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Memory is one of the most vital higher mental functions of the brain. Memory is closely related to learning because it enables us to retain information and experiences from our past to use them in our present life. It also helps us to remember facts, events, and skills, such as riding a bike or swimming. There are two types of memory — declarative memory, which involves memorizing facts or events, and procedural memory, which enables us to remember how to do something like writing or...
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Related Experiment Video

Updated: Feb 11, 2026

Homochronic Transplantation of Interneuron Precursors into Early Postnatal Mouse Brains
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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
Summary

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.

Keywords:
hippocampusmemory impairmentpostnatal mousesevoflurane

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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.