Talk:Slow-wave sleep

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Wiki Education Foundation-supported course assignment edit

  This article is or was the subject of a Wiki Education Foundation-supported course assignment. Further details are available on the course page. Peer reviewers: Arich7.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 09:30, 17 January 2022 (UTC)Reply

Physiology Lab Student Assignment: Major article edits edit

Hi everyone, for my physiology class, I chose to edit this article and would like some feedback on what I included (shown in bold and italics), and what I want to exclude (shown in strikethrough). In particular, I want to break up the current "Discussion" section into better organized sections. Also, I am having difficulty with the "Effects of Sleep deprivation" section (please help!) Please give me feedback before I go through with the major edits that I propose below. I wanted to show my edits incorporated onto the current article's descriptions. Thank you! C.q20n.17 (talk) 02:50, 29 March 2017 (UTC)Reply

Proposed rearrangement:

  • 1. Electroencephalographic characteristics
  • 2. Functions of slow-wave sleep
  • 2.1 Neural control
  • 2.2 Physical healing and growth
  • 2.3 Learning and Synaptic homeostasis
  • 3. Problems associated with slow-wave sleep
  • 3.1 Effects of sleep deprivation
  • 4. Individual differences
  • 5. Drugs
  • 6. See also I did not include this since I am not planning to change it.
  • 7. References

This is the original article writing with my incorporated edits shown in bold and italic edit

Slow-wave sleep (SWS), often referred to as deep sleep, consists of stage three of non-rapid eye movement sleep, according to the Rechtschaffen & Kales (R & K) standard of 1968.[1] There is not a clear distinction between stages three and four. Stage three has 20-50 percent delta activity, whereas stage four has more than 50 percent.[2] As of 2008, the American Academy of Sleep Medicine (AASM) has discontinued the use of stage four,[3][4][5] such that the previous stages three and four now are combined as stage three. An epoch (30 seconds of sleep) which consists of 20% or more slow-wave (delta) sleep is now considered to be stage three.

This period of sleep is called slow-wave sleep because the EEG activity is synchronized, producing slow waves with a frequency of less than 1 Hz and a relatively high amplitude. The first section of the wave signifies a down state, which is an inhibition or hyperpolarizing period phase in which the neurons in the neocortex are silent. This is the period when the neocortical neurons are able to rest. The second section of the wave signifies an "up state," which is an excitation or or depolarizing period phase in which the neurons fire briefly at a high rate. The former state is a hyperpolarizing phase and the latter is a depolarizing phase. The principal characteristics during slow-wave sleep that contrast with REM sleep are moderate muscle tone, slow or absent eye movement, and lack of genital activity.[6]

Slow-wave sleep is considered important to consolidate new memoriesfor memory consolidation.[7] This is sometimes referred to as "sleep-dependent memory processing".[8] Impaired memory consolidation has been effected in individuals with primary insomnia who thus do not perform as well as normal patients in memory tasks following a period of sleep.[9] Furthermore, slow-wave sleep improves declarative memory (which includes semantic and episodic memory). A central model has been hypothesized that the long-term memory storage is facilitated by an interaction between the hippocampal and neocortical networks.[9] In several studies, after the subjects have had training to learn a declarative memory task, the density of human sleep spindles was significantly higher compared to the non-learning control task. This is the result of the spontaneously occurring wave oscillations that account for the intracellular recordings from thalamic and cortical neurons.[10]

[Wikipedia hyperlink for memory consolidation as well as citations have been added for sleep dependent memory processing & insomnia sentence]

Sleep deprivation studies with humans suggest that the primary function of slow-wave sleep may be to allow the brain to recover from its daily activities. Glucose metabolism in the brain increases as a result of tasks that demand mental activity.[11] Another function affected by slow-wave sleep is the secretion of growth hormone, which is always greatest during this stage.[12] It is also thought to be responsible for a decrease in sympathetic and increase in parasympathetic neural activity.[12]


Electroencephalographic characteristics edit

 
Polysomnogram demonstrating SWS, stage four.
High amplitude EEG is highlighted in red.

Large 75-microvolt (0.5–3 Hz) delta waves predominate the electroencephalogram (EEG). Stage N3 is defined by the presence of 20% delta waves in any given 30-second epoch of the EEG during sleep, by the current 2007 AASM guidelines.[5]

Longer periods of SWS occur in the first part of the night, primarily in the first two sleep cycles (roughly three hours). Children and young adults will have more total SWS in a night than older adults. The elderly may not go into SWS at all during many nights of sleep.

Slow-wave sleep is an active phenomenon probably brought about by the activation of serotonergic neurons of the raphe system.[13]

[Citation added]

The slow wave seen in the cortical EEG is generated through thalamocortical communication through the thalamocortical neurons.[14] In the TC neurons this is generated by the "slow oscillation" and is dependent on membrane potential bistability, a property of these neurons due to an electrophysiological component known as "I t window". "I t window" is due to the overlap underneath activation and inactivation curves if plotted for T-type calcium channels (inward current). If these two curves are multiplied, and another line superimposed on the graph to show a small Ik leak current (outward), then the interplay between these inward (I t window) and outward (small Ik leak), three equilibrium points are seen at −90, −70 and −60 mv, −90 and −60 being stable and −70 unstable. This property allows the generation of slow waves due to an oscillation between two stable points. It is important to note that in in vitro, mGluR must be activated on these neurons to allow a small Ik leak, as seen in in vivo situations.

Discussion edit

The highest arousal thresholds (i.e. difficulty of awakening, such as by a sound of a particular volume) are observed in deep sleep. A person will typically feel more groggy when awoken from slow-wave sleep, and indeed, cognitive tests administered after awakening then indicate that mental performance is somewhat impaired for periods of up to 30 minutes, relative to awakenings from other stages. This phenomenon has been called "sleep inertia".

After sleep deprivation there is a sharp rebound of SWS, that is, the following bout of sleep will include more and deeper SWS than normal. The duration of slow-wave sleep is determined by the previous duration of this stage as well as the duration of prior wakefulness.[12]

The major factor determining how much slow-wave sleep is observed in a given sleep period is the duration of preceding wakefulness, likely related to accumulation of sleep-promoting substances in the brain. Some of the factors known to increase slow-wave sleep in the sleep period that follows them include body heating (as by immersion in a hot tub or sauna) and intense prolonged exercise. Studies have shown that slow-wave sleep is enabled when brain temperature surpasses a certain threshold. It is hypothesized that the threshold is regulated by circadian and homeostatic processes.[15] In healthy sleepers, a very low carbohydrate diet over the short-term promotes increases in the percentage of SWS (deep sleep stage four, now often called stage three) and a reduction in the percentage of REM sleep (dreaming sleep) compared to the control with a mixed diet - the sleep changes may be linked to the metabolism of the fat content of the very low carbohydrate diet.[16]

In addition to these factors, the duration of SWS periods can be increased by the ingestion of certain SSRI, and other antidepressants, [citation needed] whereas the effects of THC on SWS remain controversial.[17][18] In instances such as these, total sleep time (TST) is often unaffected due to circadian rhythms, a person's alarm clock, or early morning obligations. This increase of SWS can lead to increased REM latency and a decrease in REM duration. If the total time spent in REM sleep is decreased long enough and repeatedly over a substantial number of nights a "REM rebound" will occur in response to the removal of its inhibitor. An increase in REM sleep is believed to produce symptoms of depression and bipolar disorder in many patients for an amount of time relative to the severity of the previous REM suppression. It is debatable whether this explains the return in symptoms of depression disorder after removal of SSRI medications.

Reduced slow-wave sleep (SWS) may predict high blood pressure in older men.[19]

A study from the Department of Endocrinology at Boston Children's Hospital, an affiliate of Harvard Medical School, indicated that regular deep sleep in children is helpful in triggering the steady release of the hormones that cause puberty.[20] }}

[There should not be a discussion section. The information included in this section are random and unorganized.]

Functions of slow-wave sleep edit

Slow-wave sleep is necessary for survival. Some animals, such as dolphins and birds, have the ability to sleep with only one hemisphere of the brain, leaving the other hemisphere awake to carry out normal functions and to remain alert.

Neural control of slow-wave sleep edit

Several neurotransmitters are involved in sleep and waking patterns: acetylcholine, norepinephrine, serotonin, histamine, and orexin.[21] Neocortical neurons fire spontaneously during slow-wave sleep, thus they [What is they? the neurotransmitters?] seem to play a role during this period of sleep. Also, these neurons appear to have some sort of internal dialogue, which accounts for the mental activity during this state where there is no information from external signals because of the synaptic inhibition at the thalamic level. The rate of recall of dreams during this state of sleep is relatively high compared to the other levels of the sleep cycle. This indicates that the mental activity is closer to real life events.[10]

[Added "of the sleep cycle" to clarify what "levels" was referring to.]

Physical healing and growth edit

Slow-wave sleep is the constructive phase of sleep for recuperation of the mind-body system in which it rebuilds itself after each day. Substances that have been ingested into the body while an organism is awake are synthesized into complex proteins of living tissue. Growth hormones are also secreted to facilitate the healing of muscles as well as repairing damage to any tissues. Lastly, glial cells within the brain are restored with sugars to provide energy for the brain.[22]

Learning and Synaptic Homeostasis edit

During wakefulness, learning and memory formation occurs during wakefulness by the process of of long-term potentiation. SWS is associated with the regulation of synapses potentiated during wakefulness. SWS has been studied to be involved in the downscaling of synapses, in which strongly stimulated or potentiated synapses are kept while weakly potentiated synapses either diminish or are removed.[23] This may be helpful for recalibrating synapses for the next potentiation during wakefulness and maintaining synaptic plasticity.

[Added a section about learning and homeostatic synaptic downscaling]

Problems associated with slow-wave sleep edit

Bedwetting, night terrors, and sleepwalking are all common behaviors that can occur during stage three of sleep. These occur most frequently amongst children, who then generally outgrow them.[11] Another problem that may arise is sleep-related eating disorder. An individual will sleep-walk leaving his or her bed in the middle of the night seeking out food, and will eat not having any memory of the event in the morning.[11] Over half of individuals with this disorder become overweight.[24] Sleep-related eating disorder can usually be treated with dopaminergic agonists, or topiramate, which is an anti-seizure medication. This nocturnal eating throughout a family suggests that heredity may be a potential cause of this disorder.[11]

Effects of sleep deprivation edit

J. A. Horne (1978) reviewed several experiments with humans and concluded that sleep deprivation has no effects on people’s physiological stress response or ability to perform physical exercise. It did, however, have an effect on cognitive functions. Some people reported distorted perceptions or hallucinations and lack of concentration on mental tasks. Thus, the major role of sleep does not appear to be rest for the body, but rest for the brain.

When sleep-deprived humans sleep normally again, the recovery percentage for each stage of sleep is not the same. Only seven percent of stages one and two are regained, but 68 percent of stage-four slow-wave sleep and 53 percent of REM sleep are regained. This suggests that stage-four sleep (known today as the deepest part of stage-three sleep) is more important than the other stages.

During slow-wave sleep, there is a significant decline in cerebral metabolic rate and cerebral blood flow. The activity falls to about 75 percent of the normal wakefulness level. The regions of the brain that are most active when awake have the highest level of delta waves during slow-wave sleep. This indicates rest is geographical. The “shutting down” of the brain accounts for the grogginess and confusion if someone is awakened during deep sleep since it takes the cerebral cortex time to resume its normal functions.[25]

According to J. Siegel (2005), sleep deprivation results in the build-up of free radicals and superoxides in the brain. Free radicals are oxidizing agents that have one unpaired electron, making them highly reactive. These free radicals interact with electrons of biomolecules and damage cells. In slow-wave sleep, the decreased rate of metabolism reduces the creation of oxygen byproducts, thereby allowing the existing radical species to clear. This is a means of preventing damage to the brain.


Individual differences in slow-wave sleep edit

Though SWS is fairly consistent within the individual, it can vary across individuals. Age and gender have been noted as two of the biggest factors that affect this period of sleep. Aging is inversely proportional to the amount of SWS beginning by midlife and therefore, SWS declines with age. Sex differences have also been found, such that females tend to have higher levels of SWS compared to males, at least up until menopause. There have also been studies that have shown differences between races. The results showed that there was a lower percentage of SWS in African Americans compared to Caucasians, but since there are many influencing factors (e.g. body mass index sleep-disordered breathing, obesity, diabetes, and hypertension) this potential difference must be investigated further.[26]

Drugs edit

The chemical gamma-hydroxybutyric acid (GHB) is known to promote has been studied to increase SWS.[27][28] In the United States, the Food and Drug Administration permits the use of GHB under the trade name Xyrem to reduce cataplexy attacks and excessive daytime sleepiness in patients with narcolepsy.

[Took descriptions from "Discussion section," edited and added a citation.]

References edit

Notes

  1. ^ Rechtschaffen, A; Kales, A (1968). A Manual of Standardized Terminology, Techniques and Scoring System For Sleep Stages of Human Subjects. US Dept of Health, Education, and Welfare; National Institutes of Health.
  2. ^ Carlson, Neil R. (2012). Physiology of Behavior. Pearson. p. 291. ISBN 0205239390.
  3. ^ Schulz, Hartmut (2008). "Rethinking sleep analysis. Comment on the AASM Manual for the Scoring of Sleep and Associated Events". J Clin Sleep Med. 4 (2). American Academy of Sleep Medicine: 99–103. PMC 2335403. PMID 18468306. Although the sequence of non-REM (NREM) sleep stages one to four (R&K classification) or N1 to N3 (AASM classification) fulfills the criteria...
  4. ^ "Glossary. A resource from the Division of Sleep Medicine at Harvard Medical School, Produced in partnership with WGBH Educational Foundation". Harvard University. 2008. Retrieved 2009-03-11. The 1968 categorization of the combined Sleep Stages 3 - 4 was reclassified in 2007 as Stage N3.
  5. ^ a b Iber, C; Ancoli-Israel, S; Chesson, A; Quan, SF. for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. Westchester: American Academy of Sleep Medicine; 2007.
  6. ^ Carlson, Neil R. (2012). Physiology of Behavior. Pearson. p. 291,293. ISBN 0205239390.
  7. ^ https://www.nytimes.com/2013/01/28/health/brain-aging-linked-to-sleep-related-memory-decline.html
  8. ^ Walker, Matthew P. (1 January 2008). "Sleep-dependent memory processing". Harvard Review of Psychiatry. 16 (5): 287–298. doi:10.1080/10673220802432517. ISSN 1465-7309.
  9. ^ a b http://walkerlab.berkeley.edu/reprints/Walker_JCSM_2009.pdf
  10. ^ a b http://www.architalbiol.org/aib/article/viewFile/411/370
  11. ^ a b c d Carlson, Neil R. (2012). Physiology of Behavior. Pearson. pp. 297–298. ISBN 0205239390.
  12. ^ a b c Slow-Wave Sleep: Beyond Insomnia. Wolters Kluwer Pharma Solutions. ISBN 978-0-9561387-1-2.
  13. ^ Jones, BE (1 May 2003). "Arousal systems". Frontiers in bioscience : a journal and virtual library. 8: s438-51. ISSN 1093-9946. PMID 12700104.
  14. ^ Williams SR, Tóth TI, Turner JP, Hughes SW, Crunelli W (1997) The window component of the low threshold Ca2+ current produces input signal amplification and bistability in cat and rat thalamocortical neurones. J Physiol 505:689–705.
  15. ^ McGinty, Dennis; Ronald Szymusiak (1990). "Keeping cool: a hypothesis about the mechanisms and functions of slow-wave sleep". Science Direct. Trends in Neuroscience. 13 (12): 480–487. doi:10.1016/0166-2236(90)90081-k.
  16. ^ Afaghi A, O'Connor H, Chow CM (August 2008). "Acute effects of the very low carbohydrate diet on sleep indices". Nutr Neurosci. 11 (4): 146–54. doi:10.1179/147683008X301540. PMID 18681982.
  17. ^ Schierenbeck, T.; Riemann, D.; Berger, M.; Hornyak, M. (Oct 2008). "Effect of illicit recreational drugs upon sleep: cocaine, ecstasy and marijuana". Sleep Med Rev. 12 (5): 381–389. doi:10.1016/j.smrv.2007.12.004. PMID 18313952.
  18. ^ Gates, P.J.; Albertella, L.; Copeland, J. (Feb 2014). "The effects of cannabinoid administration on sleep: a systematic review of human studies". Sleep Med Rev. 18: 477–487. doi:10.1016/j.smrv.2014.02.005. PMID 24726015.
  19. ^ http://www.brighamandwomens.org/about_bwh/publicaffairs/news/pressreleases/PressRelease.aspx?sub=0&PageID=942
  20. ^ http://www.massgeneral.org/about/pressrelease.aspx?id=1502
  21. ^ Carlson, Neil R. (2012). Physiology of Behavior. Pearson. p. 305-307. ISBN 0205239390.
  22. ^ http://www.hgi.org.uk/archive/sleepanddream1.htm#.U2kpm8fhjys
  23. ^ Tononi, Giulio; Cirelli, Chiara (February 2006). "Sleep function and synaptic homeostasis". Sleep Medicine Reviews. 10 (1): 49–62. doi:10.1016/j.smrv.2005.05.002. PMID 16376591.
  24. ^ Carlson, Neil R. (2012). Physiology of Behavior. Pearson. p. 298. ISBN 0205239390.
  25. ^ Carlson, Neil R. (2012). Physiology of Behavior. Pearson. p. 299-300. ISBN 0205239390.
  26. ^ http://onlinelibrary.wiley.com/enhanced/doi/10.1111/j.1365-2869.2011.00959.x/
  27. ^ Roehrs, Timothy; Roth, Thomas (December 2010). "Drug-Related Sleep Stage Changes: Functional Significance and Clinical Relevance". Sleep Medicine Clinics. 5 (4): 559–570. doi:10.1016/j.jsmc.2010.08.002. PMID PMC3041980. {{cite journal}}: Check |pmid= value (help)
  28. ^ http://www.theodora.com/drugs/eu/xyrem.html

Further reading

  • M. Massimini, G. Tononi, et al., "Breakdown of Cortical Effective Connectivity During Sleep," Science, vol. 309, 2005, pp. 2228–32.
  • P. Cicogna, V. Natale, M. Occhionero, and M. Bosinelli, "Slow Wave and REM Sleep Mentation," Sleep Research Online, vol. 3, no. 2, 2000, pp. 67–72.
  • D. Foulkes et al., "Ego Functions and Dreaming During Sleep Onset," in Charles Tart, ed., Altered States of Consciousness, p. 75.
  • Rock, Andrea (2004). The Mind at Night.
  • Warren, Jeff (2007). "The Slow Wave". The Head Trip: Adventures on the Wheel of Consciousness. ISBN 978-0-679-31408-0.

Response(s) to the above edit

  • Regarding "often referred to as deep sleep, consists of stage three..." It should be made clear, before this sentence, that the original Stages 3 and 4 (less than 50%, more than 50%) are now (most often) combined to just Stage 3. It was previously a bother to decide how much of which, and the difference isn't that critical. Starting out with the quoted bit is confusing.
  • Ref 9 needs fixing?
  • "has been effected in individuals" could be reworded. Maybe: has been seen?
  • Regarding "normal patients". We avoid using the word patient where it is not necessary. Could say "healthy people/person(s)", f.ex.
  • Sleep spindle should be wikilinked.
  • "...the non-learning control task." is awkward wording.
  • 'Learning and Synaptic homeostasis' -- synaptic should not be capitalized.

--Hordaland (talk) 14:11, 30 March 2017 (UTC)Reply

Thank you for the thorough critique, Hordaland. I will definitely make these changes. C.q20n.17 (talk) 17:01, 17 April 2017 (UTC)Reply


First comments; from September 2005 to July 2006 edit

I know this page is sparse on the details.... but there are so many references to slow wave sleep in other articles.. i thought it should be given its own page.

I though adding the image would be nice..... I'll add links to the other stages in the main sleep page.

MrSandman 18:34, 19 September 2005 (UTC)Reply

The link to rebound doesn't adequately provide a context for this article.. so perhaps if someone could change that. I will meander over to it when I have some spare time.

Nudas veritas 07:44, 27 December 2005 (UTC)Reply

No one without a specific degree or whatever can understand much of this. At least articles for the other terms should be made. 24.110.21.111 04:00, 26 July 2006 (UTC)Reply

Complicated article edit

I arrived at this article as someone had mentioned to me that we need 100 minutes of "deep sleep" per day. Deep sleep redirects here which seems fine but I found the article challenging to understand. I did one minor edit to better show how Slow-wave sleep (SWS) fits into NREM but see that a couple of edits are needed by someone well versed in SWS.

Something that caught my attention is the paragraph that starts with "Certain substances, such as benzodiazepines..." and says "as do the substances mentioned above". Did a section on medications that increase SWS get edited out of the article or does the "substances mentioned above" refer to SSRI medications which are intended for an entirely different purpose than SWS modification?

The article does not address the "deep sleep" SWS questions I had in the first place. I've heard for years about the need for X minutes of REM sleep and so was curious on what the research shows on the need for "deep sleep" which I learned today is part of NREM. Oddly, both this article and Non-rapid eye movement sleep are entirely silent on this issue other than people feel groggy for ~30 minutes on being awakened from SWS and tend to fall back into SWS rapidly. I'll check back with the person that told me about the 100 minutes issue and only mention it here as it seems the lay people (me) are told we need so many minutes of such and such sleep per night and yet the Wikipedia articles, including sleep are silent on this issue other than reporting on sleep deprivation experiments. Marc Kupper (talk) (contribs) 19:49, 6 July 2008 (UTC)Reply

Disjointed Article missing section on "Possible Purposes and Function of Slow-Wave sleep" edit

This article lacks coherent information on the possible biological function of slow-wave sleep (both neurological and physical), for instance the possible role slow-wave sleep plays on declarative memory or the role slow wave sleep may play on physiological processes such as (anabolic processes) healing, growth, growth hormone production, and catabolic processes. As well as the potentially severe physical and neurological harm that can occur from the deprivation of this stage of sleep (as opposed to the impact of.... say REM sleep of stage N2 of NREM sleep). —Preceding unsigned comment added by 66.130.154.212 (talk) 16:56, 23 March 2009 (UTC)Reply

TOC edit

Missing table of contents —Preceding unsigned comment added by 66.130.154.212 (talk) 17:01, 23 March 2009 (UTC)Reply

Huh? edit

I have no idea what this statement means:

After sleep deprivation there is a sharp rebound of SWS, suggesting its homeostatic control.

What does it mean for there to "be a rebound" of SWS after sleep deprivation? What does it mean for it to "suggest its homeostatic control?" Maybe there used to be some context that has been lost? 50.39.144.199 (talk) 23:57, 28 January 2012 (UTC)Reply

Fixed, I hope. --Hordaland (talk) 11:42, 29 January 2012 (UTC)Reply




Bwrs (talk) 03:39, 29 October 2009 (UTC)Reply

"Trazadone" edit

Article stated "trazadone" (sic) was a TCA, removed. — Preceding unsigned comment added by 86.101.2.3 (talk) 20:50, 25 November 2012 (UTC)Reply

Consciousness edit

I have had multiple occasions where i was fully Aware and conscious while entering deep sleep and during deep sleep, does anyone have a link that can explain a bit about that? also, i suffer from several disorders that may cause this and am 100 percent sure i was in deep sleep since i am very connected to my subconsciousness --Lordcat33 (talk) 16:14, 14 March 2013 (UTC)Reply

Here:
http://www.sunypress.edu/p-4013-sleep-as-a-state-of-consciousne.aspx
https://en.wikipedia.org/wiki/Yoga-nidra

Ambiguity edit

"An individual will sleep-walk leaving his or her bed in the middle of the night seeking out food, and will eat not having any memory of the event in the morning."

This sentence is ambiguous. Read one way, it implies that the subject finds food and eats it in the middle of the night. Alternatively, it could suggest that he or she will simply have breakfast without remembering having sleep-walked. (--Unfree) 208.54.85.140 (talk) 08:53, 3 May 2014 (UTC)Reply

Refs for unclear statement edit

Paragraph began with an uncited statement.

  • Formerly it ended:

Some resources reject it[clarification needed].[1][2]

(That's 2 book refs, one from 2002 and one undated.)

  • Recently changed to:

Some resources reject it[clarification needed].[3]

(That's one ref, even older.)

Removed the entire paragraph -- until statement is clarified and recent ref(s) provided.

--Hordaland (talk) 02:53, 20 June 2016 (UTC)Reply

  1. ^ Practical Guide for Clinical Neurophysiologic Testing: EEG. p. 241. Benzodiazepine increase delta, spindle coma
  2. ^ Biological Psychiatry. 2002. While hypnotic drugs increase slow wave sleep, they do not increase delta wave activity, and instead increase spindle activity during slow wave sleep.
  3. ^ "Comparative effects of melatonin, zolpidem and diazepam on sleep, body temperature, blood pressure and heart rate measured by radiotelemetry in Wistar rats". Psychopharmacology (Berl). August 2001. DZ modified mean duration of SWS (L: -27%, D: +26%) and increased total duration of SWS (+47%)

Article Editing as an Assignment edit

Hello everyone, my name is Şeyma. I have taken on the responsibility of editing this Wikipedia article and would like to introduce myself briefly. I graduated from the psychology department and am currently pursuing a master's degree in 'Neuroscience' at Uskudar University in Istanbul, Turkey. I have completed all Wikipedia training modules to enhance my editing skills. As part of my assignment for the master's course 'Biotechnology in Neuroscience,' I have chosen to edit the article 'Slow-wave sleep'. My goal is to improve the overall article by enhancing references, citations, and making minor edits. If you have any questions, please feel free to ask. Additionally, I would appreciate any feedback or support for my edits.

Best regards, SeymaPsy (talk) 19:39, 14 January 2024 (UTC)Reply