ArticleBrain and behavior2023
Enriched environment ameliorates postsurgery sleep deprivation-induced cognitive impairments through the AMPA receptor GluA1 subunit.
Article in Brain and behavior, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 5 citations in OpenAlex.
- Does Enriched Environment Improve Chronic Immobilization Stress-Induced Cognitive and Behavioral Changes in Adult Male Rats?Cellular and molecular neurobiology · 2026Article
- Meningeal lymphatic dysfunction mediates postoperative sleep deprivation-induced cognitive decline via impaired neuroinflammatory clearance.Journal of neuroinflammation · 2026Article
- Propofol improves sleep deprivation-induced sleep structural and cognitive deficits via upregulating the BMAL1 expression and suppressing microglial M1 polarization.CNS neuroscience & therapeutics · 2024Article
- Enriched environment ameliorates postsurgery sleep deprivation-induced cognitive impairments through the AMPA receptor GluA1 subunit.Brain and behavior · 2023Article
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5 authors at 1 institution in 1 country.
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Abstract
backgroundAs a common postsurgery complication, sleep deprivation (SD) can severely deteriorate the cognitive function of patients. Enriched environment (EE) exposure can increase children's cognitive ability, and whether EE exposure could be utilized to alleviate postsurgery SD-induced cognitive impairments is investigated in this study.
methodsOpen inguinal hernia repair surgery without skin/muscle retraction was performed on Sprague-Dawley male rats (9-week-old), which were further exposed to EE or standard environment (SE). Elevated plus maze (EPM), novel object recognition (NOR), object location memory (OLM), and Morris Water Maze assays were utilized to monitor cognitive functions. Cresyl violet acetate staining in the Cornusammonis 3 (CA3) region of rat hippocampus was used to detect neuron loss. The relative expression of brain-derived neurotrophic factor (BDNF) and synaptic glutamate receptor 1 (GluA1) subunits in the hippocampus were detected with quantitative reverse transcription polymerase chain reaction (RT-qPCR), Western blots, enzyme-linked immunosorbent assay (ELISA), and immunofluorescence.
resultsEE restored normal levels of time spent in the center, time in distal open arms, open/total arms ratio, and total distance traveled in the EPM test; EE restored normal levels of recognition index in the NOR and OLM test; EE restored normal levels of time in the target quadrant, escape latencies, and platform site crossings in the Morris Water Maze test. EE exposure decreased neuron loss in the CA3 region of the hippocampus with increased BDNF and phosphorylated (p)-GluA1 (ser845) expression.
conclusionEE ameliorates postsurgery SD-induced cognitive impairments, which may be mediated by the axis of BDNF/GluA1. EE exposure could be considered as an aid in promoting cognitive function in postsurgery SD.
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