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Updated: Aug 14, 2026
Functional Interrogation of Adult Hypothalamic Neurogenesis with Focal Radiological Inhibition
Published on: November 14, 2013
Propofol Administration During Early Postnatal Life Suppresses Hippocampal Neurogenesis
Jing Huang1, Sheng Jing1, Xi Chen2,3
1Department of Anesthesiology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, People's Republic of China.
Insights
Propofol anesthesia in early life impairs hippocampal neurogenesis and cell proliferation in mice. This may contribute to the cognitive dysfunction observed in adults following anesthesia.
Area of Science:
- Neuroscience
- Anesthesiology
- Developmental Biology
Background:
- Propofol is a widely used intravenous anesthetic.
- Propofol anesthesia has been linked to cognitive dysfunction in adults.
- The impact of early-life propofol exposure on the developing brain remains unclear.
Purpose of the Study:
- To investigate the effects of early postnatal propofol exposure on hippocampal neurogenesis in mice.
- To determine the impact of propofol on neural stem cell proliferation and neuronal development.
Main Methods:
- Propofol was administered to mice on postnatal days 7 or 7-9.
- Cell proliferation and neurogenesis in the dentate gyrus were assessed using BrdU and Sox2 immunostaining.
- Western blotting was used to evaluate Akt and ERK1/2 phosphorylation.
- In vitro studies utilized a neural stem cell line (C17.2).
Main Results:
- Propofol exposure on postnatal day 7 reduced hippocampal cell proliferation (at 60 mg/kg).
- Propofol decreased Akt and ERK1/2 phosphorylation in the hippocampus.
- Postnatal propofol treatment (days 7-9) reduced new neuron numbers and delayed maturation in the dentate gyrus.
- In vitro, propofol suppressed neural stem cell proliferation and induced apoptosis in a dose-dependent manner.
Conclusions:
- Propofol exposure during early postnatal life impairs hippocampal cell proliferation and neurogenesis in mice.
- These effects may be mediated by reduced Akt and ERK1/2 signaling.
- The findings suggest a potential mechanism linking early-life propofol anesthesia to later cognitive dysfunction.
Abstract:
Propofol is currently one of the most widely used intravenous anesthetics and has been indicated to induce cognitive dysfunction in adults. Here, we investigated the effects of propofol exposure during early postnatal life on hippocampal neurogenesis. Propofol (30 or 60 mg/kg) was administered to mice on either postnatal day (P) 7 or P7-P9; cell proliferation and neurogenesis in the dentate gyrus (DG) were evaluated on P8 or P17. It showed that exposure to propofol on P7 decreased hippocampal cell proliferation as indicated by BrdU and Sox2 immunostaining at P8 in propofol treatment at the dosage of 60 mg/kg but not at the dosage of 30 mg/kg. Western blots revealed propofol treatment decreased Akt or extracellular signal-related kinase (ERK) 1/2 phosphorylation in the hippocampus at P8. Propofol treatment on P7 to P9 reduced the numbers of newly formed neurons in the DG at P17, which was accompanied by delay of granule neuron maturation and decreased the density of dendritic spines, particularly the mushroom-shaped mature spines. Furthermore, the in vitro findings indicated propofol suppressed cell proliferation and cell mitosis and activated apoptosis of C17.2 neural stem cell line in a dose-dependent manner. These findings suggest that propofol impairs cell proliferation and inhibits neurogenesis in the immature mouse brain and thus is possibly involved in the cognitive dysfunction induced by propofol anesthesia.
