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Acute sleep deprivation during pregnancy in rats: Rapid elevation of placental and fetal inflammation and kynurenic acid.

Authors
  • Baratta, Annalisa M1
  • Kanyuch, Nickole R1
  • Cole, Casey A2
  • Valafar, Homayoun2
  • Deslauriers, Jessica3, 4
  • Pocivavsek, Ana1, 5
  • 1 Maryland Psychiatric Research Center, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA.
  • 2 College of Engineering and Computing, University of South Carolina, Columba, South Carolina, USA.
  • 3 Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA.
  • 4 Center of Excellence for Stress and Mental Health, Veterans Affairs Hospital, La Jolla, CA, USA.
  • 5 Department of Pharmacology, Physiology, and Neuroscience, University of South Carolina School of Medicine, Columbia, SC, USA.
Type
Published Article
Journal
Neurobiology of stress
Publication Date
May 01, 2020
Volume
12
Pages
100204–100204
Identifiers
DOI: 10.1016/j.ynstr.2019.100204
PMID: 32258253
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The kynurenine pathway (KP) is the dominant pathway for tryptophan degradation in the mammalian body and emerging evidence suggests that acute episodes of sleep deprivation (SD) disrupt tryptophan metabolism via the KP. Increases in the neuroactive KP metabolite kynurenic acid (KYNA) during pregnancy may lead to a higher risk for disrupted neurodevelopment in the offspring. As pregnancy is a critical period during which several factors, including sleep disruptions, could disrupt the fetal environment, we presently explored the relationship between maternal SD and KP metabolism and immune pathways in maternal, placenta, and fetal tissues. Pregnant Wistar rat dams were sleep deprived by gentle handling for 5 h from zeitgeber time (ZT) 0 to ZT 5. Experimental cohorts included: i) controls, ii) one session of SD on embryonic day (ED) 18 or iii) three sessions of SD occurring daily on ED 16, ED 17 and ED 18. Maternal (plasma, brain), placental and fetal (plasma, brain) tissues were collected immediately after the last session of SD or after 24 h of recovery from SD. Respective controls were euthanized at ZT 5 on ED 18 or ED 19. Maternal plasma corticosterone and fetal brain KYNA were significantly elevated only after one session of SD on ED 18. Importantly, maternal plasma corticosterone levels correlated significantly with fetal brain KYNA levels. In addition, placental levels of the proinflammatory cytokines interleukin-1β (IL-1β) and interleukin-6 (IL-6) were increased following maternal SD, suggesting a relationship between placental immune response to SD and fetal brain KYNA accumulation. Collectively, our results demonstrate that sleep loss during the last week of gestation can adversely impact maternal stress, placental immune function, and fetal brain KYNA levels. We introduce KYNA as a novel molecular target influenced by sleep loss during pregnancy. © 2019 The Authors.

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