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SAHA attenuates sevoflurane-induced learning and memory impairments in fetal mice
1Department of Anesthesiology, Huashan Hospital, Fudan University, Shanghai, China.
Insights
Repeated exposure to sevoflurane anesthesia in young mice impairs learning and memory. Treatment with suberanilohydroxamic acid (SAHA) reversed these effects, suggesting SAHA as a potential therapeutic for anesthesia-induced neurotoxicity.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Multiple early-life exposures to anesthesia, particularly sevoflurane, are linked to learning and memory deficits in children.
- Sevoflurane exposure in fetal mice induces neuroinflammation, inhibits neurogenesis, and impairs cognitive functions.
- Histone acetylation plays a crucial role in memory formation processes.
Purpose of the Study:
- To investigate the therapeutic potential of suberanilohydroxamic acid (SAHA) in mitigating sevoflurane-induced learning and memory impairments.
- To evaluate the effects of SAHA on neurotoxicity caused by early-life sevoflurane exposure.
Main Methods:
- Six-day-old C57BL/6 mice underwent daily 2-hour sevoflurane exposure for three consecutive days.
- Learning and memory were assessed using the Morris water maze test.
- Gene expression related to synaptic plasticity, neuronal activity, and cell cycle was analyzed via real-time PCR.
Main Results:
- Mice exposed to sevoflurane exhibited significant learning and memory impairments.
- SAHA treatment effectively attenuated the sevoflurane-induced cognitive deficits.
- SAHA demonstrated potential in reversing anesthesia-related neurotoxicity.
Conclusions:
- Suberanilohydroxamic acid (SAHA) shows promise in ameliorating learning and memory impairments caused by early-life sevoflurane exposure.
- SAHA may serve as a viable therapeutic agent for preventing or treating anesthesia-induced neurotoxicity in developing brains.
Abstract:
Previous studies have found that children with multiple exposures to anesthesia at an early age are at increased risk of learning and memory impairment. Sevoflurane is the most commonly used inhalational anesthetic for general anesthesia in children. Multiple exposures to sevoflurane have been shown to induce neuroinflammation, inhibit neurogenesis, and cause subsequent learning and memory impairments in fetal mice. Histone-tail acetylation has been implicated in memory formation. In this study, we employed suberanilohydroxamic acid (SAHA), an inhibitor of histone deacetylases, to treat sevoflurane-induced learning and memory impairments. Six-day-old C57BL/6 mice were exposed to sevoflurane for 2 h daily for 3 days. Morris water maze test performed to evaluate learning and memory impairments and the expression of genes related in to synaptic remodeling/plasticity, or regulated by neuronal activity or the cell cycle were detected by real-time PCR. We found that SAHA attenuated sevoflurane-induced learning and memory impairments in fetal mice. Our findings suggest that SAHA may have potential as a therapeutic agent for preventing or treating the neurotoxicity associated with anesthesia.
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