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Published on: May 12, 2015
Neonatal propofol exposure impairs synaptic plasticity and cognition, associated with BAG3 upregulation and disrupted
Liurong Chen1,2, Chenlu Wang3, Yinan Lin4
1Department of Anesthesiology, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Insights
Early-life exposure to propofol impairs brain development in neonatal mice, affecting neurogenesis and synaptic plasticity. The stress-responsive protein BAG3 is upregulated, suggesting it as a potential marker for anesthetic-induced neurotoxicity.
Area of Science:
- Neuroscience
- Anesthesiology
- Developmental Biology
Background:
- Propofol is a common anesthetic in pediatric care.
- Repeated early-life exposure to propofol may adversely affect brain development.
- The co-chaperone protein Bag3 is involved in proteostasis and neuronal stress response, potentially regulating synaptic function during brain maturation.
Purpose of the Study:
- To investigate the effects of early-life propofol exposure on neurogenesis, synaptic plasticity, and behavior in neonatal mice.
- To examine the role of Bag3 expression in response to propofol-induced neurotoxicity.
Main Methods:
- Neonatal mice received propofol on postnatal days 5-7.
- Assessed hippocampal neurogenesis using BrdU immunofluorescence.
- Measured synaptic protein (PSD95, SNAP25) and Bag3 expression via Western blotting.
- Evaluated adolescent behavior using multiple maze tests and open-field tests.
Main Results:
- Propofol exposure reduced neurogenesis in the dentate gyrus and decreased PSD95/SNAP25 expression in the cortex and hippocampus.
- Bag3 expression was significantly upregulated, with a mild increase in its phosphorylated form.
- Propofol-treated mice exhibited anxiety-like behavior and deficits in spatial learning and working memory.
Conclusions:
- Early-life propofol exposure impairs neurogenesis and synaptic plasticity.
- Upregulation of the stress-responsive protein BAG3 is associated with these effects.
- BAG3 is identified as a potential correlative marker for anesthetic-induced neurotoxicity and a target for future research.
Background:
Propofol is widely used in pediatric anesthesia, but it has been implicated in adverse effects on brain development following repeated early-life exposure. Bag3, a co-chaperone protein involved in proteostasis and the neuronal stress response, may play a critical role in regulating synaptic function during early brain maturation.
Methods:
Neonatal mice were treated with propofol on postnatal days 5-7. Hippocampal neurogenesis was assessed via BrdU immunofluorescence. Synaptic proteins (PSD95, SNAP25) and Bag3 expression were measured by Western blotting. Behavioral performance in adolescence was evaluated using open-field, elevated plus-maze, Morris water maze, Y-maze, and T-maze tests.
Results:
Propofol exposure significantly reduced proliferative activity (BrdU incorporation) in the dentate gyrus and decreased PSD95 and SNAP25 expression in both the cortex and hippocampus. Bag3 expression was markedly upregulated, accompanied by a mild increase in its phosphorylated form. Behaviorally, propofol-treated mice showed anxiety-like behavior and impairments in spatial learning and working memory.
Conclusion:
These findings suggest that early-life exposure to propofol impairs neurogenesis and synaptic plasticity. This process is temporally associated with the upregulation of stress-responsive co-chaperone BAG3, which precedes the of synaptic protein homeostasis. While causal relationship remains to be established, these findings identifies BAG3 as a candidate correlative marker of anesthetic-induced neurotoxicity and highlights it as a target for future mechanistic studies.
