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Brain oxidation is an initial process in sleep induction.

M Ikeda1, M Ikeda-Sagara, T Okada

  • 1Department of Molecular Behavioral Biology, Osaka Bioscience Institute, 6-2-4 Furuedai, Suita, Osaka 565-0874, Japan. msikeda@obi.or.jp

Neuroscience
|January 18, 2005
PubMed
Summary
This summary is machine-generated.

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Low-level brain oxidation, specifically reactive oxygen species (ROS), can promote sleep by triggering the release of sleep-inducing neuromodulators in the preoptic/anterior hypothalamus (POAH). This process is regulated by the antioxidant glutathione and involves calcium signaling.

Area of Science:

  • Neuroscience
  • Sleep Research
  • Oxidative Stress Biology

Background:

  • Central nervous system (CNS) activity correlates with vigilance states, being high during wakefulness and low during sleep.
  • Neuronal activity consumes oxygen, producing reactive oxygen species (ROS), which can be cytotoxic.
  • Glutathione, an antioxidant, protects against ROS, and is proposed to influence sleep, but the link between sleep and cerebral oxidation is unclear.

Purpose of the Study:

  • To investigate the relationship between cerebral oxidation and sleep induction.
  • To determine if low-level oxidative stress can promote sleep.
  • To elucidate the mechanisms underlying peroxide-induced sleep promotion in the preoptic/anterior hypothalamus (POAH).

Main Methods:

  • Intracerebroventricular (i.c.v.) infusion of t-butyl-hydroperoxide in rats to assess sleep promotion.

Related Experiment Videos

  • Microinjection and microdialysis of t-butyl-hydroperoxide into the POAH to measure neuromodulator release.
  • In vitro studies using organotypic cultures of the POAH to visualize calcium dynamics and assess neuroprotection.

    • Main Results:

    • Low-dose t-butyl-hydroperoxide infusion promoted sleep in rats.
    • Peroxide exposure in the POAH induced nitric oxide and adenosine release, mediated by N-methyl-D-aspartate (NMDA) receptor activation.
    • In vitro, peroxides caused intracellular calcium mobilization, which was inhibited by NMDA receptor antagonists and glutathione, protecting neurons.

    Conclusions:

    • Low-level oxidative stress in the POAH can trigger sleep via calcium-dependent release of sleep-inducing neuromodulators.
    • The antioxidant system, involving glutathione, plays a role in regulating this sleep-promoting oxidative pathway.
    • A moderate increase in ROS during wakefulness may act as an initial trigger for sleep induction.