Literature DB >> 22354242

Delayed environmental enrichment reverses sevoflurane-induced memory impairment in rats.

Jennifer Shih1, Laura D V May, Heidi E Gonzalez, Elaine W Lee, Rehan S Alvi, Jeffrey W Sall, Vinuta Rau, Philip E Bickler, Gopal R Lalchandani, Marianna Yusupova, Elliott Woodward, Heejae Kang, Alan J Wilk, Colleen M Carlston, Mortay V Mendoza, Jeremy N Guggenheim, Maximilian Schaefer, Allison M Rowe, Greg Stratmann.   

Abstract

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.

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Year:  2012        PMID: 22354242      PMCID: PMC4146425          DOI: 10.1097/ALN.0b013e318247564d

Source DB:  PubMed          Journal:  Anesthesiology        ISSN: 0003-3022            Impact factor:   7.892


  49 in total

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4.  Isoflurane and sevoflurane affect cell survival and BCL-2/BAX ratio differently.

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Journal:  Brain Res       Date:  2005-03-10       Impact factor: 3.252

Review 5.  Enriched environments, experience-dependent plasticity and disorders of the nervous system.

Authors:  Jess Nithianantharajah; Anthony J Hannan
Journal:  Nat Rev Neurosci       Date:  2006-09       Impact factor: 34.870

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10.  Xenon mitigates isoflurane-induced neuronal apoptosis in the developing rodent brain.

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  62 in total

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3.  Using animal models to evaluate the functional consequences of anesthesia during early neurodevelopment.

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Authors:  Eunchai Kang; Daniel A Berg; Orion Furmanski; William M Jackson; Yun Kyoung Ryu; Christy D Gray; C David Mintz
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Review 6.  Developmental anesthetic neurotoxicity: from animals to humans?

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7.  Androgenic Modulation of the Chloride Transporter NKCC1 Contributes to Age-dependent Isoflurane Neurotoxicity in Male Rats.

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9.  Long-lasting behavioral effects in neonatal mice with multiple exposures to ketamine-xylazine anesthesia.

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10.  Cell age-specific vulnerability of neurons to anesthetic toxicity.

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