Nicholas W. Gentry , Thomas McMahon , Maya Yamazaki , John Webb , Thomas D. Arnold , Susanna Rosi , Louis J. Ptáček , Ying-Hui Fu
{"title":"Microglia are involved in the protection of memories formed during sleep deprivation","authors":"Nicholas W. Gentry , Thomas McMahon , Maya Yamazaki , John Webb , Thomas D. Arnold , Susanna Rosi , Louis J. Ptáček , Ying-Hui Fu","doi":"10.1016/j.nbscr.2021.100073","DOIUrl":null,"url":null,"abstract":"<div><p>Sleep deprivation can generate inflammatory responses in the central nervous system. In turn, this inflammation increases sleep drive, leading to a rebound in sleep duration. Microglia, the innate immune cells found exclusively in the CNS, have previously been found to release inflammatory signals and exhibit altered characteristics in response to sleep deprivation. Together, this suggests that microglia may be partially responsible for the brain's response to sleep deprivation through their inflammatory activity. In this study, we ablated microglia from the mouse brain and assessed resulting sleep, circadian, and sleep deprivation phenotypes. We find that microglia are dispensable for both homeostatic sleep and circadian function and the sleep rebound response to sleep deprivation. However, we uncover a phenomenon by which microglia appear to be essential for the protection of fear-conditioning memories formed during the recovery sleep period following a period of sleep deprivation. This phenomenon occurs potentially through the upregulation of synaptic-homeostasis related genes to protect nascent dendritic spines that may be otherwise removed or downscaled during recovery sleep. These findings further expand the list of known functions for microglia in synaptic modulation.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"12 ","pages":"Article 100073"},"PeriodicalIF":0.0000,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ce/99/main.PMC8741522.pdf","citationCount":"8","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurobiology of Sleep and Circadian Rhythms","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2451994421000146","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 8
Abstract
Sleep deprivation can generate inflammatory responses in the central nervous system. In turn, this inflammation increases sleep drive, leading to a rebound in sleep duration. Microglia, the innate immune cells found exclusively in the CNS, have previously been found to release inflammatory signals and exhibit altered characteristics in response to sleep deprivation. Together, this suggests that microglia may be partially responsible for the brain's response to sleep deprivation through their inflammatory activity. In this study, we ablated microglia from the mouse brain and assessed resulting sleep, circadian, and sleep deprivation phenotypes. We find that microglia are dispensable for both homeostatic sleep and circadian function and the sleep rebound response to sleep deprivation. However, we uncover a phenomenon by which microglia appear to be essential for the protection of fear-conditioning memories formed during the recovery sleep period following a period of sleep deprivation. This phenomenon occurs potentially through the upregulation of synaptic-homeostasis related genes to protect nascent dendritic spines that may be otherwise removed or downscaled during recovery sleep. These findings further expand the list of known functions for microglia in synaptic modulation.
期刊介绍:
Neurobiology of Sleep and Circadian Rhythms is a multidisciplinary journal for the publication of original research and review articles on basic and translational research into sleep and circadian rhythms. The journal focuses on topics covering the mechanisms of sleep/wake and circadian regulation from molecular to systems level, and on the functional consequences of sleep and circadian disruption. A key aim of the journal is the translation of basic research findings to understand and treat sleep and circadian disorders. Topics include, but are not limited to: Basic and translational research, Molecular mechanisms, Genetics and epigenetics, Inflammation and immunology, Memory and learning, Neurological and neurodegenerative diseases, Neuropsychopharmacology and neuroendocrinology, Behavioral sleep and circadian disorders, Shiftwork, Social jetlag.