Sleep Deprivation in Mood Disorders

Benedetti, Francesco; Colombo, Cristina

doi:10.1159/000328947

Cited by 105 publications

(64 citation statements)

References 265 publications

(157 reference statements)

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“…The limited efficacy of the current antidepressants underlines the need to look for novel fast-acting and effective antidepressant measures. Treatment with a low dose of ketamine and non-pharmacological interventions, such as sleep deprivation (SD) and electroconvulsive therapy (ECT) emerged as rapid and effective antidepressant therapies, though their mechanism of action is not well understood (Berman et al, 2000;Kato, 2009;Benedetti and Colombo, 2011). A solid knowledge of the mechanism of action and the neurobiological effects of the current antidepressant therapies would facilitate the development of new antidepressant drugs.…”

Section: Introductionmentioning

confidence: 99%

Signaling pathways regulating Homer1a expression: implications for antidepressant therapy

Serchov

Heumann

Calker

et al. 2016

Biological Chemistry

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Homer1a is upregulated by several different antidepressant measures, including non-pharmacological treatments, like sleep deprivation (SD) and electroconvulsive therapy (ECT) and antidepressant drugs, such as imipramine, fluoxetine and ketamine. Homer1a induction might thus be a crucial joint mechanism for antidepressant therapy in general. However, the upstream signaling pathways that regulate or induce Homer1a expression are still not well understood. The main focus of the present review is to offer an overview of the current knowledge about the potential role of Homer1a in depression and the signaling pathways responsible for Homer1a regulation. It is suggested here that a detailed characterization of the signaling mechanisms leading to Homer1a expression might provide novel therapeutic targets for antidepressant drug development.

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Section: Introductionmentioning

confidence: 99%

Signaling pathways regulating Homer1a expression: implications for antidepressant therapy

Serchov

Heumann

Calker

et al. 2016

Biological Chemistry

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“…A related possibility is that sleep deprivationinduced upregulation of ENK could have a normalizing influence on mood in pathological states associated with already-elevated DYN levels. A specific case could be the palliative effect of acute sleep deprivation in depression (Benedetti and Colombo, 2010;Giedke and Schwarzler, 2002;Gillin et al, 2001;Wu et al, 2009). Although speculative, these hypotheses lead to testable predictions, particularly with the advent of PET imaging techniques capable of detecting in vivo opioid signaling.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Gene Expression in Reward-Modulatory Striatal Opioid Systems by Sleep Loss

Baldo

Hanlon

Obermeyer

et al. 2013

Neuropsychopharmacol

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Epidemiological studies have shown a link between sleep loss and the obesity 'epidemic,' and several observations indicate that sleep curtailment engenders positive energy balance via increased palatable-food 'snacking.' These effects suggest alterations in rewardmodulatory brain systems. We explored the effects of 10 days of sleep deprivation in rats on the expression of striatal opioid peptide (OP) genes that subserve food motivation and hedonic reward, and compared effects with those seen in hypothalamic energy balanceregulatory systems. Sleep-deprived (Sleep-Dep) rats were compared with yoked forced-locomotion apparatus controls (App-Controls), food-restricted rats (Food-Restrict), and unmanipulated controls (Home-Cage). Detection of mRNA levels with in situ hybridization revealed a subregion-specific upregulation of striatal preproenkephalin and prodynorhin gene expression in the Sleep-Dep group relative to all other groups. Neuropeptide Y (NPY) gene expression in the hippocampal dentate gyrus and throughout neocortex was also robustly upregulated selectively in the Sleep-Dep group. In contrast, parallel gene expression changes were observed in the Sleep-Dep and Food-Restrict groups in hypothalamic energy-sensing systems (arcuate nucleus NPY was upregulated, and cocaine-and amphetamine-regulated transcript was downregulated), in alignment with leptin suppression in both groups. Together, these results reveal a novel set of sleep deprivation-induced transcriptional changes in reward-modulatory peptide systems, which are dissociable from the energy-balance perturbations of sleep loss or the potentially stressful effects of the forced-locomotion procedure. The recruitment of telencephalic food-reward systems may provide a feeding drive highly resistant to feedback control, which could engender obesity through the enhancement of palatable feeding.

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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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Sleep Deprivation in Mood Disorders

Cited by 105 publications

References 265 publications

Signaling pathways regulating Homer1a expression: implications for antidepressant therapy

Signaling pathways regulating Homer1a expression: implications for antidepressant therapy

Upregulation of Gene Expression in Reward-Modulatory Striatal Opioid Systems by Sleep Loss

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

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