Balancing brain metabolic states during sickness and recovery sleep.

Eur J Neurosci

Howard Hughes Medical Institute, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Published: December 2024

AI Article Synopsis

  • Sleep deprivation, sickness sleep, and rebound sleep all elevate levels of cytokines, particularly interleukins, but they involve distinct brain activity and physiological responses.
  • A study using metabolomics on mouse cortex and hippocampus revealed that sickness sleep and rebound sleep have unique biochemical signatures, with more pronounced differences observed in the cortex.
  • Both conditions increased tryptophan levels, but sickness sleep reduced glycolysis intermediates while rebound sleep enhanced energy production through nucleotides, indicating that rebound sleep creates a more energy-rich environment in the brain compared to sickness sleep.

Article Abstract

Sickness sleep and rebound following sleep deprivation share humoral signals including the rise of cytokines, in particular interleukins. Nevertheless, they represent unique physiological states with unique brain firing patterns and involvement of specific circuitry. Here, we performed untargeted metabolomics of mouse cortex and hippocampus to uncover changes with sickness and rebound sleep as compared with normal daily sleep. We found that the three settings are biochemically unique with larger differences in the cortex than in the hippocampus. Both sickness and rebound sleep shared an increase in tryptophan. Surprisingly, these two sleep conditions showed opposite modulation of the methionine-homocysteine cycle and differences in terms of the energetic signature, with sickness impinging on glycolysis intermediates whilst rebound increased the triphosphorylated form of nucleotides. These findings indicate that rebound following sleep deprivation stimulates an energy rich setting in the brain that is devoid during sickness sleep.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11612838PMC
http://dx.doi.org/10.1111/ejn.16588DOI Listing

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