Jennifer R Goldschmied1, Philip Gehrman2. 1. Center for Sleep and Circadian Neurobiology, University of Pennsylvania, 125 S.31st St., Philadelphia, PA, 19104, USA. jrgolds2@pennmedicine.upenn.edu. 2. Center for Sleep and Circadian Neurobiology, University of Pennsylvania, 125 S.31st St., Philadelphia, PA, 19104, USA.
Abstract
PURPOSE OF REVIEW: In this review, we aim to integrate the most recent research highlighting alterations in sleep slow-wave activity (SWA), and impairments in neuroplasticity in major depressive disorder (MDD) into a novel model of disorder maintenance. RECENT FINDINGS: Sleep homeostasis has been shown to be impaired in MDD, with a subset of individuals also demonstrating impaired SWA. SWA is considered a marker of the homeostatic regulation of sleep, and is implicated in the downscaling of synaptic strength in the context of maintaining homeostatic plasticity. Individuals with MDD have been shown to exhibit impairments in both neural plasticity such as loss of dendritic branching, and synaptic plasticity such as decreased long-term potentiation-dependent learning and memory. Alterations in the homeostatic regulation of sleep, SWA, and synaptic plasticity in MDD suggest an underlying impairment in the modulation of synaptic strength. One candidate mechanism for this impairment is AMPA receptor trafficking.
PURPOSE OF REVIEW: In this review, we aim to integrate the most recent research highlighting alterations in sleep slow-wave activity (SWA), and impairments in neuroplasticity in major depressive disorder (MDD) into a novel model of disorder maintenance. RECENT FINDINGS:Sleep homeostasis has been shown to be impaired in MDD, with a subset of individuals also demonstrating impaired SWA. SWA is considered a marker of the homeostatic regulation of sleep, and is implicated in the downscaling of synaptic strength in the context of maintaining homeostatic plasticity. Individuals with MDD have been shown to exhibit impairments in both neural plasticity such as loss of dendritic branching, and synaptic plasticity such as decreased long-term potentiation-dependent learning and memory. Alterations in the homeostatic regulation of sleep, SWA, and synaptic plasticity in MDD suggest an underlying impairment in the modulation of synaptic strength. One candidate mechanism for this impairment is AMPA receptor trafficking.
Authors: Graham H Diering; Raja S Nirujogi; Richard H Roth; Paul F Worley; Akhilesh Pandey; Richard L Huganir Journal: Science Date: 2017-02-02 Impact factor: 47.728
Authors: Elaine M Boland; Hengyi Rao; David F Dinges; Rachel V Smith; Namni Goel; John A Detre; Mathias Basner; Yvette I Sheline; Michael E Thase; Philip R Gehrman Journal: J Clin Psychiatry Date: 2017 Sep/Oct Impact factor: 4.384
Authors: Okko Alitalo; Roosa Saarreharju; Ioline D Henter; Carlos A Zarate; Samuel Kohtala; Tomi Rantamäki Journal: Prog Neurobiol Date: 2021-08-14 Impact factor: 10.885
Authors: Boram Kim; Suzanne De La Monte; Virginia Hovanesian; Aparna Patra; Xiaodi Chen; Ray H Chen; Miles C Miller; Mehmet Halit Pinar; Yow-Pin Lim; Edward G Stopa; Barbara S Stonestreet Journal: J Neurosci Res Date: 2019-12-04 Impact factor: 4.164
Authors: Amandine Valomon; Brady A Riedner; Stephanie G Jones; Keith P Nakamura; Giulio Tononi; David T Plante; Ruth M Benca; Melanie Boly Journal: Sci Rep Date: 2021-02-26 Impact factor: 4.379
Authors: Daniela Dudysová; Karolina Janků; Michal Šmotek; Elizaveta Saifutdinova; Jana Kopřivová; Jitka Bušková; Bryce Anthony Mander; Martin Brunovský; Peter Zach; Jakub Korčák; Veronika Andrashko; Michaela Viktorinová; Filip Tylš; Anna Bravermanová; Tom Froese; Tomáš Páleníček; Jiří Horáček Journal: Front Pharmacol Date: 2020-12-03 Impact factor: 5.810