Lecture 6: Sleep and biological rhythms Flashcards

1
Q

How is sleep measured?

A

EEG-Electrical activity
EMG- Muscle activity
EOG-Eye movements
PSG-the whole system of assessment plus O2 levels, heart and breathing

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2
Q

Beta activity

A

Arousal

Irregular electrical activity of 13-30 Hz

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3
Q

Alpha activity

A

Relaxation

Smooth electrical activity of 8-12Hz

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4
Q

Theta activity

A

transition between wakefulness and sleep

EEG activity of 3.5-7.5 Hz

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5
Q

Delta activity

A

Regular, synchronous electrical activity less than 4Hz

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6
Q

Sleep stage 1

A

sleep is characterised by drowsiness, muscle activity slows, eye movement slows down, its not uncommon to experience hypnic myoclonia “Startle-like muscle jerks often preceded by the sensation of having to fall.”

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7
Q

Sleep stage 2

A

eye movement stops and brain activity slows down – k complexes and sleep spindles observed in eeg / definitely asleep but easy to wake up.

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8
Q

Sleep stage 3/4

A

sleep characterised by delta activity (v slow) and deep sleep. S3 30%, S4 50%. Very difficult to wake. Lose all muscle tone. Groggy if woken up. Number of sleep disorders occur during S4

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9
Q

REM sleep

A

brain activity becomes desynchronised and resembles alert state / breathing becomes irregular and shallow / eyes jerk rapidly in different directions (hence REM) / limb muscles become paralys ed (paradoxical sleep) / heart rate and blood pressure rises / erections and vaginal excretions occur / dreaming happens.

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10
Q

Sleep cycle

A

Sleep cycles through these stages approximately every 90 minutes. Most slow wave sleep (stages 3 and 4) occurs in the first half of the night. As the night draws on most of our sleep is stage 2 and we see that periods of REM become longer and stage 4 sleep becomes shorter.

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11
Q

Typical nights sleep

A
•	50% Stage 2
•	20% REM
•	30% other stages
•	Sleep needs across species:
	Two-toed sloth – 20 hours
	Infants – 16 hours (50% REM)
	Teenagers – 9 hours
	Adults – 7-8 hours
	Elderly - <7
	Horses – 2 hours

Prem babies 80% in REM

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12
Q

How many people suffer from sleep disorder?

A

33%

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13
Q

Insomnia

A

Occurrence - 25% of pop occasionally and 9% regularly

•Inability to fall asleep, sleep through the night, and / or fall back to sleep after early waking

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14
Q

Sleep apnea

A

Occurrence: 1-6% adults and 2% children

pauses in breathing or periods of shallow breathing during sleep. Pauses can last for a few seconds to a few minutes and occur many times a night

During sleep apnea, carbon dioxide in the blood stimulates chemoreceptors and person wakes up gasping for air. The oxygen levels return to normal, the person falls asleep and the cycle happens over again.

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15
Q

Narcolepsy

A

affects less than 1% of the population

-frequent and intense urges to sleep at inappropriate times

Sleep paralysis: inability to move just before sleep or just after waking while lying down

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16
Q

Cataplexy

A

=varying amount of muscle weakness
sometimes completely paralysed but can still see/hear

-triggered by strong emotional reactions or by sudden physical effort

17
Q

Hypnogogic hallucinations

A

=dreaming whilst aware and awake

18
Q

Evolutionary hypothesis

A

sleep allows us to conserve energy and evade risk
• Animals who have fewer predators tend to sleep longer
• Predatory danger negatively correlates with NREM
and REM sleep
• Only adaptive if safety assured
Importance of REM sleep for brain development
• Early brain development? – premature infants spend 80% in REM sleep vs 50% in non-prem, decreases to 30% in 6 month olds and 22% in 8 year olds
• Sleep facilitates maze learning in rats
• Link with REM time and giftedness in children

19
Q

Rebound phenomenon

A

-particular stages of sleep seem to have more importance for survival

rebound effects
-deprivation followed by increase in proportion of stage 4 and REM sleep, at the expense of other stages

-sleep efficiency rather than length of sleep increases

20
Q

Repair and restoration theory

A
  • Function of sleep is to enable body/brain to repair after exertions of the day
  • Priority given to recovery of stage 4 sleep suggests this type may be particularly important for recuperation
21
Q

Support for repair and restoration theory

A

 Growth hormone mainly secreted during S4 important for tissue growth and cell repair, i.e. “beauty sleep”
 Lowered cerebral metabolic rate – delta waves falls to 75% of waking levels – people in S4 can only be woken by intense stimuli and it takes them a long time to become alert – suggesting the brain is resting

22
Q

Problems with repair and restoration theory

A

 Forced sedentariness does not decrease time in sleep
 No effect of physical exercise on sleep duration
 Fitter active people do not sleep longer than unfit sedentary people

23
Q

Refinement to RR theory: recovery from cerebral activity specifically

A

 Sleep and sleepiness increases following a behaviourally and mentally but not physically “active” day
 Similar sleep duration in an active compared to non-active day
 Increased time spent in S4 slow wave sleep

24
Q

Refinement to RR theory: role in learning and memory?

A

 Improvement in declarative memory following nap or overnight sleep
 Brain appears to rehearse newly learned information during SWS
 Consolidation effects of word learning from ST to LT memory with sleep and napping: gets rid of information that isnt needed

25
Q

What neurotransmitters control arousal system?

A
	   Acetylcholine (Ach)
	   Norepinephrine (NE)
	   Serotonin (5-HT)
	   Histamine
	   Orexin (Ox)
26
Q

VLPA

A

=key switch in the hypothalamus that inhibits arousal system

 Destruction of VLPA causes insomnia
 Stimulation of VLPA causes sleep
• Other hypothalamic neurons stabilize the switch, and their
absence results in inappropriate switching of behavioural states, such as occurs in narcolepsy

27
Q

Flip-flop switch

A

What is interesting about the VLPA and brain stem arousal systems is that they have reciprocal pathways that inhibit each other

-because these systems inhibit each other, explains how bursts of arousal might then inadvertently trigger the VLPA circuit as the arousal system tries to regulate itself – explains symptoms of narcolepsy and sudden flip-flop between excitement to deep sleep

28
Q

ARAS

A

inhibits neurons in the VLPA and releases Its that mediate arousal

29
Q

VLPA

A

GABAergic neurons inhibit ARAS followed by drowsiness and sleep

unstable-always rapidly one or other, no in-between

30
Q

Orexin

A

Neurons in the lateral hypothalamus secrete orexin to prevent suddenly collapsing to the floor

-activated when there’s motivation to stay awake or when something brings you out of sleep eg noise

support the maintenance of arousal and work to stabilize the flip-flop switch – by keeping VLPA inhibited.

31
Q

Acetylcholine and REM sleep

A
  • exposure to an insecticide associated with acetylcholine release caused vivid hallucinations
  • stimulation of Ach by agonist during sleep prolonged the cycle duration of REM sleep while antagonists shortened it
32
Q

Circadian rhythms

A

Zeitgeber = a stimulus (usually light) that resets the biological clock responsible for circadian rhythms

  • Studies conducted in animals and humans where the influence of zeitgebers has been removed to see if the circadian rhythm persists:
  • they find is that there are individual differences within species (so everyone’s cycle length might differ) and that the sleep-wake cycle in humans tends towards 25 hours rather than 24.
  • What keeps everyone’s cycles together is the presence of zeitgebers which entrain the biological rhythms.
33
Q

Suprachiasmatic nucleus (SCN)

A

• Regulates circadian rhythm
• Lesions = circadian rhythms (wheel running, drinking, hormone secretion, body temp and sleep) become
less consistent (occur throughout 24 hr period rather than just one half of the day)
• If removed from brain, SCN neurons
continue to produce circadian rhythm of
action potentials
• Transplants of SCN’s producing “faulty”
rhythms caused recipients to develop similarly
faulty circadian cycles (in hamsters)

34
Q

SCN and sleep cycle

A
  • SCN appears to regulate wake-sleep via its effects on other brain areas (e.g. pineal gland)
  • In response to signals from the SCN, the pineal gland releases a hormone called melatonin
  • Melatonin, released almost exclusively at night, increases sleepiness