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<p>Rapid-eye-movement (REM) sleep is generated in the brainstem, but the brainstem population dynamics that drive transitions to REM sleep remain largely unknown. Here, combining mouse Neuropixels recordings and dimensionality reduction, we found that population activity in the midbrain and pons is dominated by two components, one of which captures strong infraslow fluctuations in neural activity. During transitions from non-REM (NREM) to REM sleep, the population activity followed a stereotypic trajectory that was preceded by an increase in the infraslow component. Our analysis revealed—across all brainstem areas—subpopulations of REM sleep-activated and REM sleep-inhibited neurons with opposing infraslow dynamics and diverging ramping activity between REM sleep episodes, reinforced through antagonistic functional connections. Activation of REM sleep-promoting medullary neurons rapidly enhanced the infraslow component, whose strength gated the ability of upstream circuits to induce REM sleep. Collectively, our results identify a population-level mechanism for gating REM sleep, suggesting that NREM-to-REM sleep transitions are coordinated by low-dimensional, antagonistic brainstem dynamics.</p>

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Low-dimensional population dynamics in the brainstem gate REM sleep

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月25日

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  • David E. Lozano,
  • Jiso Hong,
  • Xi Jin,
  • Joseph A. Stucynski,
  • Christian K. Machens,
  • Shinjae Chung,
  • Franz Weber

摘要

Rapid-eye-movement (REM) sleep is generated in the brainstem, but the brainstem population dynamics that drive transitions to REM sleep remain largely unknown. Here, combining mouse Neuropixels recordings and dimensionality reduction, we found that population activity in the midbrain and pons is dominated by two components, one of which captures strong infraslow fluctuations in neural activity. During transitions from non-REM (NREM) to REM sleep, the population activity followed a stereotypic trajectory that was preceded by an increase in the infraslow component. Our analysis revealed—across all brainstem areas—subpopulations of REM sleep-activated and REM sleep-inhibited neurons with opposing infraslow dynamics and diverging ramping activity between REM sleep episodes, reinforced through antagonistic functional connections. Activation of REM sleep-promoting medullary neurons rapidly enhanced the infraslow component, whose strength gated the ability of upstream circuits to induce REM sleep. Collectively, our results identify a population-level mechanism for gating REM sleep, suggesting that NREM-to-REM sleep transitions are coordinated by low-dimensional, antagonistic brainstem dynamics.