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Research Articles, Behavioral/Cognitive

Baseline Levels of Rapid Eye Movement Sleep May Protect Against Excessive Activity in Fear-Related Neural Circuitry

Itamar Lerner, Shira M. Lupkin, Neha Sinha, Alan Tsai and Mark A. Gluck
Journal of Neuroscience 15 November 2017, 37 (46) 11233-11244; DOI: https://doi.org/10.1523/JNEUROSCI.0578-17.2017
Itamar Lerner
Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, New Jersey 07102
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Shira M. Lupkin
Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, New Jersey 07102
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Neha Sinha
Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, New Jersey 07102
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Alan Tsai
Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, New Jersey 07102
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Mark A. Gluck
Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, New Jersey 07102
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Abstract

Sleep, and particularly rapid eye movement sleep (REM), has been implicated in the modulation of neural activity following fear conditioning and extinction in both human and animal studies. It has long been presumed that such effects play a role in the formation and persistence of posttraumatic stress disorder, of which sleep impairments are a core feature. However, to date, few studies have thoroughly examined the potential effects of sleep prior to conditioning on subsequent acquisition of fear learning in humans. Furthermore, these studies have been restricted to analyzing the effects of a single night of sleep—thus assuming a state-like relationship between the two. In the current study, we used long-term mobile sleep monitoring and functional neuroimaging (fMRI) to explore whether trait-like variations in sleep patterns, measured in advance in both male and female participants, predict subsequent patterns of neural activity during fear learning. Our results indicate that higher baseline levels of REM sleep predict reduced fear-related activity in, and connectivity between, the hippocampus, amygdala and ventromedial PFC during conditioning. Additionally, skin conductance responses (SCRs) were weakly correlated to the activity in the amygdala. Conversely, there was no direct correlation between REM sleep and SCRs, indicating that REM may only modulate fear acquisition indirectly. In a follow-up experiment, we show that these results are replicable, though to a lesser extent, when measuring sleep over a single night just before conditioning. As such, baseline sleep parameters may be able to serve as biomarkers for resilience, or lack thereof, to trauma.

SIGNIFICANCE STATEMENT Numerous studies over the past two decades have established a clear role of sleep in fear-learning processes. However, previous work has focused on the effects of sleep following fear acquisition, thus neglecting the potential effects of baseline sleep levels on the acquisition itself. The current study provides the first evidence in humans of such an effect. Specifically, the results of this study suggest that baseline rapid eye movement (REM) sleep may serve a protective function against enhanced fear encoding through the modulation of connectivity between the hippocampus, amygdala, and the ventromedial PFC. Building on this finding, baseline REM measurements may serve as a noninvasive biomarker for resilience to trauma or, conversely, to the potential development of posttraumatic stress disorder following trauma.

  • fear learning
  • fMRI
  • PTSD
  • rapid eye movement sleep
  • REM sleep
  • sleep
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The Journal of Neuroscience: 37 (46)
Journal of Neuroscience
Vol. 37, Issue 46
15 Nov 2017
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Baseline Levels of Rapid Eye Movement Sleep May Protect Against Excessive Activity in Fear-Related Neural Circuitry
Itamar Lerner, Shira M. Lupkin, Neha Sinha, Alan Tsai, Mark A. Gluck
Journal of Neuroscience 15 November 2017, 37 (46) 11233-11244; DOI: 10.1523/JNEUROSCI.0578-17.2017

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Baseline Levels of Rapid Eye Movement Sleep May Protect Against Excessive Activity in Fear-Related Neural Circuitry
Itamar Lerner, Shira M. Lupkin, Neha Sinha, Alan Tsai, Mark A. Gluck
Journal of Neuroscience 15 November 2017, 37 (46) 11233-11244; DOI: 10.1523/JNEUROSCI.0578-17.2017
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Keywords

  • fear learning
  • fMRI
  • PTSD
  • rapid eye movement sleep
  • REM sleep
  • sleep

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  • RE: DHEA Levels During Sleep may Explain Lerner, et al
    James M. Howard
    Published on: 24 October 2017
  • Published on: (24 October 2017)
    Page navigation anchor for RE: DHEA Levels During Sleep may Explain Lerner, et al
    RE: DHEA Levels During Sleep may Explain Lerner, et al
    • James M. Howard, Biologist, Independent

    I suggest the basis of Lerner, et al., is dehydroepiandrosterone (DHEA).

    Very briefly, it is my hypothesis of 1985 that the function of sleep is to produce dehydroepiandrosterone (DHEA) which stimulates consciousness. My mechanism suggests that the light-dark cycle is involved in stimulating DHEA. This requires melatonin production during the dark phase which then results in the production of DHEA. Melatonin triggers prolactin production which is a direct and specific stimulator of DHEA. As DHEA is literally used during the day, melatonin increases at sleep. During sleep the melatonin - prolactin cycle increases until sufficient levels of DHEA are produced to induce awakening and consciousness during the day. The function of sleep / circadian rhythm is production of DHEA. "Sleep deprivation" is caused by low / insufficient DHEA. During periods of increasing DHEA, I suggest DHEA not only maintains brainstem activity but also causes REM sleep.

    It is my hypothesis that cortisol evolved to counteract the effects of DHEA and is the basis of the "fight or flight" mechanism. ("A Theory of the Control of the Ontogeny and Phylogeny of Homo sapiens by the Interaction of Dehydroepiandrosterone and the Amygdala," Copyright 1985, James Michael Howard, Fayetteville, Arkansas, U.S.A. (Registered Copyright TXu220580).) The "cortisol to DHEA ratio" appears numerous times in the medical literature; it is becoming an important m...

    Show More

    I suggest the basis of Lerner, et al., is dehydroepiandrosterone (DHEA).

    Very briefly, it is my hypothesis of 1985 that the function of sleep is to produce dehydroepiandrosterone (DHEA) which stimulates consciousness. My mechanism suggests that the light-dark cycle is involved in stimulating DHEA. This requires melatonin production during the dark phase which then results in the production of DHEA. Melatonin triggers prolactin production which is a direct and specific stimulator of DHEA. As DHEA is literally used during the day, melatonin increases at sleep. During sleep the melatonin - prolactin cycle increases until sufficient levels of DHEA are produced to induce awakening and consciousness during the day. The function of sleep / circadian rhythm is production of DHEA. "Sleep deprivation" is caused by low / insufficient DHEA. During periods of increasing DHEA, I suggest DHEA not only maintains brainstem activity but also causes REM sleep.

    It is my hypothesis that cortisol evolved to counteract the effects of DHEA and is the basis of the "fight or flight" mechanism. ("A Theory of the Control of the Ontogeny and Phylogeny of Homo sapiens by the Interaction of Dehydroepiandrosterone and the Amygdala," Copyright 1985, James Michael Howard, Fayetteville, Arkansas, U.S.A. (Registered Copyright TXu220580).) The "cortisol to DHEA ratio" appears numerous times in the medical literature; it is becoming an important mechanism.

    Therefore, I submit that the basis of Lerner, et al., is the effects of DHEA during sleep. DHEA, prolactin, melatonin, and cortisol are not mentioned in Lerner, et al.

    Show Less
    Competing Interests: None declared.

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