Short-term sleep deprivation stimulates hippocampal neurogenesis in rats following global cerebral ischemia/reperfusion.

Oumei Cheng,Lijuan Yu,Junqing Yang,Lei Zhao,Beibei Chen,Bin Yang,Jia Wang,Rong Li,Quanguang Zhang

doi:10.1371/journal.pone.0125877

Abstract

BackgroundSleep deprivation (SD) plays a complex role in central nervous system (CNS) diseases. Recent studies indicate that short-term SD can affect the extent of ischemic damage. The aim of this study was to investigate whether short-term SD could stimulate hippocampal neurogenesis in a rat model of global cerebral ischemia/reperfusion (GCIR).MethodsOne hundred Sprague-Dawley rats were randomly divided into Sham, GCIR and short-term SD groups based on different durations of SD; the short-term SD group was randomly divided into three subgroups: the GCIR+6hSD*3d-treated, GCIR+12hSD-treated and GCIR+12hSD*3d-treated groups. The GCIR rat model was induced via the bilateral occlusion of the common carotid arteries and hemorrhagic hypotension. The rats were sleep-deprived starting at 48 h following GCIR. A Morris water maze test was used to assess learning and memory ability; cell proliferation and differentiation were analyzed via 5-bromodeoxyuridine (BrdU) and neuron-specific enolase (NSE), respectively, at 14 and 28 d; the expression of hippocampal BDNF was measured after 7 d.ResultsThe different durations of short-term SD designed in our experiment exhibited improvement in cognitive function as well as increased hippocampal BDNF expression. Additionally, the short-term SD groups also showed an increased number of BrdU- and BrdU/NSE-positive cells compared with the GCIR group. Of the three short-term SD groups, the GCIR+12hSD*3d-treated group experienced the most substantial beneficial effects.ConclusionsShort-term SD, especially the GCIR+12hSD*3d-treated method, stimulates neurogenesis in the hippocampal dentate gyrus (DG) of rats that undergo GCIR, and BDNF may be an underlying mechanism in this process.

Highlights

Short-term sleep deprivation (SD), especially the Global cerebral ischemia/reperfusion (GCIR)+12hSD*3d-treated method, stimulates neurogenesis in the hippocampal dentate gyrus (DG) of rats that undergo GCIR, and Brain-derived neurotrophic factor (BDNF) may be an underlying mechanism in this process
Global cerebral ischemia/reperfusion (GCIR), a syndrome characterized by the rapid interruption of cerebral blood flow, occurs in patients who suffer from cardiac arrest, shock or complex cardiac surgery and is usually accompanied by a broad range of neuronal death in the brain[1,2,3]
Compared with the S group, the rats subjected to GCIR showed a prolonged escape latency, which implies that global ischemia significantly impaired spatial learning ability, and this impairment occurred from training day 1 onward (p

Summary

Introduction

Global cerebral ischemia/reperfusion (GCIR), a syndrome characterized by the rapid interruption of cerebral blood flow, occurs in patients who suffer from cardiac arrest, shock or complex cardiac surgery and is usually accompanied by a broad range of neuronal death in the brain[1,2,3]. Many of these patients suffer from various degrees of memory loss and learning dysfunction, suggesting an impairment in the hippocampus, which is the primary region of the brain that controls the formation of memories and learned behaviors[4, 5]. The aim of this study was to investigate whether short-term SD could stimulate hippocampal neurogenesis in a rat model of global cerebral ischemia/reperfusion (GCIR).

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