Flashcards Psychology of Sleep: Stages, EEG, REM, and Circadian Rhythms

Cortisol and sleep?

Stress hormone; it must decrease for you to fall asleep. When cortisol is high, growth hormone is low.

Who reports more subjective sleep disturbance, and when does it increase?

Women; it increases around menopause.

Daytime fatigue with age?

Increases as you get older.

Sleep need?

Average amount of sleep needed daily to maintain alertness and not have sleep debt.

Large sleep debt leads to?

Microsleeps (2-3 seconds of sleep).

17 hours awake equals what BAC impairment?

0.05% BAC (0.08 = DUI).

24 hours awake equals what BAC impairment?

0.10% BAC.

Sleepiness in residents is equivalent to?

Patients with serious sleep disorders, between sleep apnea and narcolepsy.

Behavioral definition of sleep?

Behavioral inactivity, sleep posture, decreased responsiveness, and return to waking with moderate stimulation.

Electroencephalography (EEG)?

Recording of average electrical activity of groups of neurons in the cortex; invented by Hans Berger.

NREM: what does it stand for and how much of the night?

Non-Rapid Eye Movement; Stages 1-4; about 75% of the night.

NREM Stage 1 features?

Wake-to-sleep transition, twitching/hypnic jerks, easily awoken, theta waves, slow eye rolling.

NREM Stage 2 features?

Lose consciousness of environment; K-complexes and sleep spindles.

K-complex?

Big isolated deflection = single slow wave, generated by the neocortex (Stage 2).

Sleep spindles: description and frequency?

Waxing and waning oscillations (12-15 Hz); Stage 2.

Other names for Stage 3/4 sleep?

Slow Wave Sleep (SWS) or deep sleep; you need enough to satisfy need.

SWS features?

Neurons synchronize to a slow rhythm, extremely hard to waken, delta waves.

Slow waves?

Low-frequency oscillations (neurons firing together).

What drives SWS?

The sleep-wake restorative process; the amount of SWS depends on how long you have been awake.

REM: what does it stand for and how much of the night?

Rapid Eye Movement; dreams; about 25% of the night.

REM EEG pattern?

Looks similar to the awake mind (desynchronized activity); alpha and theta waves.

PGO waves?

Ponto-geniculo-occipital waves: high-amplitude electrical potentials generated by the pons.

REM deprivation and PGO?

REM deprivation = high density of PGO. Increase in PGO = learning in animals (and vice versa).

REM body signs?

Eyes dart back and forth; body muscles paralyzed.

REM is regulated by which neurotransmitters?

Serotonin and acetylcholine.

Effect of stimulating acetylcholine on REM?

You move quickly into REM.

Effect of serotonin / SSRIs / antidepressants on REM?

They shorten REM sleep.

REM in people with depression?

They have lots of REM.

What drives REM?

Circadian rhythm (internal biological clock); not affected by wake hours.

Brain areas with increased activity in REM?

Pons, limbic system, parietal cortex, temporal cortex.

Brain areas with decreased activity in REM?

Primary visual cortex, motor cortex, dorsolateral prefrontal cortex (PFC).

Why are the limbic cortex and amygdala active in REM?

They are freed from the prefrontal cortex's inhibition.

Length of a sleep cycle?

About 90 minutes.

Order of stages in Cycle 1?

N1 (light) > N2 (medium) > N3/4 (deep/SWS) > N2 (medium) > REM.

Order of stages in later cycles?

After an hour it cycles back: N2 > N3/4 > N2 > REM. N1 is usually skipped after you first fall asleep.

SWS (Stage 3/4) across the night?

Early in the night; decreases in length as the night progresses.

REM across the night?

Later in the night, toward morning; increases in length as the night progresses.

Wakefulness EEG pattern?

Desynchronized activity.

Theta waves (4-9 Hz) in wakefulness?

Spatial navigation, memory, sensory.

Alpha waves frequency?

7-12 Hz.

Beta waves (10-30 Hz)?

Learning.

Gamma waves (30-80 Hz)?

Attention.

EOG?

Activity from muscles around your eyes. Slow rolling = Stage 1; rapid = REM.

EMG?

Activity from other muscles. REM = atonia (total muscle paralysis).

Two Process Model of Sleep Regulation?

Process S (sleep homeostat) and Process C (circadian).

Process S (sleep homeostat)?

Balances wake and sleep (SWS). SWS = restorative, growth hormone.

Homeostasis?

Maintenance of equilibrium by regulation of internal states.

Process C (circadian)?

REM; internally driven, consistent; about 24 hrs; light-dark cycle/social time.

Circadian clock genes?

CLOCK, BMAL1, CRY1, CRY2, PER1, PER2, PER3.

What does the circadian rhythm regulate?

Organs, humors, urine production; stays consistent despite lack of environmental cues about time of day.

Zeitgebers?

'Time givers': environmental factors that regulate your circadian rhythm (exercise, noise, meals, temperature).

Free run?

Without zeitgebers, you settle into a rhythm of activity and rest but drift out of phase with the 12 hr day/light cycle.

Which light affects circadian rhythm?

Blue/green light, but not red light.

Blue vs. red light sources?

Blue: morning light and LED. Red: sunset and lightbulbs.

Ultradian rhythm?

Less than one day (e.g., stages of sleep).

Infradian rhythm?

More than one day (e.g., PMS).

Circannual rhythm?

Yearly (e.g., hibernation).

Suprachiasmatic nucleus (SCN): location and function?

Part of the hypothalamus; controls temperature and sleep circadian rhythms.

SCN damage?

Less consistent rhythms; not synchronized to light/dark.

How does light information reach the SCN?

SCN cells are modulated by light via retinal ganglion cells (RGCs) that contain melanopsin (a photopigment).

RGCs signal daylight to the SCN: result?

Stop creating melatonin.

SCN and the pineal gland?

SCN regulates the pineal gland, which secretes melatonin. RGC signals no light (night) = more melatonin.

Jet lag?

Disruption of circadian rhythms due to crossing time zones.

Traveling west vs. east: phase effects?

West = phase delays; east = phase advances.

Social jet lag?

Difference between weekday sleep pattern and weekend sleep pattern.

Within-subjects design?

Same person in all conditions; reduces variability between groups/individuals.

Between-subjects design?

Control vs. experimental groups.

Psychomotor Vigilance Task (PVT)?

Sustained attention/reaction time task.

PVT: well rested vs. sleep deprived?

Well rested = stable, within ms, no lapses. Sleep deprived = unstable, lots of lapses (good then bad).

Brainstem parts and role?

Midbrain, pons, medulla. All sensory and motor info passes through; autonomic NS (consciousness, heart rate, respiration); communicates with hypothalamus (wake/sleep transition).

Medulla?

Life sustaining (breathing, swallowing, heart rate, blood pressure); most important, involuntary; helps transfer neural messages from brain to spinal cord. Damage = vegetative state, fatal.

Reticular formation?

Loosely clustered neurons in white matter; waking/alertness, arousal, attention, sleep, awareness.

Reticular formation damage?

Coma (inhibits waking), death, fatigue, sexual arousal changes, disrupted sleep.

Which structure prevents motor movement during REM?

The pons.

Thalamus: location and function?

Forebrain; sensory relay station from sensory receptors to brain areas.

Thalamus in NREM vs. REM?

Turned off during NREM (shuts out the world); activated during REM (vivid dreams).

Thalamus and sleep spindles?

Produces sleep spindles (NREM Stage 2) = rehearses old memory.

Thalamus damage?

Sensory confusion, cannot stay awake, hypersomnolence (daytime sleepiness).

Sleep spindles in coma patients?

Excitation/active brain; patient might regain consciousness.

Locus coeruleus (LC)?

In the pons; axons release norepinephrine to arouse cortex = wakefulness.

LC during sleep?

Dormant, but bursts of LC activity remind the brain of important/emotionally salient experiences to process.

Basal forebrain in arousal and sleep?

Releases inhibitory GABA = sleep; other axons release excitatory acetylcholine = increased arousal.

Hypothalamus and histamine?

Releases histamine = excitatory. Antihistamine = sleepy.

Orexin/hypocretin?

Released by the hypothalamus; ability to stay awake; stimulates acetylcholine-releasing cells (increases wakefulness and arousal).

Orexin and narcolepsy?

Neurons that create orexin/hypocretin die off in narcolepsy.

Wake-promoting neurotransmitters?

Glutamate; histamine and orexin/hypocretin (hypothalamus); acetylcholine; dopamine (monoamine); norepinephrine (locus coeruleus); serotonin (raphe and pons).

NREM-promoting neurotransmitters?

GABA, galanin, adenosine, melatonin (pineal gland, SCN).

Adenosine and sleepiness?

Accumulation of adenosine inhibits basal forebrain cells for arousal; lots of adenosine = sleepy.

How does caffeine work?

Blocks adenosine receptors = wakefulness.

Prostaglandins and sleep?

Accumulate through the day, inducing sleep by stimulating the basal forebrain to release adenosine and inhibiting histamine release from the hypothalamus.

REM-promoting neurotransmitters?

Acetylcholine and GABA (basal forebrain), glutamate, glycine (muscle atonia).