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Sleeping Sickness Disrupts the Sleep-Regulating Adenosine System.

Filipa Rijo-Ferreira1,2, Theresa E Bjorness3,4, Kimberly H Cox1

  • 1Department of Neuroscience, Peter O'Donnell Jr. Brain Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9111.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|October 24, 2020
PubMed
Summary
This summary is machine-generated.

Sleeping sickness disrupts sleep by altering the brain's adenosine system. Trypanosoma brucei infection in mice reduced their response to sleep deprivation, suggesting a link to adenosine signaling changes.

Keywords:
adenosinehomeostasissleepsleeping sickness

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Area of Science:

  • Neuroscience
  • Parasitology
  • Sleep Medicine

Background:

  • Sleeping sickness, caused by *Trypanosoma brucei*, leads to significant sleep disturbances.
  • The precise neurological mechanisms underlying these sleep disruptions remain unclear.

Purpose of the Study:

  • To investigate the impact of *T. brucei* infection on sleep architecture and homeostatic sleep regulation in a mouse model.
  • To explore the role of the adenosine system in *T. brucei*-induced sleep alterations.

Main Methods:

  • Assessed sleep architecture in male mice infected with *T. brucei* under normal and sleep-deprived conditions.
  • Evaluated the electrophysiological response to an adenosine receptor antagonist.
  • Measured adenosine receptor gene expression.

Main Results:

  • *T. brucei*-infected mice exhibited significantly altered sleep patterns.
  • Infected mice showed a diminished homeostatic sleep response following sleep deprivation.
  • Electrophysiological responses to adenosine receptor antagonists were reduced, with increased adenosine receptor gene expression.

Conclusions:

  • *Trypanosoma brucei* infection alters sleep patterns and impairs homeostatic sleep regulation in mice.
  • Findings suggest that disrupted adenosine signaling may contribute to the sleep disturbances observed in sleeping sickness.
  • Further research is needed to elucidate the exact mechanisms linking *T. brucei* infection to these neurological changes.