Related Experiment Video

Updated: Jan 18, 2026

A Neonatal Mouse Spinal Cord Compression Injury Model
13:31

A Neonatal Mouse Spinal Cord Compression Injury Model

Published on: March 27, 2016

13.1K

Developmental neuroplasticity enables recovery from anesthetic-induced synaptic perturbations in the immature brain

Lixi Chen1, Zhiduo Zhang1, Shana Yang2

  • 1Guangdong Provincial Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China; Advanced Medical Technology Center, the First Affiliated Hospital, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.

Neurochemistry International
|September 10, 2025
PubMed

Insights

Pediatric anesthesia with sevoflurane causes temporary brain changes in mice, but the developing brain shows remarkable resilience. Full recovery occurs within 24 hours, reassuring its safe use in children.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Anesthesiology

Background:

  • General anesthetics are crucial for pediatric procedures.
  • Concerns exist about potential neurotoxicity of anesthetics on the developing brain.
  • The long-term effects of transient synaptic disruptions from anesthesia are not fully understood.

Purpose of the Study:

  • To investigate the structural and functional consequences of sevoflurane exposure on the developing brain.
  • To determine if anesthesia-induced effects are transient or lead to long-term deficits.
  • To assess the role of endogenous neuroplasticity in mitigating anesthetic effects.

Main Methods:

  • Longitudinal in vivo two-photon imaging in awake mice.
  • Clinically relevant exposure to sevoflurane at postnatal day 20.
  • Electrophysiological recording and calcium imaging.

Main Results:

  • Sevoflurane caused transient hyperactivity and suppressed filopodia elimination, fully reversed within 24 hours.
  • No persistent alterations in synaptogenesis, neuronal activity, motor learning, or anxiety-like behavior were observed over 10 days.
  • Restoration of normal neuronal firing and synaptic transmission was confirmed.

Conclusions:

  • The developing brain exhibits intrinsic resilience to transient anesthetic insults.
  • A dual-phase recovery mechanism (acute plasticity followed by chronic convergence) is involved.
  • Sevoflurane acts as a temporary challenge buffered by neuroplasticity, not a source of irreversible neurotoxicity.

Keywords:
AnesthesiaIn vivo imagingLong-term anesthetic neurotoxicitySevofluraneSynaptogenesis

More Related Videos

Adaptation of Microelectrode Array Technology for the Study of Anesthesia-induced Neurotoxicity in the Intact Piglet Brain08:23

Adaptation of Microelectrode Array Technology for the Study of Anesthesia-induced Neurotoxicity in the Intact Piglet Brain

Published on: May 12, 2018

9.9K
Assessing Changes in Synaptic Plasticity Using an Awake Closed-Head Injury Model of Mild Traumatic Brain Injury09:49

Assessing Changes in Synaptic Plasticity Using an Awake Closed-Head Injury Model of Mild Traumatic Brain Injury

Published on: January 20, 2023

3.6K

Related Concept Videos

Neuroplasticity01:01

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
1.6K
Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
1.6K
Long-term Potentiation01:35

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
58.3K
Long-term Potentiation01:25

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when...
3.4K