{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T13:33:07Z","timestamp":1784813587224,"version":"3.55.0"},"posted":{"date-parts":[[2024,2,22]]},"group-title":"Neuroscience","reference-count":61,"publisher":"openRxiv","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2024,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  AMPA-type glutamate receptors (AMPAR) mediate excitatory cochlear transmission. However, the unique roles of AMPAR subunits are unresolved. Lack of subunit GluA3 (\n                  <jats:italic>\n                    Gria3\n                    <jats:sup>KO<\/jats:sup>\n                  <\/jats:italic>\n                  ) in male mice reduced cochlear output by 8-weeks of age. Since\n                  <jats:italic>Gria3<\/jats:italic>\n                  is X-linked and considering sex differences in hearing vulnerability, we hypothesized accelerated presbycusis in\n                  <jats:italic>\n                    Gria3\n                    <jats:sup>KO<\/jats:sup>\n                  <\/jats:italic>\n                  females. Here, auditory brainstem responses (ABR) were similar in 3-week-old female\n                  <jats:italic>\n                    Gria3\n                    <jats:sup>WT<\/jats:sup>\n                  <\/jats:italic>\n                  and\n                  <jats:italic>\n                    Gria3\n                    <jats:sup>KO<\/jats:sup>\n                  <\/jats:italic>\n                  mice. However, when raised in ambient sound, ABR thresholds were elevated and wave-1 amplitudes were diminished at 5-weeks and older in\n                  <jats:italic>\n                    Gria3\n                    <jats:sup>KO<\/jats:sup>\n                  <\/jats:italic>\n                  . In contrast, these metrics were similar between genotypes when raised in quiet. Paired synapses were similar in number, but lone ribbons and ribbonless synapses were increased in female\n                  <jats:italic>\n                    Gria3\n                    <jats:sup>KO<\/jats:sup>\n                  <\/jats:italic>\n                  mice in ambient sound compared to\n                  <jats:italic>\n                    Gria3\n                    <jats:sup>WT<\/jats:sup>\n                  <\/jats:italic>\n                  or to either genotype raised in quiet. Synaptic GluA4:GluA2 ratios increased relative to\n                  <jats:italic>\n                    Gria3\n                    <jats:sup>WT<\/jats:sup>\n                  <\/jats:italic>\n                  , particularly in ambient sound, suggesting an activity-dependent increase in calcium-permeable AMPARs in\n                  <jats:italic>\n                    Gria3\n                    <jats:sup>KO<\/jats:sup>\n                  <\/jats:italic>\n                  . Swollen afferent terminals were observed by 5-weeks only in\n                  <jats:italic>\n                    Gria3\n                    <jats:sup>KO<\/jats:sup>\n                  <\/jats:italic>\n                  females reared in ambient sound. We propose that lack of GluA3 induces sex-dependent vulnerability to AMPAR-mediated excitotoxicity.\n                <\/jats:p>","DOI":"10.1101\/2024.02.21.581467","type":"posted-content","created":{"date-parts":[[2024,2,27]],"date-time":"2024-02-27T13:04:27Z","timestamp":1709039067000},"source":"Crossref","is-referenced-by-count":2,"title":["Female GluA3-KO mice show early onset hearing loss and afferent swellings in ambient sound levels"],"prefix":"10.64898","author":[{"given":"Indra","family":"Pal","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Atri","family":"Bhattacharyya","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Babak","family":"V-Ghaffari","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Essence D.","family":"Williams","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maolei","family":"Xiao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark A.","family":"Rutherford","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mar\u00eda Eulalia","family":"Rubio","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2024041806050901000_2024.02.21.581467v2.1","doi-asserted-by":"crossref","first-page":"403","DOI":"10.1007\/s10162-012-0319-2","article-title":"Maturation and aging of the human cochlea: a view through the DPOAE looking glass","volume":"13","year":"2012","journal-title":"DJournal of the Association for Research in Otolaryngology: JARO"},{"key":"2024041806050901000_2024.02.21.581467v2.2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.2573-19.2020"},{"key":"2024041806050901000_2024.02.21.581467v2.3","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2007.12.002"},{"key":"2024041806050901000_2024.02.21.581467v2.4","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-013-1309-1"},{"key":"2024041806050901000_2024.02.21.581467v2.5","doi-asserted-by":"crossref","first-page":"761","DOI":"10.1016\/j.dib.2015.10.033","article-title":"Identification of genes escaping X inactivation by allelic expression analysis in a novel hybrid mouse model","volume":"5","year":"2015","journal-title":"Data in brief"},{"key":"2024041806050901000_2024.02.21.581467v2.6","doi-asserted-by":"publisher","DOI":"10.1038\/nature03479"},{"key":"2024041806050901000_2024.02.21.581467v2.7","doi-asserted-by":"crossref","unstructured":"Chakrabarti R , Fung TS , Kang T , Elonkirjo PW , Suomalainen A , Usherwood EJ , Higgs HN (2022) Mitochondrial dysfunction triggers actin polymerization necessary for rapid glycolytic activation. 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