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<p><i>Nr4a2</i> (<i>Nurr1</i>) is well known to be vital for midbrain dopaminergic neurons. Recent single-cell RNA analyses reveal that <i>Nr4a2</i> is expressed in lateral cerebral regions, within neurons named L4/L5/L6 IT <i>Car3</i>. These neurons have attracted intense attention for the molecular mechanisms underlying their development and functions. We classified <i>Car3</i> neurons into neocortical (Ncx-<i>Car3</i>), claustral (CLA-<i>Car3</i>), and dorsal endopiriform nucleus (dEn-<i>Car3</i>) subpopulations, focusing on the characterization of Ncx-<i>Car3</i> neurons. These neurons exhibit distinct birthdates and migratory morphologies compared to CLA- and dEn-<i>Car3</i> neurons, but share a common transcriptomic profile when <i>Nr4a2</i> is deleted at the embryonic stage or in adulthood. Notably, <i>Nr4a2</i> misexpression ectopically induces <i>Car3</i>-enriched genes <i>in vivo</i>. Mice lacking <i>Nr4a2</i> in <i>Car3</i> ensembles during the embryonic stage or in adulthood display hyperactivity and reduced anxiety-like behaviors. Therefore, our results demonstrate that Nr4a2 is a key factor in regulating the development and functional maintenance of the forebrain <i>Car3</i> neurons.</p>

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Nr4a2, A Key Factor Controlling the Development and Functional Maintenance of Forebrain Car3 Neurons

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月8日

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  • Yun-Chao Tao,
  • Li Zhao,
  • Qiong Zhang,
  • Xi-Yue Liu,
  • Wei-Tang Liu,
  • Ze-Xuan Li,
  • Ling Hu,
  • Lei Zhang,
  • Jia-Yin Chen,
  • Yu-Qiang Ding,
  • Ning-Ning Song

摘要

Nr4a2 (Nurr1) is well known to be vital for midbrain dopaminergic neurons. Recent single-cell RNA analyses reveal that Nr4a2 is expressed in lateral cerebral regions, within neurons named L4/L5/L6 IT Car3. These neurons have attracted intense attention for the molecular mechanisms underlying their development and functions. We classified Car3 neurons into neocortical (Ncx-Car3), claustral (CLA-Car3), and dorsal endopiriform nucleus (dEn-Car3) subpopulations, focusing on the characterization of Ncx-Car3 neurons. These neurons exhibit distinct birthdates and migratory morphologies compared to CLA- and dEn-Car3 neurons, but share a common transcriptomic profile when Nr4a2 is deleted at the embryonic stage or in adulthood. Notably, Nr4a2 misexpression ectopically induces Car3-enriched genes in vivo. Mice lacking Nr4a2 in Car3 ensembles during the embryonic stage or in adulthood display hyperactivity and reduced anxiety-like behaviors. Therefore, our results demonstrate that Nr4a2 is a key factor in regulating the development and functional maintenance of the forebrain Car3 neurons.