REM Sleep Deprivation Reverses Neurochemical and Other Depressive-Like Alterations Induced by Olfactory Bulbectomy

Maturana, Maira J.; Pudell, Cláudia; Targa, Adriano; Rodrigues, Laís S.; Noseda, Ana Carolina D.; Fortes, Mariana H.; Santos, Patricia C. Dos; Cunha, Cláudio Da; Zanata, Sı́lvio M.; Ferraz, Anete Curte; Lima, Marcelo M.S.

doi:10.1007/s12035-014-8721-x

Cited by 27 publications

(15 citation statements)

References 52 publications

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“…The genetic basis of both amygdala hyperactivity and increased REM density should also be investigated, as the identification of specific genetic variants involved in these two vulnerability factors is likely to improve the way in which we understand the development and underlying pathophysiology of depression. Finally, mechanisms underlying sleep deprivation therapy (Benedetti & Colombo, 2011;Maturana et al, 2015) and antidepressant medications which suppress REM sleep (Mayers & Baldwin, 2005;Palagini et al, 2013;Steiger & Kimura, 2010) should be investigated. It seems likely that their efficacy may relate to the prevention of emotional memory processing which typically occurs during REM sleep.…”

Section: Mmentioning

confidence: 99%

The influence of REM sleep and SWS on emotional memory consolidation in participants reporting depressive symptoms

Harrington

Johnson

Croom

et al. 2018

Cortex

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Negative emotional memory bias is thought to play a causal role in the onset and maintenance of major depressive disorder. Rapid Eye Movement (REM) sleep has been shown to selectively consolidate negative emotional memories in healthy participants, and is greater in quantity and density in depressed patients. Slow-Wave Sleep (SWS) is typically associated with the consolidation of non-emotional memories. However, the effects of REM sleep and SWS on emotional memory consolidation have not been investigated in participants reporting depressive symptoms. In this study, we recruited two groups of healthy participants; one reporting mild-to-moderate depressive symptoms, and another reporting minimal depressive symptoms (assessed using the Beck Depression Inventory; BDI-II). Using a within-subjects split-night design, we measured consolidation of positive, neutral and negative images across a 3 h retention interval rich in either REM sleep or SWS. We found a significant sleep condition x image valence interaction in participants reporting depressive symptoms [F (2, 20) = 4.73, p = .021], but not participants reporting minimal depressive symptoms [F (2, 22) = .17, p = .845]. Participants reporting depressive symptoms consolidated significantly more neutral memories during SWS, and marginally more negative memories during REM sleep, than those reporting minimal depressive symptoms [t (21) = 2.44, p = .023; t (21) = 1.96, p = .064, respectively]. Our preliminary results demonstrate that REM sleep and SWS have differential effects on the consolidation of emotional and neutral images in participants reporting depressive symptoms. Further studies including larger sample sizes are required to investigate whether REM sleep alterations promote the development of negative memory bias in major depressive disorder.

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Section: Mmentioning

confidence: 99%

The influence of REM sleep and SWS on emotional memory consolidation in participants reporting depressive symptoms

Harrington

Johnson

Croom

et al. 2018

Cortex

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“…( 40 , 41 ) for reviews]. Finally, manipulations of the sleep/wake cycle can alleviate depression symptoms ( 42 , 43 ). Together, these data suggest that factors that increase vulnerability to sleep disruption could contribute to the development of stress-related psychiatric disorders.…”

Section: Introductionmentioning

confidence: 99%

Repeated Exposure to Conditioned Fear Stress Increases Anxiety and Delays Sleep Recovery Following Exposure to an Acute Traumatic Stressor

et al. 2014

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Repeated stressor exposure can sensitize physiological responses to novel stressors and facilitate the development of stress-related psychiatric disorders including anxiety. Disruptions in diurnal rhythms of sleep–wake behavior accompany stress-related psychiatric disorders and could contribute to their development. Complex stressors that include fear-eliciting stimuli can be a component of repeated stress experienced by human beings, but whether exposure to repeated fear can prime the development of anxiety and sleep disturbances is unknown. In the current study, adult male F344 rats were exposed to either control conditions or repeated contextual fear conditioning for 22 days followed by exposure to no, mild (10), or severe (100) acute uncontrollable tail shock stress. Exposure to acute stress produced anxiety-like behavior as measured by a reduction in juvenile social exploration and exaggerated shock-elicited freezing in a novel context. Prior exposure to repeated fear enhanced anxiety-like behavior as measured by shock-elicited freezing, but did not alter social exploratory behavior. The potentiation of anxiety produced by prior repeated fear was temporary; exaggerated fear was present 1 day but not 4 days following acute stress. Interestingly, exposure to acute stress reduced rapid eye movement (REM) and non-REM (NREM) sleep during the hours immediately following acute stress. This initial reduction in sleep was followed by robust REM rebound and diurnal rhythm flattening of sleep/wake behavior. Prior repeated fear extended the acute stress-induced REM and NREM sleep loss, impaired REM rebound, and prolonged the flattening of the diurnal rhythm of NREM sleep following acute stressor exposure. These data suggest that impaired recovery of sleep/wake behavior following acute stress could contribute to the mechanisms by which a history of prior repeated stress increases vulnerability to subsequent novel stressors and stress-related disorders.

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“…Furthermore, research in humans and animals demonstrates that selective REM sleep deprivation can produce rapid antidepressant effects (Benedetti & Colombo, 2011;Maturana et al, 2015). Findings such as these have led researchers to hypothesise that REM sleep suppression may be an essential component of any effective form of MDD therapy (Vogel, McAbee, Barker, & Thurmond, 1977).…”

Section: Figmentioning

confidence: 99%

The ‘affect tagging and consolidation’ (ATaC) model of depression vulnerability

Harrington

Pennington

Durrant

2017

Neurobiology of Learning and Memory

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Please cite this article as: Harrington, M.O., Pennington, K., Durrant, S.J., The 'Affect Tagging and Consolidation' (ATaC) Model of Depression Vulnerability, Neurobiology of Learning and Memory (2017), doi: http://dx.doi.org/10. 1016/j.nlm.2017.02.003 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. patients, suggesting that they may be vulnerability markers of major depressive disorder (MDD), rather than mere epiphenomena of the disorder. Neuroimaging studies have revealed that depression is also associated with heightened amygdala reactivity to negative emotional stimuli, which may also be a vulnerability marker for MDD. Several models have been developed to explain the respective roles of REM sleep alterations and negatively-biased amygdala activity in the pathology of MDD, however the possible interaction between these two potential risk-factors remains uncharted. This paper reviews the roles of the amygdala and REM sleep in the encoding and consolidation of negative emotional memories, respectively. We present our 'affect tagging and consolidation' (ATaC) model, which argues that increased REM sleep density and negatively-biased amygdala activity are two separate, genetically influenced risk-factors for depression which interact to promote the development of negative memory bias -a well-known cognitive vulnerability marker for depression.Predictions of the ATaC model may motivate research aimed at improving our understanding of sleep dependent memory consolidation in depression aetiology.

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REM Sleep Deprivation Reverses Neurochemical and Other Depressive-Like Alterations Induced by Olfactory Bulbectomy

Cited by 27 publications

References 52 publications

The influence of REM sleep and SWS on emotional memory consolidation in participants reporting depressive symptoms

The influence of REM sleep and SWS on emotional memory consolidation in participants reporting depressive symptoms

Repeated Exposure to Conditioned Fear Stress Increases Anxiety and Delays Sleep Recovery Following Exposure to an Acute Traumatic Stressor

The ‘affect tagging and consolidation’ (ATaC) model of depression vulnerability

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