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<p>To facilitate precise genetic access to auditory circuits, we firstly developed a <i>Scrt1</i><sup><i>3</i>×<i>HA‑P2A‑iCreER‑T2A‑EGFP</i></sup> knock‑in mouse model. This tool enables tamoxifen‑inducible, permanent labeling of <i>Scrt1</i>‑expressing cells. Systematic analysis from neonatal to adult stages revealed that <i>Scrt1</i> is constitutively and specifically expressed in all type I spiral ganglion neurons (SGNs), with no detection in hair cells or type II SGNs. Furthermore, <i>Scrt1</i> is expressed in neurons across all subdivisions of the cochlear nucleus (CN). These findings establish the <i>Scrt1</i>‑iCreER line as a potent genetic driver for targeting the primary sensory relay neurons in the auditory pathway. This model provides a valuable resource for mapping connectivity, monitoring activity, and functionally manipulating type I SGNs and their central targets in the CN, thereby advancing mechanistic studies of auditory processing and related disorders.</p>

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Scrt1-iCreER: An Inducible Mouse Model for Genetic Access to Type I Spiral Ganglion and Cochlear Nucleus Neurons

  • 期刊论文

  • 发表日期：

    2026年1月1日

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  • Xiang Mengya,
  • Li Jian,
  • Fan Shuwen,
  • Luo Zhengnan,
  • Yu Hongzhe,
  • Liu Zhiyong,
  • Li Xiang,
  • Li Huawei,
  • Wang Yunfeng

摘要

To facilitate precise genetic access to auditory circuits, we firstly developed a Scrt13×HA‑P2A‑iCreER‑T2A‑EGFP knock‑in mouse model. This tool enables tamoxifen‑inducible, permanent labeling of Scrt1‑expressing cells. Systematic analysis from neonatal to adult stages revealed that Scrt1 is constitutively and specifically expressed in all type I spiral ganglion neurons (SGNs), with no detection in hair cells or type II SGNs. Furthermore, Scrt1 is expressed in neurons across all subdivisions of the cochlear nucleus (CN). These findings establish the Scrt1‑iCreER line as a potent genetic driver for targeting the primary sensory relay neurons in the auditory pathway. This model provides a valuable resource for mapping connectivity, monitoring activity, and functionally manipulating type I SGNs and their central targets in the CN, thereby advancing mechanistic studies of auditory processing and related disorders.