Enriched environment ameliorates postsurgery sleep deprivation-induced cognitive impairments through the AMPA receptor GluA1 subunit.

Abstract

As 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. Open 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. EE 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. EE 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.