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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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  • RE: DHEA Levels During Sleep may Explain Lerner, et al
    James M. Howard
    Submitted on: 24 October 2017
  • Submitted 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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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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Jump to comment:

  • 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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