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Sevoflurane-induced memory impairment in the postnatal developing mouse brain

Zhijun Lu1, Jihui Sun1, Yichun Xin1

  • 1Department of Anesthesia, Rui Jin Hospital Luwan Branch, Shanghai Jiao Tong University School of Medicine, Shanghai 200020, P.R. China.

Experimental and Therapeutic Medicine
|May 8, 2018
PubMed

Insights

Sevoflurane exposure in developing mice impairs memory. This is linked to increased caspase-3 and cleaved PARP, and altered levels of BDNF signaling proteins, suggesting a mechanism for neurotoxicity.

Area of Science:

  • Neuroscience
  • Anesthesiology
  • Developmental Biology

Background:

  • Anesthetic agents like sevoflurane are widely used in pediatric procedures.
  • Emerging evidence suggests potential neurotoxic effects of anesthetics on the developing brain.
  • Understanding the mechanisms of sevoflurane-induced neurotoxicity is crucial for patient safety.

Purpose of the Study:

  • To confirm sevoflurane-induced memory impairment in postnatal developing mouse brains.
  • To elucidate the underlying molecular mechanisms of this impairment.
  • To investigate the roles of apoptosis and neurotrophic factors in sevoflurane neurotoxicity.

Main Methods:

  • Postnatal C57BL/6 mice (7 days old) were exposed to sevoflurane (2.6% or 1.3%) or control conditions.
  • Morris Water Maze (MWM) test assessed spatial learning and memory.
  • Hippocampal tissues were analyzed for caspase-3, cleaved PARP, BDNF, Ntrk2, pro-BDNF, p75NTR, and PKB/Akt levels.
  • Blood gas analysis monitored for hypoxia and respiratory depression.

Main Results:

  • Sevoflurane exposure significantly impaired memory performance in the MWM test.
  • Increased levels of caspase-3 and cleaved poly adenosine diphosphate-ribose polymerase (PARP) were observed.
  • Elevated pro-brain-derived neurotrophic factor (pro-BDNF) and p75 neurotrophin receptor (p75NTR) were detected.
  • Decreased protein kinase B (PKB/Akt) levels were noted in sevoflurane-exposed groups.

Conclusions:

  • Sevoflurane induces memory impairment in the developing mouse brain.
  • The mechanism involves apoptosis, indicated by caspase-3 and cleaved PARP.
  • Alterations in the BDNF signaling pathway (pro-BDNF, p75NTR, PKB/Akt) contribute to sevoflurane-induced neurotoxicity.
Keywords:
hippocampusmemory impairmentpostnatal mousesevoflurane

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