Sleep and Emotional Memory Processing

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Sleep

The sleep of mammalian species has been broadly classified into 2 distinct types; non-REM (NREM) sleep and REM sleep, with NREM sleep being further divided in primates and cats into 4 substages (1–4) corresponding, in that order, to increasing depth of sleep.4 In humans, NREM and REM sleep alternate or “cycle” across the night in an ultradian pattern every 90 minutes (Fig. 1). Although this NREM-REM cycle length remains largely stable across the night, the ratio of NREM to REM within each

Sleep loss, mood stability, and emotional brain (re)activity

Together with impairments of attention and alertness, sleep deprivation is commonly associated with increased subjective reports of irritability and affective volatility.60 Using a sleep restriction paradigm (5 hours/night), Dinges and colleagues61 have reported a progressive increase in emotional disturbance across a 1-week period based on questionnaire mood scales. In addition, subjective descriptions in the daily journals of the participants also indicated increasing complaints of emotional

A heuristic model of sleep-dependent emotional processing

Based on the emerging interaction between sleep and emotion, a synthesis of these findings is provided next, which converge on a functional role for sleep in affective brain modulation. A model of sleep-dependent emotional information processing is described, offering provisional brain-based explanatory insights on the effect of sleep abnormalities in the initiation and maintenance of certain mood disorders and leading to testable predictions for future experimental investigations.

The findings

Emotional memory processing: a sleep to forget and sleep to remember hypothesis

Founded on the emerging interaction between sleep and emotion, the authors outline a model of affective information processing that may offer brain-based explanatory insights regarding the effect of sleep abnormalities, particularly REM sleep, on the initiation or maintenance of mood disturbance.

Although there is abundant evidence to suggest that emotional experiences persist in our autobiographies over time, an equally remarkable but less noted change is a reduction in the affective tone

Summary

When viewed as a whole, findings at the cellular, systems, cognitive, and clinical level all point to a crucial role for sleep in the affective modulation of human brain function. Based on the remarkable neurobiology of sleep, and REM sleep in particular, a unique capacity for the overnight modulation of affective networks and previously encountered emotional experiences may be possible, redressing and maintaining the appropriate connectivity and hence the next-day reactivity throughout limbic

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      Crucial to the topic of this paper, however, is the notion that independent of the type of memory process during treatment, the resulting new or updated memory needs to be consolidated during post-treatment sleep to solidify the treatment effect (Lane et al., 2015). During this period the new memory gets integrated into long-term memory networks, stabilizing the memory and further reducing its affective charge (van der Helm and Walker, 2011). In addition, irrespective of newly formed therapeutic memories, healthy sleep by itself will promote the consolidation process of the traumatic memory.

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      The lack of consistency in the literature suggests that further studies are needed to elucidate the effect of TMR during SWS on emotional memory consolidation and arousal processing. Regions known to be important for emotional memory include amygdala, hippocampus and parahippocampus (Cairney et al., 2014; Rasch et al., 2007; Murty et al., 2010; Van Der Helm and Walker, 2011), insula (Gu et al., 2013; Gasquoine, 2014) and orbitofrontal cortex (OFC) (Rolls, 2019). Activity in the amygdala (van der Helm et al., 2011) and the hippocampus (Cairney et al., 2014) elicited by emotional experiences has been shown to be modulated by REM sleep, and memory reactivations experimentally induced using TMR during SWS have been shown to trigger hippocampal activation (Rasch et al., 2007).

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