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5d ago

UC Berkeley Maps Sleep-Stage Circuit That Controls Growth Hormone—and Primes Wakefulness

A mouse study in Cell outlines a hypothalamus–locus coeruleus feedback loop that links nightly hormone pulses to arousal.

During sleep, the brain produces growth hormone to help build muscle and bone and reduce fat. UC Berkeley research in mice reveals the brain circuits that regulate growth hormone release, along with a brainstem feedback mechanism that promotes wakefulness after a good night's sleep.
Scientists track how growth hormone reinforces our muscles and bones while we're asleep
Sleep is known to promote tissue growth and regulate metabolism, partly by enhancing growth hormone (GH) release, but the underlying circuit mechanism is unknown. Ding et al. demonstrate how GH release, which is enhanced during both rapid eye movement (REM) and non-REM (NREM) sleep, is regulated by sleep-wake-dependent activity of distinct hypothalamic neurons expressing GH-releasing hormone (GHRH) and somatostatin (SST). SST neurons in the arcuate nucleus suppress GH release by inhibiting nearby GHRH neurons that stimulate GH release, whereas periventricular SST neurons inhibit GH release by projecting to the median eminence. GH release is associated with strong surges of both GHRH and SST activity during REM sleep but moderately increased GHRH and decreased SST activity during NREM sleep. Furthermore, Ding et al. identified a negative feedback pathway in which GH enhances the excitability of locus coeruleus neurons and increases wakefulness. Image credit: Ding et al., doi: 10.1016/j.cell.2025.05.039.

Overview

  • Researchers identified opposing GHRH and somatostatin neurons in the hypothalamus that drive growth hormone during REM and non‑REM sleep.
  • Released growth hormone heightened the excitability of locus coeruleus arousal neurons, forming a feedback that promotes transitions toward wakefulness.
  • Deleting growth hormone receptors from those brainstem cells abolished the arousal effect, while hormone infusion increased alertness in receptor‑intact mice.
  • The team used optogenetics, chemogenetics, calcium imaging, electrophysiology, virus-based circuit tracing, and CRISPR in young adult mice to map the mechanism and its sleep‑state dependence.
  • Authors emphasize that results are preclinical in mice, though the circuit could inform future therapies for sleep and metabolic disorders; funding came from HHMI and UC Berkeley’s Pivotal Life Sciences Chancellor’s Chair fund.