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Updated: Apr 8, 2026
Automated High-throughput Behavioral Analyses in Zebrafish Larvae
Published on: July 4, 2013
Zebrafish as a model for studying the developmental neurotoxicity of propofol
Peipei Guo1, Zhibin Huang2, Tao Tao1
1Department of Anesthesiology, Nanfang Hospital of Southern Medical University, Guangzhou, Guangdong, China.
Insights
Propofol anesthesia during embryonic development in zebrafish increases cell death and decreases myelin basic protein (MBP) expression, indicating potential neurotoxicity. Zebrafish serve as a model to study these adverse effects.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Anesthetics can induce neurodegeneration and affect synaptogenesis in early life.
- Myelin basic protein (MBP) is crucial for synaptogenesis, but propofol's impact on MBP during embryonic development is largely unknown.
Purpose of the Study:
- To investigate the effects of propofol exposure on embryonic development, apoptosis, and MBP expression in zebrafish.
- To establish zebrafish as a model for studying propofol-induced neurotoxicity.
Main Methods:
- Zebrafish embryos were exposed to varying concentrations of propofol (1-3 µg/mL) from 6 to 48 hours postfertilization.
- Assessed survival, hatchability, developmental aberrations, cell apoptosis (caspase-3, -8, -9), and MBP gene/protein expression.
Main Results:
- Propofol exposure led to decreased hatchability and increased developmental aberrations.
- Significant increases in apoptotic cells and caspase expression were observed in propofol-treated embryos and larvae.
- Propofol exposure dose-dependently reduced MBP gene and protein expression in the zebrafish central nervous system.
Conclusions:
- Embryonic exposure to propofol is neurotoxic to zebrafish, inducing apoptosis and reducing MBP expression.
- Zebrafish provide a valuable model for elucidating the mechanisms underlying propofol neurotoxicity.
Abstract:
Anesthetics can cause widespread apoptotic neurodegeneration and adverse effects on synaptogenesis during early postnatal life. Synaptogenesis correlates with several proteins, including myelin basic protein (MBP). However, little is known about the adverse effects of exposure to propofol on MBP, particularly during embryonic development. Our goal was to use zebrafish to explore the effect of propofol on embryonic development, apoptosis and MBP expression. Zebrafish embryos were exposed to propofol at defined doses and stages from 6 to 48 h postfertilization by immersion. The survival rate, hatchability, aberration rate, cell apoptosis and gene expression were analyzed at defined stages. Analysis revealed that doses of 1, 2 and 3 µg ml(-1) propofol were reasonable anesthetic concentrations for zebrafish embryos. These doses of propofol caused a significant decrease in hatchability and an increase in aberration rate. Moreover, 6 days postfertilization (dpf) larvae are anesthetized by immersion into water containing 1, 2 or 3 µg ml(-1) of propofol. The number of apoptotic cells in the head of propofol-treated 36 h postfertilization embryos were significantly increased, and the expression of caspases-3, -8 and -9 were upregulated. Apoptosis was also induced in the brain of 3 dpf larvae exposed to propofol. However, propofol caused a decrease in mbp gene and protein (dose-dependent) expression levels in the central nervous system of 3 dpf zebrafish. These data show that embryonic exposure to propofol is neurotoxic, causing increased apoptosis and decreased MBP expression. We believe zebrafish can be used as a novel model to explore the mechanisms of propofol neurotoxicity.
