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Astroglial dysfunctions drive aberrant synaptogenesis and social behavioral deficits in mice with neonatal exposure

Bin Zhou1,2,3, Lingmin Chen1,2,3, Ping Liao1,2,3

  • 1Laboratory of Anesthesia and Critical Care Medicine, Sichuan University, Chengdu, Sichuan, China.

Plos Biology
|August 22, 2019
PubMed

Insights

General anesthetics like sevoflurane can harm developing brains. This study shows astrocytes are key targets, and restoring Ezrin protein function can reverse neurobehavioral deficits in young mice.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Anesthesiology

Background:

  • General anesthetics (GAs) pose risks to the developing brain, prompting FDA warnings for young children.
  • Mechanisms of GA-induced neurotoxicity are not fully understood.
  • Sevoflurane (Sevo) is a widely used pediatric GA.

Purpose of the Study:

  • Investigate the molecular and cellular mechanisms of sevoflurane-induced neurotoxicity in the developing brain.
  • Determine the role of astrocytes in GA neurotoxicity.
  • Identify potential therapeutic targets to mitigate GA-induced neurodevelopmental deficits.

Main Methods:

  • Exposed developing mice to sevoflurane.
  • Assessed astrocyte morphogenesis, synaptic function, and Ca2+ homeostasis.
  • Investigated the role of Ezrin protein in astrocyte function and development.
  • Utilized overexpression of Ezrin to rescue Sevo-induced deficits.

Main Results:

  • Sevoflurane exposure impaired astrocyte development and synaptic function in a region-, duration-, and age-specific manner.
  • Sevoflurane disrupted astrocyte calcium (Ca2+) homeostasis, leading to decreased Ezrin levels.
  • Overexpressing astrocyte Ezrin reversed astrocytic, neuronal, and social behavior deficits in mice exposed to sevoflurane.

Conclusions:

  • Astrocytes, not just neurons, are critical targets for GA neurotoxicity.
  • Astrocyte morphological integrity, regulated by Ezrin, is essential for proper synaptogenesis and neurological behavior.
  • Targeting astrocyte Ezrin may offer a therapeutic strategy against GA-induced neurodevelopmental harm.

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