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<p>Central respiratory chemoreception is a vital homeostatic mechanism maintaining arterial blood gas levels. Central respiratory chemoreceptors in the retrotrapezoid nucleus (RTN) and nucleus tractus solitarius (NTS) form interconnected circuits to regulate respiratory homeostasis. We hypothesized that NTS GABAergic neurons (NTS<sup>GABA</sup>) modulate hypercapnic ventilatory responses by targeting ventrolateral medulla Phox2b neurons (VLM<sup>Phox2b</sup>), particularly Phox2b-expressing RTN neurons. Stimulation of NTS<sup>GABA</sup> neurons significantly attenuated CO<sub>2</sub>-evoked ventilatory responses, accompanied by a reduction in CO<sub>2</sub>-activated Phox2b-expressing RTN neurons. Neural tracing revealed that monosynaptic inputs to the VLM<sup>Phox2b</sup> neurons primarily originate from the ventrolateral and dorsolateral subdivisions of the NTS. Photostimulation of NTS<sup>GABA</sup> neurons retrogradely labeled from the VLM markedly suppressed respiratory drive, while chemogenetic activation of these neurons induced hypoventilation, increased spontaneous apnea, and attenuated hypercapnic ventilatory response. These findings demonstrate that activation of the NTS-VLM inhibitory circuit diminishes respiratory motor output, offering novel insights into the regulatory mechanisms of respiratory homeostasis.</p>

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GABAergic Inhibition from the Nucleus Tractus Solitarius to Ventrolateral Medulla Phox2b Neurons Modulates Central Respiratory Chemoreflex and Ventilatory Homeostasis

  • 期刊论文

  • 发表日期：

    2026年1月26日

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  • Liuqi Shao,
  • Yake Ji,
  • Hongxiao Yu,
  • Zixuan Cheng,
  • Fanrao Kong,
  • Xiaoyi Wang,
  • Bingwen Zhang,
  • Yinchang Wang,
  • Yimeng Song,
  • Fang Yuan,
  • Congrui Fu,
  • Sheng Wang

摘要

Central respiratory chemoreception is a vital homeostatic mechanism maintaining arterial blood gas levels. Central respiratory chemoreceptors in the retrotrapezoid nucleus (RTN) and nucleus tractus solitarius (NTS) form interconnected circuits to regulate respiratory homeostasis. We hypothesized that NTS GABAergic neurons (NTSGABA) modulate hypercapnic ventilatory responses by targeting ventrolateral medulla Phox2b neurons (VLMPhox2b), particularly Phox2b-expressing RTN neurons. Stimulation of NTSGABA neurons significantly attenuated CO2-evoked ventilatory responses, accompanied by a reduction in CO2-activated Phox2b-expressing RTN neurons. Neural tracing revealed that monosynaptic inputs to the VLMPhox2b neurons primarily originate from the ventrolateral and dorsolateral subdivisions of the NTS. Photostimulation of NTSGABA neurons retrogradely labeled from the VLM markedly suppressed respiratory drive, while chemogenetic activation of these neurons induced hypoventilation, increased spontaneous apnea, and attenuated hypercapnic ventilatory response. These findings demonstrate that activation of the NTS-VLM inhibitory circuit diminishes respiratory motor output, offering novel insights into the regulatory mechanisms of respiratory homeostasis.