Related Experiment Video
Updated: May 24, 2026
The Use of the Puzzle Box as a Means of Assessing the Efficacy of Environmental Enrichment
Published on: December 29, 2014
Delayed environmental enrichment reverses sevoflurane-induced memory impairment in rats
Jennifer Shih1, Laura D V May, Heidi E Gonzalez
1Department of Anesthesia, University of California San Francisco, San Francisco, California 94143, USA.
Insights
General anesthesia in young rodents can impair cognitive function, but this effect is treatable. Delayed environmental enrichment can reverse anesthesia-induced short-term memory deficits in rats, offering hope for pediatric anesthesia.
Area of Science:
- Neuroscience
- Anesthesiology
- Developmental Biology
Background:
- General anesthesia in immature rodents causes cognitive decline.
- This raises concerns for children undergoing surgery under anesthesia.
- The study investigated if anesthesia-induced cognitive decline is treatable and aggravated by tissue injury.
Purpose of the Study:
- To determine if anesthesia-induced cognitive decline in rats is reversible.
- To assess if tissue injury exacerbates anesthesia-induced cognitive deficits.
- To explore potential therapeutic interventions for anesthesia-related cognitive impairments.
Main Methods:
- Seven-day-old rats received sevoflurane anesthesia (1 MAC, 4h) with or without tail clamping.
- Rats were housed in enriched or standard environments from 4 weeks.
- Neurocognitive testing at 8 weeks assessed memory consolidation and different memory types.
Main Results:
- Sevoflurane anesthesia impaired short-term memory in rats, evidenced by increased escape latency with longer delays.
- Delayed environmental enrichment successfully reversed sevoflurane-induced short-term memory deficits.
- Tail clamping did not worsen anesthesia-induced memory impairment.
Conclusions:
- Anesthesia-induced cognitive decline in rats is treatable.
- Environmental enrichment is a potential intervention for sevoflurane-induced memory impairment.
- Tissue injury does not appear to exacerbate anesthesia-related cognitive deficits in this model.
Background:
Anesthesia given to immature rodents causes cognitive decline, raising the possibility that the same might be true for millions of children undergoing surgical procedures under general anesthesia each year. We tested the hypothesis that anesthesia-induced cognitive decline in rats is treatable. We also tested if anesthesia-induced cognitive decline is aggravated by tissue injury.
Methods:
Seven-day old rats underwent sevoflurane anesthesia (1 minimum alveolar concentration, 4 h) with or without tail clamping. At 4 weeks, rats were randomized to environmental enrichment or normal housing. At 8 weeks rats underwent neurocognitive testing, which consisted of fear conditioning, spatial reference memory, and water maze-based memory consolidation tests, and interrogated working memory, short-term memory, and early long-term memory.
Results:
Sevoflurane-treated rats had a greater escape latency when the delay between memory acquisition and memory retrieval was increased from 1 min to 1 h, indicating that short-term memory was impaired. Delayed environmental enrichment reversed the effects of sevoflurane on short-term memory and generally improved many tested aspects of cognitive function, both in sevoflurane-treated and control animals. The performance of tail-clamped rats did not differ from those rats receiving anesthesia alone.
Conclusion:
Sevoflurane-induced cognitive decline in rats is treatable. Delayed environmental enrichment rescued the sevoflurane-induced impairment in short-term memory. Tissue injury did not worsen the anesthesia-induced memory impairment. These findings may have relevance to neonatal and pediatric anesthesia.
