Showing posts with label amygdala. Show all posts
Showing posts with label amygdala. Show all posts

REM sleep and memory processing

The role of rapid eye movement sleep for amygdala-related memory processing.
Genzel L, Spoormaker V, Konrad BN, Dresler M.
Neurobiol Learn Mem. 2015 Jan 28.

Over the years, rapid eye movement (REM) sleep has been associated with general memory consolidation, specific consolidation of perceptual, procedural, emotional and fear memories, brain maturation and preparation of waking consciousness. More recently, some of these associations (e.g. general and procedural memory consolidation) have been shown to be unlikely, while others (e.g. brain maturation and consciousness) remain inconclusive. In this review, we argue that both behavioral and neurophysiological evidence supports a role of REM sleep for amygdala-related memory processing: the amygdala-hippocampus-medial prefrontal cortex network involved in emotional processing, fear memory and valence consolidation shows strongest activity during REM sleep, in contrast to the hippocampus-medial prefrontal cortex only network which is more active during non-REM sleep. However, more research is needed to fully understand the mechanisms.

Poor sleep increases desire to eat

The impact of sleep deprivation on food desire in the human brain.
Stephanie Greer, Andrea Goldstein and Matthew Walker.
Nature Communications, August 6, 2013

Epidemiological evidence supports a link between sleep loss and obesity. However, the detrimental impact of sleep deprivation on central brain mechanisms governing appetitive food desire remains unknown. Here we report that sleep deprivation significantly decreases activity in appetitive evaluation regions within the human frontal cortex and insular cortex during food desirability choices, combined with a converse amplification of activity within the amygdala. Moreover, this bi-directional change in the profile of brain activity is further associated with a significant increase in the desire for weight-gain promoting high-calorie foods following sleep deprivation, the extent of which is predicted by the subjective severity of sleep loss across participants. These findings provide an explanatory brain mechanism by which insufficient sleep may lead to the development/maintenance of obesity through diminished activity in higher-order cortical evaluation regions, combined with excess subcortical limbic responsivity, resulting in the selection of foods most capable of triggering weight-gain.

Sleep depotentiates prior emotional experiences/painful memories

REM Sleep Depotentiates Amygdala Activity to Previous Emotional Experiences
Current Biology, 23 November 2011 (Link)
Els van der Helm, Justin Yao, Shubir Dutt, Vikram Rao, Jared M. Saletin, Matthew P. Walker

Highlights:
  • Sleep decreases amygdala activity to prior waking emotional experiences 
  • The amygdala decrease is associated with reestablished prefrontal connectivity 
  • These neural changes are accompanied by overnight reductions in subjective reactivity 
  • Reductions in both brain and behavioral reactivity are associated with REM physiology 
Summary: Clinical evidence suggests a potentially causal interaction between sleep and affective brain function; nearly all mood disorders display co-occurring sleep abnormalities, commonly involving rapid-eye movement (REM) sleep. Building on this clinical evidence, recent neurobiological frameworks have hypothesized a benefit of REM sleep in palliatively decreasing next-day brain reactivity to recent waking emotional experiences. Specifically, the marked suppression of central adrenergic neurotransmitters during REM (commonly implicated in arousal and stress), coupled with activation in amygdala-hippocampal networks that encode salient events, is proposed to (re)process and depotentiate previous affective experiences, decreasing their emotional intensity. In contrast, the failure of such adrenergic reduction during REM sleep has been described in anxiety disorders, indexed by persistent high-frequency electroencephalographic (EEG) activity; a candidate factor contributing to hyperarousal and exaggerated amygdala reactivity. Despite these neurobiological frameworks, and their predictions, the proposed benefit of REM sleep physiology in depotentiating neural and behavioral responsivity to prior emotional events remains unknown. Here, we demonstrate that REM sleep physiology is associated with an overnight dissipation of amygdala activity in response to previous emotional experiences, altering functional connectivity and reducing next-day subjective emotionality.

Resolving emotional conflict

Dissociated responses in the amygdala and orbitofrontal cortex to bottom-up and top-down components of emotional evaluation.
Wright P, Albarracin D, Brown RD, Li H, He G, Liu Y.
Neuroimage. 2007 Sep 19

Background: Although emotional responses to stimuli may be automatic, explicit evaluation of emotion is a voluntary act. These bottom-up and top-down processes may be supported by distinct neural systems. Previous studies reported bottom-up responses in the amygdala, top-down responses in the orbital and ventromedial prefrontal cortices, and top-down modulation of the amygdalar response.

Methods: The current study used event-related fMRI on fifteen healthy males to examine these responses in the absence of stimulus anticipation or task repetition. Factorial analysis distinguished bottom-up responses in the amygdala from top-down responses in the orbitofrontal cortex.

Results: Activation of ventromedial prefrontal cortex and modulation of amygdalar response were not observed, and future studies may investigate whether these effects are contingent upon anticipation or cognitive set.