Time is of the essence : Coupling sleep-wake and circadian neurobiology to the antidepressant effects of ketamine

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Kohtala , S , Alitalo , O , Rosenholm , M , Rozov , S & Rantamäki , T 2021 , ' Time is of the essence : Coupling sleep-wake and circadian neurobiology to the antidepressant effects of ketamine ' , Pharmacology & Therapeutics , vol. 221 , 107741 , pp. 107741 . https://doi.org/10.1016/j.pharmthera.2020.107741

Titel: Time is of the essence : Coupling sleep-wake and circadian neurobiology to the antidepressant effects of ketamine
Författare: Kohtala, S.; Alitalo, O.; Rosenholm, M.; Rozov, S.; Rantamäki, T.
Upphovmannens organisation: Division of Pharmacology and Pharmacotherapy
Laboratory of Neurotherapeutics
Drug Research Program
SLEEPWELL Research Program
Medicum
INDIVIDRUG - Individualized Drug Therapy
Doctoral Programme Brain & Mind
Divisions of Faculty of Pharmacy
Datum: 2021-05
Språk: eng
Sidantal: 17
Tillhör serie: Pharmacology & Therapeutics
ISSN: 0163-7258
DOI: https://doi.org/10.1016/j.pharmthera.2020.107741
Permanenta länken (URI): http://hdl.handle.net/10138/330390
Abstrakt: Several studies have demonstrated the effectiveness of ketamine in rapidly alleviating depression and suicidal ideation. Intense research efforts have been undertaken to expose the precise mechanism underlying the antidepressant action of ketamine; however, the translation of findings into new clinical treatments has been slow. This translational gap is partially explained by a lack of understanding of the function of time and circadian timing in the complex neurobiology around ketamine. Indeed, the acute pharmacological effects of a single ketamine treatment last for only a few hours, whereas the antidepressant effects peak at around 24 hours and are sustained for the following few days. Numerous studies have investigated the acute and long-lasting neurobiological changes induced by ketamine; however, the most dramatic and fundamental change that the brain undergoes each day is rarely taken into consideration. Here, we explore the link between sleep and circadian regulation and rapid-acting antidepressant effects and summarize how diverse phenomena associated with ketamine’s antidepressant actions – such as cortical excitation, synaptogenesis, and involved molecular determinants – are intimately connected with the neurobiology of wake, sleep, and circadian rhythms. We review several recently proposed hypotheses about rapid antidepressant actions, which focus on sleep or circadian regulation, and discuss their implications for ongoing research. Considering these aspects may be the last piece of the puzzle necessary to gain a more comprehensive understanding of the effects of rapid-acting antidepressants on the brain.Several studies have demonstrated the effectiveness of ketamine in rapidly alleviating depression and suicidal ideation. Intense research efforts have been undertaken to expose the precise mechanism underlying the antidepressant action of ketamine; however, the translation of findings into new clinical treatments has been slow. This translational gap is partially explained by a lack of understanding of the function of time and circadian timing in the complex neurobiology around ketamine. Indeed, the acute pharmacological effects of a single ketamine treatment last for only a few hours, whereas the antidepressant effects peak at around 24 hours and are sustained for the following few days. Numerous studies have investigated the acute and long-lasting neurobiological changes induced by ketamine; however, the most dramatic and fundamental change that the brain undergoes each day is rarely taken into consideration. Here, we explore the link between sleep and circadian regulation and rapid -acting antidepressant effects and summarize how diverse phenomena associated with ketamine's antidepressant actions - such as cortical excitation, synaptogenesis, and involved molecular determinants - are intimately connected with the neurobiology of wake, sleep, and circadian rhythms. We review several recently proposed hypotheses about rapid antidepressant actions, which focus on sleep or circadian regulation, and discuss their implications for ongoing research. Considering these aspects may be the last piece of the puzzle necessary to gain a more comprehensive understanding of the effects of rapid-acting antidepressants on the brain. (c) 2020 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY license (http:// creativecommons.org/licenses/by/4.0/).
Subject: Sleep
Circadian
Plasticity
Depression
Rapid-acting antidepressant
Slow-wave sleep
GLYCOGEN-SYNTHASE KINASE-3
RESISTANT MAJOR DEPRESSION
LONG-TERM POTENTIATION
CLOCK GENE-EXPRESSION
BRIGHT LIGHT THERAPY
BLOOD-BRAIN-BARRIER
SLOW-WAVE ACTIVITY
SUPRACHIASMATIC NUCLEUS
NEUROTROPHIC FACTOR
PREFRONTAL CORTEX
317 Pharmacy
3112 Neurosciences
Referentgranskad: Ja
Licens: cc_by
Användningsbegränsning: openAccess
Parallelpublicerad version: publishedVersion


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