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dolphins
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whales
sperm whale (off the coast of Chilé)
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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….
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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)
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)
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tells us about the n of EPSPs that occur at the same point in
time
n of neurons firing in synchrony
high frequency, low amplitude
beta waves
start seeing higher amplitude, lower
frequency alpha waves
1st sleep stage – still fairly high frequency
low amplitude but clear difference from
alert and awake state
often will deny being asleep
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?–
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
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first bout of REM sleep
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low amplitude, high frequency
desynchronous EEG
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low amplitude, high frequency desynchronous EEG
rapid eye movement (REM)
narrative dreams
muscle atonia
◦ look at motor cortex – extremely active but descending
motor pathways paralyzed
◦ REM without atonia
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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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changes in amount of time spent in REM over
the night
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……
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restoration and repair
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Sleep more if:
◦ No predators
◦ Safe place for sleeping
◦ Dangerous to yourself in the dark
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Sleep less if:
◦ Fear of predation
◦ Food of low nutritional value
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evolutionary theory
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restoration and repair
◦ marathon runner studies
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Insomnia
1.
Insomnia
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primary cause - sleep medications
1.
Insomnia
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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)
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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)
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First in a new class of sleep medications
non BZ
non sedative
melatonin agonist
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Insomnia
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primary cause - sleep medications
- develop tolerance; REM rebound
- we are often poor estimators of how
much sleep we get
-sleep apnea – difficulty sleeping and
breathing at the same time
-two types
- 1. CNS mediated – very rare
- 2. obstructive sleep apnea- main cause
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
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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
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What does it do during sleep?
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locus coerulus- in hindbrain (NE transmitter)
◦ important for arousal
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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 asleepvery vivid dreams and nightmares!
 PGO waves –
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Increases in tryptophan – increases in 5HT
Increases in 5HT – increases in drowsiness (?)