Sleep-wake cycle: Difference between revisions

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The '''Sleep-wake cycle''' is a diurnal rhythm the human body oscillates in between awake and sleeping states, the mechanics of which span several fields of science including psychophysiology, endopharmacology, metabolomics, and psychology. In this cycle a person will optimally spend 7 hours in the sleep state<ref>{{cite journal | vauthors=((Kripke, D. F.)), ((Garfinkel, L.)), ((Wingard, D. L.)), ((Klauber, M. R.)), ((Marler, M. R.)) | journal=Archives of General Psychiatry | title=Mortality Associated With Sleep Duration and Insomnia | volume=59 | issue=2 | pages=131 | date=1 February 2002 | url=http://archpsyc.jamanetwork.com/article.aspx?doi=10.1001/archpsyc.59.2.131 | issn=0003-990X | doi=10.1001/archpsyc.59.2.131}}</ref> which is similar on the surface to unconsciousness (although the phenomenon of [[lucid dreaming]] is contradictory to the term unconsciousness). The sleep state is often preformed at night as this is the evolutionary norm for humans, as evidenced by the fact that the hormone [[melatonin]] is released during darkness and contributes to the desire to sleep.<ref>{{cite journal | vauthors=((Zhdanova, I. V.)), ((Wurtman, R. J.)), ((Lynch, H. J.)), ((Ives, J. R.)), ((Dollins, A. B.)), ((Morabito, C.)), ((Matheson, J. K.)), ((Schomer, D. L.)) | journal=Clinical Pharmacology and Therapeutics | title=Sleep-inducing effects of low doses of melatonin ingested in the evening | volume=57 | issue=5 | pages=552–558 | date= May 1995 | issn=0009-9236 | doi=10.1016/0009-9236(95)90040-3}}</ref> Although melatonin in this instance serves as a regulatory mechanism for making sure humans sleep once a day during night, it is not the causative factor as humans are able to sleep even during daylight if they are sleepy enough. Though it should be noted that this can lead to [[circadian rhythm]] sleep disorders.

*Lack of Adenosine activating the (A(2A)R) receptor is sufficient to have decreased GABA release in the tuberomammillary nucleus enough to have enabled histamine to wake one up and cause vigilance.<ref name="Hong2005">{{cite journal | vauthors=((Hong, Z.-Y.)), ((Huang, Z.-L.)), ((Qu, W.-M.)), ((Eguchi, N.)), ((Urade, Y.)), ((Hayaishi, O.)) | journal=Journal of Neurochemistry | title=An adenosine A receptor agonist induces sleep by increasing GABA release in the tuberomammillary nucleus to inhibit histaminergic systems in rats | volume=92 | issue=6 | pages=1542–1549 | date= March 2005 | issn=0022-3042 | doi=10.1111/j.1471-4159.2004.02991.x}}</ref><ref name="Thakkar2011">{{cite journal | vauthors=((Thakkar, M. M.)) | journal=Sleep medicine reviews | title=HISTAMINE IN THE REGULATION OF WAKEFULNESS | volume=15 | issue=1 | pages=65–74 | date= February 2011 | url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3016451/ | issn=1087-0792 | doi=10.1016/j.smrv.2010.06.004}}</ref>

*Exposure to blue light frequencies mainly between 460 and 480nm<ref>{{cite journal | vauthors=((Brainard, G. C.)), ((Hanifin, J. P.)), ((Greeson, J. M.)), ((Byrne, B.)), ((Glickman, G.)), ((Gerner, E.)), ((Rollag, M. D.)) | journal=The Journal of Neuroscience: The Official Journal of the Society for Neuroscience | title=Action spectrum for melatonin regulation in humans: evidence for a novel circadian photoreceptor | volume=21 | issue=16 | pages=6405–6412 | date=15 August 2001 | issn=1529-2401}}</ref> trigger [[melanopsin]] cells in the eyes to send a signal to the suprachiasmatic nucleus<ref name="Colwell2011">{{cite journal | vauthors=((Colwell, C. S.)) | journal=Nature Reviews Neuroscience | title=Linking neural activity and molecular oscillations in the SCN | volume=12 | issue=10 | pages=553–569 | date= October 2011 | url=https://www.nature.com/articles/nrn3086 | issn=1471-0048 | doi=10.1038/nrn3086}}</ref> which sends [[GABA]] to the [[pineal gland]], inhibiting it from releasing melatonin thereby causing levels to decline.<ref name="Kalsbeek1999">{{cite journal | vauthors=((Kalsbeek, A.)), ((Cutrera, R. A.)), ((Heerikhuize, J. J. van)), ((Vliet, J. van der)), ((Buijs, R. M.)) | journal=Neuroscience | title=GABA release from suprachiasmatic nucleus terminals is necessary for the light-induced inhibition of nocturnal melatonin release in the rat | volume=91 | issue=2 | pages=453–461 | date= June 1999 | url=https://linkinghub.elsevier.com/retrieve/pii/S0306452298006356 | issn=03064522 | doi=10.1016/S0306-4522(98)00635-6}}</ref>

*The food eaten before sleep has been digested and the stomach is empty which releases ghrelin, this causes hunger by inducing the release of the hormone orexin and thereby pushing one to eat.<ref>{{Citation | title=GHRL ghrelin and obestatin prepropeptide [Homo sapiens (human)] - Gene - NCBI | url=https://www.ncbi.nlm.nih.gov/gene/51738}}</ref>

*ATP from the food is metabolized into adenosine which begins to accumulate around the adenosine receptors.<ref>{{Citation | title=MOLECULES THAT BUILD UP AND MAKE YOU SLEEP | url=https://thebrain.mcgill.ca/flash/a/a_11/a_11_m/a_11_m_cyc/a_11_m_cyc.html}}</ref>

*The decreasing of the light levels which were activating melanopsin cells begins to shut off the signal to the suprachiasmatic nucleus,<ref name="Colwell2011"/> stopping GABA from being sent to the pineal gland allowing melatonin to be released.<ref name="Kalsbeek1999"/>

*In the presence of insulin melatonin causes upregulation of leptin, thereby inhibiting the hunger hormone orexin allowing one to fast while they sleep.<ref name="Alonso-Vale2005">{{cite journal | vauthors=((Alonso-Vale, M. I. C.)), ((Andreotti, S.)), ((Peres, S. B.)), ((Anhê, G. F.)), ((Neves Borges-Silva, C. das)), ((Neto, J. C.)), ((Lima, F. B.)) | journal=American Journal of Physiology. Endocrinology and Metabolism | title=Melatonin enhances leptin expression by rat adipocytes in the presence of insulin | volume=288 | issue=4 | pages=E805-812 | date= April 2005 | issn=0193-1849 | doi=10.1152/ajpendo.00478.2004}}</ref> (If one has been fasting before sleep insulin levels will be low causing melatonin to downregulate leptin instead of upregulating it, thus encouraging one to eat before they sleep)

*High levels of adenosine activating the adenosine receptor A1 inhibit cholinergic neurons in the basal forebrain<ref name="Hawryluk2012">{{cite journal | vauthors=((Hawryluk, J. M.)), ((Ferrari, L. L.)), ((Keating, S. A.)), ((Arrigoni, E.)) | journal=Journal of Neurophysiology | title=Adenosine inhibits glutamatergic input to basal forebrain cholinergic neurons | volume=107 | issue=10 | pages=2769–2781 | date=15 May 2012 | url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3362278/ | issn=0022-3077 | doi=10.1152/jn.00528.2011}}</ref> thus gradually causing cognitive decline.<ref>{{cite journal | vauthors=((Hasselmo, M. E.)) | journal=Current opinion in neurobiology | title=The Role of Acetylcholine in Learning and Memory | volume=16 | issue=6 | pages=710–715 | date= December 2006 | url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659740/ | issn=0959-4388 | doi=10.1016/j.conb.2006.09.002}}</ref>

*In addition activation of adenosine receptor (A(2A)R) causes the release of GABA in the tuberomammillary nucleus to inhibit histamine, thus gradually inducing sleepiness.<ref name="Hong2005"/>

*Food is Digested throughout the night, sustaining insulin levels which in combination with melatonin cause the upregulation of leptin. This inhibits orexin allowing one to sleep without being distracted by hunger.<ref name="Alonso-Vale2005"/>

*The falling levels of adenosine enable the cholinergic neurons in the basal forebrain to become uninhibited to activation.<ref name="Thakkar2011"/><ref name="Hawryluk2012"/>

*As adenosine is metabolized and it's levels decrease it no longer leads to the [[GABAergic]] inhibition of histamine, allowing vigilance to increase.<ref>{{cite journal | vauthors=((Huang, Z.-L.)), ((Urade, Y.)), ((Hayaishi, O.)) | journal=Current Topics in Medicinal Chemistry | title=The role of adenosine in the regulation of sleep | volume=11 | issue=8 | pages=1047–1057 | date= 2011 | issn=1873-4294 | doi=10.2174/156802611795347654}}</ref><ref name="Hong2005"/>