrasonic vocalization (USV) patterns in neonatal mice lacking the neuronal glycine transporter (GlyT2). GlyT2\u2010knockout (KO) mice have a profound reduction of glycinergic synaptic currents already at birth, develop a severe motor phenotype and survive only until the second postnatal week. At this stage, GlyT2\u2010KO mice are smaller, have a reduced respiratory rate and still display a neonatal breathing pattern with active expiration for the production of USV. By contrast, wild\u2010type mice acquire different USV\u2010associated breathing patterns that depend on post\u2010inspiratory control of air flow. Nonetheless, USVs <jats:italic>per se<\/jats:italic> remain largely indistinguishable between both genotypes. We conclude that GlyT2\u2010KO mice, despite the strong impairment of glycinergic inhibition, can produce sufficient expiratory airflow to produce ultrasonic vocalization.<\/jats:p><\/jats:sec>","DOI":"10.1113\/jp276976","type":"journal-article","created":{"date-parts":[[2018,10,8]],"date-time":"2018-10-08T19:06:38Z","timestamp":1539025598000},"page":"173-191","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["The postnatal development of ultrasonic vocalization\u2010associated breathing is altered in glycine transporter 2\u2010deficient mice"],"prefix":"10.1113","volume":"597","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5042-8724","authenticated-orcid":false,"given":"Swen","family":"H\u00fclsmann","sequence":"first","affiliation":[{"name":"Clinic for Anesthesiology University Medical Center  G\u00f6ttingen Germany"},{"name":"Center for Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB)  G\u00f6ttingen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoshihiko","family":"Oke","sequence":"additional","affiliation":[{"name":"Division of Physiome, Department of Physiology Hyogo College of Medicine  Nishinomiya Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guillaume","family":"Mesuret","sequence":"additional","affiliation":[{"name":"Clinic for Anesthesiology University Medical Center  G\u00f6ttingen Germany"},{"name":"Center for Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB)  G\u00f6ttingen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. 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