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<p>Perception of external temperature is essential for maintaining homeostasis and avoiding thermal injury. Although molecular thermosensors such as transient receptor potential melastatin type 8 (TRPM8) have been identified, the neural circuits responsible for transmitting cool signals remain unclear. Here we show that a spinal circuit in mice conveys cool signals from the skin to the brain. Excitatory interneurons in the spinal dorsal horn expressing thyrotropin-releasing hormone receptor (Trhr<sup>+</sup>) act as a central hub for cool sensation. These Trhr<sup>+</sup> neurons receive monosynaptic input from TRPM8<sup>+</sup> sensory afferents and are selectively activated by innocuous cool stimuli. Ablating Trhr<sup>+</sup> interneurons abolishes behavioral responses to cool, but not to warm or cold stimuli. We also identify a population of calcitonin receptor-like receptor-positive (Calcrl<sup>+</sup>) spinal projection neurons that receive convergent input from both TRPM8<sup>+</sup> afferents and Trhr<sup>+</sup> interneurons, and transmit cool-specific signals to the lateral parabrachial nucleus (lPBN). Our findings define a feedforward amplification circuit for cool sensation and reveal a modality-specific spinal pathway for thermal processing.</p>

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A dedicated skin-to-brain circuit for cool sensation in mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月28日

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  • Hankyu Lee,
  • Chia Chun Hor,
  • Lorraine R. Horwitz,
  • Ailin Xiong,
  • Xin-Yu Su,
  • Daniel R. Soden,
  • Sarah Yang,
  • Wei Cai,
  • Wenwen Zhang,
  • Chen Li,
  • Christopher Radcliff,
  • Abbey Dinh,
  • Tin Long Rex Fung,
  • Ilma Rovcanin,
  • Kevin P. Pipe,
  • X. Z. Shawn Xu,
  • Bo Duan

摘要

Perception of external temperature is essential for maintaining homeostasis and avoiding thermal injury. Although molecular thermosensors such as transient receptor potential melastatin type 8 (TRPM8) have been identified, the neural circuits responsible for transmitting cool signals remain unclear. Here we show that a spinal circuit in mice conveys cool signals from the skin to the brain. Excitatory interneurons in the spinal dorsal horn expressing thyrotropin-releasing hormone receptor (Trhr+) act as a central hub for cool sensation. These Trhr+ neurons receive monosynaptic input from TRPM8+ sensory afferents and are selectively activated by innocuous cool stimuli. Ablating Trhr+ interneurons abolishes behavioral responses to cool, but not to warm or cold stimuli. We also identify a population of calcitonin receptor-like receptor-positive (Calcrl+) spinal projection neurons that receive convergent input from both TRPM8+ afferents and Trhr+ interneurons, and transmit cool-specific signals to the lateral parabrachial nucleus (lPBN). Our findings define a feedforward amplification circuit for cool sensation and reveal a modality-specific spinal pathway for thermal processing.