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Published byJaiden Hopp Modified over 9 years ago
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dolphins whales
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sperm whale (off the coast of Chilé)
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http://www.nature.com/news/2008/080221/ multimedia/news.2008.613.mov http://www.nature.com/news/2008/080221/ multimedia/news.2008.613.mov
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135,000 hours of your life asleep (1/3) How do we study sleep? What do we know about it? What are some sleep disorders What do we know about brain regions and neurotransmitters involved in sleep?
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typically in a sleep lab…. EEG – electroencephalogram EPSPs of cortical neurons ◦ EMG – electromyelogram looking at muscle tone (usually electrodes on jaw) ◦ EOG – electrooculogram looking at eye movements (electrodes around eye)
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look at 2 components of the EEG 1.the frequency of the wave (n of peaks/unit time) –tells you about the number of cortical neurons generating EPSPs 2.the amplitude of the wave (height of wave) –tells us about the n of EPSPs that occur at the same point in time –n of neurons firing in synchrony
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high frequency, low amplitude beta waves
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start seeing higher amplitude, lower frequency alpha waves
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1 st sleep stage – still fairly high frequency low amplitude but clear difference from alert and awake state often will deny being asleep
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15 min later (if not disturbed) stage 2 – characterized by high frequency low amplitude sleep spindles and high amp low f k complexes role of these wave forms?–
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15 min later if not disturbed stage 3 – first of the slow wave sleep stages characterized by delta waves high amplitude, low frequency waves less than 50% delta waves is stage 3; more than 50% stage 4 (15 min later)
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during SWS, parasympathetic NS activity seems to predominate (hr and bp decrease, respiration decreases, gastric motility increases) person relaxed but still motor activity; normal sleeper changes position every 20 min or so stage 4 deepest stage ?
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typical 90 min sleep cycles goes from ◦ stage 1 (15 min) to stage 2 (15 min) to stage 3 (15 min) to stage 4 (15 min) to stage 3 (15 min) to stage 2 (15 min) to first bout of REM sleep
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low amplitude, high frequency desynchronous EEG
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rapid eye movement (REM) narrative dreams muscle atonia ◦ look at motor cortex – extremely active but descending motor pathways paralyzed ◦ REM without atonia penile erections and vaginal secretions deepest stage? ◦ incorporate things into our dreams ◦ more likely to spontaneously awaken
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changes in amount of time spent in REM over the night
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maturational changes in pattern ◦ species with underdeveloped CNS – spend more time in REM
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changes in amount of time spent in REM over the night maturational changes in pattern ◦ species with underdeveloped CNS – spend more time in REM ◦ human newborns ~ 50% sleep time in REM ◦ human premies ~ 80% sleep time in REM
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evolutionary theory ◦ predictions…… restoration and repair
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Sleep more if: ◦ No predators ◦ Safe place for sleeping ◦ Dangerous to yourself in the dark Sleep less if: ◦ Fear of predation ◦ Food of low nutritional value
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evolutionary theory restoration and repair ◦ marathon runner studies
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1. Insomnia
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-primary cause - sleep medications
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1. Insomnia -primary cause - sleep medications -develop tolerance; REM rebound
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short-acting benzodiazepenes ◦ triazolam (Halcion®)
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short-acting benzodiazepenes ◦ triazolam (Halcion®) problems with BZ tolerance REM suppression (and REM rebound) WD
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Zolpidem- (Ambien) ◦ non hypnotic sedative ◦ Also a muscle relaxant and anticonvulsant ◦ Still works on GABA A receptors ◦ Works quickly (15 min) and with a short ½ life (how quickly it clears out of the body
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releases hormone melatonin at night
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Ramelteon (Rozerem) ◦ First in a new class of sleep medications ◦ non BZ ◦ non sedative ◦ melatonin agonist
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1. Insomnia -primary cause - sleep medications -develop tolerance; REM rebound -we are often poor estimators of how much sleep we get
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-sleep apnea – difficulty sleeping and breathing at the same time -two types -1. CNS mediated – very rare -2. obstructive sleep apnea- main cause
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weight loss, reducing alcohol consumption (or other muscle relaxants), elevated sleeping, CPAP machine – continuous postive airway pressure surgical procedures to remove or tighten tissue
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SIDS – sudden infant death syndrome ◦ possible link
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Nocturnal myoclonus – twitching of the body, usually the legs, during sleep – most are not aware of why they don’t feel rested (now called periodic limb movement disorder); involuntary Restless legs – sufferers complain of legs being uncomfortable that prevents sleep- can occur when awake or asleep Txt can include DA agonists; anticonvulsants Copyright © 2006 by Allyn and Bacon
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~ 250,000 people in US ◦ symptoms: uncontrollable recurring sleep during daytime (usually during mundane tasks) ◦ subcategories cataplexy- hypnagogic hallucinations REM sleep behavior disorder
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often (not always) older males often (not always) associated with other neurodegenerative diseases
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brainstem structures – pons, medulla abnormalities in noradrenergic, cholinergic, and serotonergic systems, seems to exist in the pathogenesis of RBD clonazepam (Klonopin) ◦ anticonvulsant – ◦ benzodiazpene
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unusual sleep characteristics ◦ short latency to REM ◦ persistent muscle tone ◦ excessive muscle twitching Treatment for narcolepsy ◦ stimulants; caffeine, ◦ GHB – gamma hydroxy butyrate**
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genetics of narcolepsy ◦ people with family history + are 50X more likely to have disorder than families without history + ◦ animal species
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Non-REM sleep disorders ◦ Enuresis ◦ Sleep walking
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locus coerulus- in hindbrain (NE transmitter) ◦ important for arousal What does it do during sleep?
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locus coerulus- in hindbrain (NE transmitter) ◦ important for arousal What does it do during sleep? ◦ active when awake; inhibited during sleep – particularly REM
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Acetylcholine – in pons – important for REM onset ◦ AChE poisoning (mustard gas or pesticides) people go into REM immediately after falling asleep- very vivid dreams and nightmares! PGO waves –
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Increases in tryptophan – increases in 5HT Increases in 5HT – increases in drowsiness (?)
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