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Related Experiment Video

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The decrease of NMDAR subunit expression and NMDAR EPSC in hippocampus by neonatal exposure to desflurane in mice.

Xinyu Xu1, Chen Zheng1, Nan Li2

  • 1Laboratory of Neurobiology in Medicine, School of Biomedical Engineering, Tianjin Medical University, Tianjin 300070, China.

Behavioural Brain Research
|September 19, 2016
PubMed
Summary

Neonatal exposure to high concentrations of desflurane (1.5MAC) impaired memory function in mice. This desflurane exposure reduced N-methyl-D-aspartate receptor (NMDAR) expression and activity in the hippocampus.

Keywords:
DesfluraneHippocampusMiceNMDARNeonatal

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Area of Science:

  • Neuroscience
  • Anesthesiology
  • Developmental Biology

Background:

  • Desflurane is a modern inhaled anesthetic used in pediatric and obstetric care.
  • The impact of neonatal desflurane exposure on brain development remains largely uncharacterized.

Purpose of the Study:

  • To investigate the effects of neonatal desflurane exposure on memory and N-methyl-D-aspartate receptor (NMDAR) function in mice.

Main Methods:

  • Neonatal mice (6 days old) were exposed to desflurane (1.0 or 1.5 Minimum Alveolar Concentration [MAC]) for 2 hours.
  • Cognitive functions (activity, working memory, long-term memory) were assessed at 28 days old.
  • Hippocampal NMDAR subunit expression and NMDAR-mediated excitatory postsynaptic current (EPSC) were analyzed.

Main Results:

  • Exposure to 1.5 MAC desflurane significantly impaired working memory and fear conditioning memory in 28-day-old mice.
  • A significant decrease in hippocampal NMDAR subunits (NR1, NR2B) protein expression and NMDAR-mediated EPSC was observed.
  • No significant cognitive or molecular changes were found in mice exposed to 1.0 MAC desflurane compared to controls.

Conclusions:

  • Neonatal exposure to high-concentration desflurane (1.5 MAC) leads to lasting memory deficits in mice.
  • Reduced NMDAR expression and function in the hippocampus may underlie these cognitive impairments.