Scholarlink

<p>Vocal communication is fundamental for social interaction across species, yet the neural mechanisms that shape vocal circuit development remain poorly understood despite their relevance to neurodevelopmental disorders. Here, we investigate vocal circuit development in mice using isolation-induced ultrasonic vocalizations (USVs) in neonates. An activity-tagging approach identifies the ventromedial prefrontal cortex (vmPFC) as a cortical region strongly activated during USV emission. We find a predictable temporal correlation between vmPFC activity and USV emission using in vivo fiber photometry. Selective activation and inhibition of vmPFC neurons establishes a causal role of vmPFC in vocalization. Interestingly, chronic activation of vmPFC neurons not only increases <i>Foxp2</i>, a gene implicated in childhood speech apraxia, but also Vglut1-labeled synapses in the striatum, suggesting that activity-dependent increases in Foxp2 may promote corticostriatal synaptogenesis. Consistent with this finding, neonatal vmPFC activation partially rescues USV deficits in Foxp2 heterozygous mutant mice. Collectively, our results identify the vmPFC-striatal circuit as a key regulator of neonatal vocalization and suggest that Foxp2 may mediate activity-dependent development of vocal circuits.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Activity-dependent development of vocal circuits in the neonatal rodent forebrain

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月19日

查看全文
  • Shih-Yun Chen,
  • Hao-Yu Pang,
  • Pao-Wen Fan,
  • Guan-Ying Wu,
  • Wan-Ting Lin,
  • Fu-Chin Liu,
  • Hsiao-Ying Kuo

摘要

Vocal communication is fundamental for social interaction across species, yet the neural mechanisms that shape vocal circuit development remain poorly understood despite their relevance to neurodevelopmental disorders. Here, we investigate vocal circuit development in mice using isolation-induced ultrasonic vocalizations (USVs) in neonates. An activity-tagging approach identifies the ventromedial prefrontal cortex (vmPFC) as a cortical region strongly activated during USV emission. We find a predictable temporal correlation between vmPFC activity and USV emission using in vivo fiber photometry. Selective activation and inhibition of vmPFC neurons establishes a causal role of vmPFC in vocalization. Interestingly, chronic activation of vmPFC neurons not only increases Foxp2, a gene implicated in childhood speech apraxia, but also Vglut1-labeled synapses in the striatum, suggesting that activity-dependent increases in Foxp2 may promote corticostriatal synaptogenesis. Consistent with this finding, neonatal vmPFC activation partially rescues USV deficits in Foxp2 heterozygous mutant mice. Collectively, our results identify the vmPFC-striatal circuit as a key regulator of neonatal vocalization and suggest that Foxp2 may mediate activity-dependent development of vocal circuits.