Sleep and Arousal
Sleep
Circadian Rhythms
Suprachiasmatic nucleus
"blocking clock"
Light stimulates the SCN and results in decreased melatonin production by pineal gland in the morning
Low light (darkness) leads to increased melatonin production by pineal gland
Chronotype
Alters with age
Young
Night owls
Performance is worst in the morning
Older
Morning larks
Performance is best in the morning
Why do we sleep?
Recuperation Theories of Sleep
Restorative Theory
Repair and regeneration of the body?
Muscle repair, tissue growth, protein synesis, growth hormone release
Necessary for optimal functioning of physiological systems
Elimination Theory
Rid the brain of excess sensory information?
Certain synaptic connections are strengthened, and others are weakened (or not established) during sleep
Synaptic pruning
Brain Plasticity Theory
Neural reorganization, growth of neurons, and brain structures
Adaptation Theories of Sleep
Immobilization Theory
Early theory of sleep
Why we sleep is to encourage us to be less active where we are most vulnerable
What prompts early humans to have about 8 hours of sleep?
Why do we sleep during the dark part of the cycle?
We can't see in the dark
Predators
Invasions
Ability to navigate is weak
Increased risk of injury
Innate response with species specific patterns
Keeps one inactive and safe during least efficient part of day/nigh cycle
Energy Conservation Theory
We can survive by having a period of time where we are conserving energy
Following survival activities, periods of inactivity are a good way to conserve energy
Such as, hunting, gathering, food preparation, and eating
About 1/3 of the day or our life is spent sleep
Time to digest the food we eat
Metabolism rate decreases about 10% during sleep
Burning less energy during sleep
Functions of Slow-Wave Sleep
Deeper state of sleep that seems to be when our recuperation and recovery takes place
50-70% of growth hormone is released
Seems essential for survival
E.g., Fatal familial insomnia
Hereditary disease
Protein in the brain start to unfold in unseal ways and disrupts activity in part of the brain
Thalamus
Malfunctions
Slow wave sleep stops first
6 months within them not sleeping they die
Lack of SWS correlated with various disorders
Cardiovascular
Diabetes
Obesity
Alzheimer's
Consolidation of declarative memory
Explicit memory
Allows you to talk about your experiences
Dates
Times
Information you can talk about and review
Information you can describe
Functions of REM Sleep
Dreaming
Promote brain development
Facilitate learning
Consolidation of nondeclarative memory
Implicit memory
Things we can't talk about
More about remembering how to do particular tasks
Tying your shoe
Riding a bike
More important for learning tasks
REM rebound phenomenon
Indicated biologically than REM sleep is better than Slow-Wave sleep
If you are sleep deprived, you will have more REM sleep
Make up REM first and then Slow-Wave
True or False?
"Driving sleepy is just as bad as driving drunk"
"Therefore, after 17 hours of sustained wakefulness cognitive psychomotor
performance decreased to a level equivalent to the performance impairment
observed at a blood alcohol concentration of 0.05%. This is the proscribed
level of alcohol intoxication in many western industrialized countries. After 24
hours of sustained wakefulness cognitive psychomotor performance
decreased to a level equivalent to the performance deficit observed at a blood
alcohol concentration of roughly 0.10%.”
Dawson, D., & Reid, K. (1997). Fatigue, alcohol and performance impairment. Nature,
388(6639), 235-235
REM Sleep and Development
Infants and Toddlers sleep a lot
Brain develops faster
Dream more
The older we get the less sleep we get
Brain growth and development slows down
Cognitive decline in elders
Dream less
Species Specific Hours of Sleep per Day
Large differences found between species
Bat
19.9 ( a lot)
Horse
2.9 (little)
Metabolic rate
Measurement of Arousal and Sleep
Physiological Measures of Arousal and Sleep
Electroencephalogram (EEG)
Electrical potential recorded from electrodes placed on the scalp
"Brain Waves"
Swimmers cap
Looks at patterns where particular waves show wakefulness and levels of wakefulness
Different stages of sleep have different patterns of waves
Electrooculogram (EOG)
Measure of eye movements seen during sleep
Electrodes placed on eyebrow, below eye, and on each side
SWS
Slow rolling eye movements
Think: Eyeball floating in water
REM
Rapid eye movements
Left-right (fast)
Electromyogram (EMG)
Electrical potential recorded from an electrode placed on muscle
Measures changes in muscle tension particularly facial and neck muscles
Mentalis muscle
Muscle on chin
Connects lower lip to chin
Muscle completely relaxes when asleep
Other muscles still have tone
Theories of Sleep
Passive Theory of Sleep
Bremer (1936)
Cerveau isole
Isolating the forebrain
Continuous state of slow-wave sleep
Strong odor could wake then up and within minutes fell back asleep
Encephale isole
Cut the brain from the spinal cord
Normal sleep-wave cycle
Ignored data
Focused more on isolating the forebrain
Active Theory of Sleep
Moruzzi and Magoun (1949)
Discovered the reticular formation
Four Pieces of Evidence that the Reticular Activating System is Involved in Sleep
(2) only cutting the small section of reticular
When they cut just reticular information, the tasks show the exact same slow-wave pattern as if the cut the whole brain
Bremer is WRONG
Sleep Characteristics and Neurotransmitters
Sleep-Wake Cycle
More through sleep in particular order
Stage 1 sleep
Only occurs when we are coming out of wakefulness (falling asleep)
Roughly, 1-7 minutes before descending into stage 2
Stage 2 sleep
You feel like you have been asleep, but you also feel your are right on the edge
Roughly, 10-20 minutes
About 50% of total sleep time
Gets longer towards later cycles
Slow-Wave sleep
Deepest sleep
Roughly, 20-40 minutes
Difficulty waking up
One thing that can wake people up is calling their name
Nightmares tend to occur
Sleepwalking can occur
More time in stage 3 earlier than later
Stage 2 sleep
REM sleep
Dream stage
Roughly, 20-25% of total sleep time
Early in the night is shorter
On average, 1-1.5 hours per cycle
Sleep Stages and Brain Waves
Gamma Wave
Irregular
Low amplitude
Highest frequency
About 30 - 120 Hz
Hyper focused
Beta Wave
Irregular
Low amplitude
High frequency
About 13- 30 Hz
Thinking and processing
Alpha Wave
Fairly regular
Low amplitude
High frequency
About 8 - 13 Hz
Occur when we are relaxed
Theta Wave
Low amplitude
Moderate frequency
About 4 - 8 Hz
Indicator of falling asleep
Sleep Spindles
Short bursts
About 12 - 14 Hz
Extremely short
Correlated with noises
K Complexes
Sudden sharp waveforms
Tactile stimulation
Delta Wave
High amplitude
Low frequency
About 1 - 4 Hz
Activation synesis
Arousal and Neurotransmitters
Acetylcholine
Dorsal pons and basal forebrain
Plays role in arousal of cerebral cortex
Levels high during wakefulness and REM
Project to
Medial pons, thalamus, cortex
Involved in cortex and hippocampus arousal
Norepinephrine
Locus coeruleus (in pons)
Plays roles in attention and vigilance
Possible role in "behavioral" arousal
Levels high only during wakefulness
Lower levels during SWS and lowest during REM
Project and impact
Cortex, thalamus, hippocampus, cerebellum, pons, and medulla
Serotonin (5-HT)
Raphe nuclei
Medial pons
Near caudal end of reticular formation
Levels high during wakefulness
Levels lowering as descending towards REM
Cortical and behavioral arousal
Plays role in activating behavior
Pacing, chewing, grooming in rodents
Projects to and impact
Thalamus, hypothalamus, cortex, hippocampus, basal ganglia
Histamine
Tuberomammillary nucleus
In hypothalamus
Levels high during wakefulness
Levels low during SWS and REM
Implicated in control of wakefulness and arousal
i.e., an antihistamine is Benadryl
Project to and impact
Cortex, thalamus, hypothalamus, basal ganglia, basal forebrain
Orexin
From lateral hypothalamus
Levels high during wakefulness
Low during rest and all sleep stages
Increase activity in the brain stem and forebrain arousal systems
Has a stimulatory effect on all other areas of the brain talked about previously
Slow-Wave Sleep and Neurotransmitters
GABA (GABAergic neuron)
Major inhibitory neurotransmitter
Doesn't promote Slow-Wave sleep
Indirect role
From ventrolateral preoptic area (vlPOA)
Quite down and inhibit the arousal areas of the brain
Suppress alertness and behavioral arousal and promote sleep
Disruption to the brain stem, thalamus, hypothalamus, and cortex
Adenosine
Peptide released by neurons during high levels of metabolic activity through out the day
More active you are, more adenosine released
Highest when you fall asleep
Increases activity in the vlPOA
Brain Mechanisms
The Sleep/Waking Flip Flop
When the flip-flop is in the "wake" state, the arousal systems are active and the vlPOA in inhibited (a)
GABA is coming from the arousal areas and having an effect on vlPOA
Result is vlPOA is inhibited
When the flip-flop is in the "sleep" state, the vlPOA is active and the arousal systems are inhibited (b)
Solid line
Neurotransmitters are being released
vlPOA
Ventrolateral preoptic area
vlPAG
Ventrolateral periaqueductal gray
SLD
Sublaterodorsal nucleus
REM Sleep Brain Mechanisms
Narcolepsy
Symptoms of Narcolepsy
Sleep attack
Cataplexy
Sleep paralysis
Hallucinations
Hypnagogic
Hypnopompic
Additional symptoms
Difficulty staying awake during the day
Difficulty staying asleep during night
Fragmented sleep
REM sleep intrudes into waking state
Seem to skip SWS and enter REM sleep quickly
Prevalence
1 in 2000
Causes of Narcolepsy
Seems to be related to deficiency of peptide neurotransmitter orexin
Mutation in orexin B receptor (causes canine narcolepsy)
In humans
Complete absence of orexin in 7 out of 9 persons with narcolepsy
Most are born with orexin, but during adolescence the immune system may attack these neurons and symptoms begin
Treatment of Narcolepsy
Stimulants
Ritalin and Amphetamine
Methylphenidate (Ritalin)
Dopamine and norepinephrine agonist
Reuptake inhibitor
Amphetamine
Dopamine & norepinephrine agonist
Reuptake inhibitor
Modafinil (Provigil)
Orexin agonist
Typically taken in the morning
Help to reduce daytime sleepiness
I.e., decrease sleep attacks
SSRIs and SNRIs
Fluoxetine
Prozac, Serafem, others - SSRI
Venlafaxine
Effexor - SSRI
Atomoxetine
Strattera - SNRI
Typically taken later in the day
Help to reduce episodes of REM sleep components
I.e., episodes of cataplexy, sleep paralysis, and hallucinations
Tricyclic Antidepressants
Norepinephrine, serotonin, dopamine agonist
Reuptake inhibitor
Protriptyline
Vivactil
Imipramine
Tofranil
Typically taken later in the day
Help to reduce episodes of REM sleep components
I.e., cataplexy, sleep paralysis, and hallucinations
Sodium Oxybate
Xyrem
CNS depressant that reduces excessive daytime sleepiness and cataplexy
GABA-B receptor agonist
Taken at night
Immediately before bed
Second dose 3-4 hours later
Middle of the night
