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Clocks, Sleep & Rhythms Of Life > Lectures 10-12 > Flashcards

Lectures 10-12 Flashcards

1
Q

What are the two main definitions of sleep?

A

Behavioural: A normal absence of consciousness.

Electrophysiological: A pattern of specific brain wave activity.

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2
Q

What is the transition from waking to ‘sleep’ associated with?

A

An overall decrease in neuronal activity.

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3
Q

Why is sleep NOT a global ‘turning down’ of brain activity?

A

It’s a deliberate and active process:

Sleep is a series of precisely controlled brain states and the sequence is determined by activity of specific brain nuclei.

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4
Q

Why do we sleep?

A

Sleep is a basic homeostatic function that occurs in some fashion in all multicell organisms.

The requirement for sleep increases with the time spent awake.

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5
Q

What is the relationship between sleep duration and organism size?

A

The duration of sleep appears to increase with organism size.

Smaller organisms tend to alternate between short bouts of sleeping/waking - suggested due to reduced capacity for wakefulness or as a requirement for increased vigilance

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6
Q

Describe the general trend of sleep duration in humans as they age.

A

From when you are born, there is a downwards trend from ~16 hours of sleep to ~6-7 hours per night.

This goes from 16 -> 12 hours in the first year, then 12 -> 10 hours when you are 10 years old, and sloping down from 10 -> 8 and below once you’re 20 years old.

It’s also not just the amount of time that you sleep for that changes, it’s also the patterns of sleep (when a child it’s more sporadic, adults it’s more consistent).

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7
Q

Why do you need to sleep?

A

Across all organisms, we know that sleep is critical for the maintenance of cognitive function - without sleep you will die.

STUDY: used electrophysiological recordings in rats and just as they were showing that they were about to sleep, they would then shake the cage keeping them in perpetual sleep deprivation.

After 2 weeks, the rats would die. This is impressive given their relative lifespan.

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8
Q

What is the main methodology to measure sleep?

A

Electroencephalography (EEG).

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9
Q

What are the main advantages of using EEG in sleep research?

A

It provides a continuous recording of brain activity.

It’s cheap and non-invasive - it can be taken home to be worn during sleep.

It allows a quantitative measure of whether someone is actually asleep or not.

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10
Q

What is ECoG?

A

Electrocorticogram - it’s when the cortex is exposed and the electrodes are placed directly on its surface.

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11
Q

What are the two main measurements in which EEG waveforms are measured?

A

According to their amplitude and frequency.

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12
Q

What is the general rule about the brain waves waveform as you fall asleep?

A

The amplitude gets bigger and the frequency gets slower as you get into deeper sleep.

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13
Q

Provide an overview of EEG sleep stages.

A

EEG Sleep Stages Overview

  • NREM Sleep:
    • Stage 1: Alpha → theta waves; light sleep, easy to wake.
    • Stage 2: Theta waves with sleep spindles & K-complexes; stable sleep.
    • Stage 3: Delta waves; deep sleep, hard to wake, essential for recovery.
  • REM Sleep:
    • EEG resembles wakefulness (low amplitude, mixed frequency).
    • Rapid eye movements, muscle paralysis, vivid dreams.
  • Sleep Cycles: ~90 min; more deep sleep early, more REM later.
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14
Q

Outline the key details of alpha waves

A
  • Frequency: 8-13 Hz
  • Associated with: Relaxed wakefulness, calm focus (e.g., eyes closed but awake).
  • Common location: Occipital and parietal regions.
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15
Q

Outline the key details of beta waves

A
  • Frequency: 13-30 Hz
  • Associated with: Active thinking, problem-solving, and alertness.
  • Common location: Frontal and central regions.
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16
Q

Outline the key details of theta waves

A
  • Frequency: 4-8 Hz
  • Associated with: Light sleep, deep relaxation, and drowsiness.
  • Common location: Temporal and parietal regions.
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17
Q

Outline the key details of delta waves

A
  • Frequency: 0.5-4 Hz
  • Associated with: Deep sleep (Stage 3 NREM), restorative processes.
  • Common location: Frontal regions during deep sleep.
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18
Q

Outline the key details of gamma waves

A
  • Frequency: 30-100 Hz
  • Associated with: High-level cognition, attention, and memory binding.
  • Common location: Distributed across the brain.
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19
Q

What did Kleitman and Aserinsky show about sleep in 1953?

A

Using EEG recordings they showed that sleep consists of a number of ages that occur in a characteristic sequence.

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20
Q

What is the average amount of sleep cycles per night and what type of chart would show you this?

A

Average of 5 sleep cycles/night.

A hypnogram.

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21
Q

What are the unique characteristics of REM/SWS and deep sleep as a person goes through all the sleep cycles?

A

REM duration increases/SWS decreases throughout the sleep bout.

Deep sleep is only present in the first two cycles.

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22
Q

What is an EOG?

A

Electrooculogram

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23
Q

What is an EMG?

A

Electromyogram

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24
Q

What does a hypnogram show?

A

The proportion of time spent in different sleep stages

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25
Q

What do EOGs reveal about sleep?

A

That eye movement is most active during REM.

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26
Q

What do EMGs reveal about sleep?

A

Neck movement is most prominent at waking and REM transitions.

27
Q

What happens to heart rate and respiration levels during REM?

A

They peak to waking levels.

28
Q

What are the three interacting neural systems that actively control sleep (at least)?

A

Forebrain System - can independently support SWS.

Brainstem System - activates the forebrain into waking.

System in the Pons - triggers REM sleep.

29
Q

What studies were critical for identifying the 3 interacting neural systems that actively control sleep?

A

Frederic Bremer nerve transection studies performed in Cats.

30
Q

What is the role of the forebrain in actively controlling sleep?

A

It can independently support SWS.

31
Q

What is the role of the brainstem in actively controlling sleep?

A

It activates the forebrain into waking.

32
Q

What is the role of the system in the Pons in actively controlling sleep?

A

It triggers REM sleep.

33
Q

Outline the Encephale Isole study by Frederic Bremer (1935).

A

METHODS:
- Used cats and performed a transection between the medulla and the spinal cord.
- This left the brain fully isolated and would highlight the role of the spinal input.

RESULTS:
- The brain went through all the stages of sleep.
- This showed that Spinal Input is not required for waking.

34
Q

Outline the Cerveau Isole study by Frederic Bremer (1935).

A

METHODS:
- He performed a transection between the brainstem and the midbrain so that only the forebrain was present.
- Looked to see what happened to sleep.

RESULTS:
- He found that the brain was stuck in a constant state of SWS.
- This showed that there was a region in the forebrain that was causing SWS (later found to be the VLPO).

35
Q

What is known about the VLPOs role in sleep?

A

Frederic Bremer first showed that isolating the forebrain meant that the brain was stuck in SWS, showing the presence of it’s production here.

Later, studies showed that if you stimulated the VLPO you can make animals fall asleep and that lesions would abolish this type of sleep.

Thus, it seems to be a crucial site for SWS initiation.

36
Q

Provide a general overview as to how the VLPO in involved in sleep.

A

Neurons in the VLPO become active at sleep onset.

It’s neurons are inhibitory (GABAergic) and project widely across the brain.

Their stimulation/activation induces SWS.

VLPO neurons are inhibited by neurochemicals associated with arousal (Noradrenaline, ACh, Histamine and 5HT).

37
Q

If an isolated Forebrain leads to a brain stuck in SWS, what can be inferred about the rest of the brains role in sleep?

A

Forebrain = SWS only.

Brainstem & Forebrain = Can shift between all sleep stages.

Thus, the parts controlling waking and REM must be controlled in the brainstem.

38
Q

What is the ARAS?

A

Ascending Reticular Activation System.

It’s a set of major brainstem arousal pathways that plays a major role in generating waking and REM sleep.

39
Q

Describe in detail the Flip-flop model by Saper et al., (2005).

A

This is the current conceptual model about how the control between sleep and wake works.

There are two sets of mutually antagonistic/opposing cells.

VLPO is sleep promoting and inhibits the wake-promoting cells via Galanin/GABA.

Inputting the following wake-promoting regions:
- TMN - Tuberomammillary Nucleus (Hypothalamus)
- DR - Dorsal Raphe (Brainstem)
- LC - Locus Coeruleus (Brainstem)
- LDT/PPT - Laterodorsal tegmental/pedunculopontine tegmental (Brainstem).

The reverse is true too; the wake-promoting regions input the VLPO and inhibit it using the following neurotransmitters:

  • TMN - GABA/Histamine
  • DR - Serotonin
  • LC - Noradrenaline
  • LDT/PPT - Acetylcholine.

*These connections between cell groups are not necessarily direct.

Via interneurons their signals can be flipped.

So as this stands, everyone is inhibiting everyone.

For the model to work, you need something to come tip the ‘balance’ between wake and sleep.

40
Q

What are the wake promoting areas in the Flip-Flop model? (4)

A
  • TMN - Tuberomammillary Nucleus (Hypothalamus)
  • DR - Dorsal Raphe (Brainstem)
  • LC - Locus Coeruleus (Brainstem)
  • LDT/PPT - Laterodorsal tegmental/pedunculopontine tegmental (Brainstem)
41
Q

What is the neurotransmitter used by the Tuberomamillary Nucleus in the Flip-Flop model? What does it do?

A

GABA/Histamine - Inhibit the sleep-promoting VLPO.

42
Q

What is the neurotransmitter used by the Dorsal Raphe in the Flip-Flop model? What does it do?

A

Serotonin - Inhibit the sleep-promoting VLPO.

43
Q

What is the neurotransmitter used by the Locus Coeruleus in the Flip-Flop Model? What does it do?

A

Noradrenaline - Inhibit the sleep-promoting VLPO.

44
Q

What is the neurotransmitter used by the Laterodorsal Tegmental/Pedunculopontine Tegmental in the Flip-Flop model? What does it do?

A

Acetylcholine - Inhibit the sleep-promoting VLPO.

45
Q

What is the neurotransmitter used by the Ventral Lateral Preoptic Area in the Flip-Flop Model? What does it do?

A

Galanin/GABA - inhibits the wake-promoting areas.

  • TMN - Tuberomammillary Nucleus (Hypothalamus)
  • DR - Dorsal Raphe (Brainstem)
  • LC - Locus Coeruleus (Brainstem)
  • LDT/PPT - Laterodorsal tegmental/pedunculopontine tegmental (Brainstem)
46
Q

What seems to be the neurotransmitter that provides excitatory input to wake-promoting neurons in the Flip-Flop model?

A

Orexin/Hypocretin.

47
Q

What seems to be the neurotransmitter that provides excitatory input to sleep-promoting neurons in the Flip-Flop model?

A

Adenosine seems to be a likely candidate.

It’s not agreed upon yet…

48
Q

Outline the potential reason for Adenosine to be a sleep regulator.

A

Adenosine is a by product of energy metabolism.

During intense neural activity, it will build up in the extracellular space.

So, the longer you’re awake, the more of it you have in your brain - whilst you sleep it will be cleared.

49
Q

What are 4 major pieces of evidence as to why Adenosine might be a sleep regulator?

A

Adenosine levels increase during waking and decrease during sleep.

Adenosine agonists increase sleep.

Adenosine receptor antagonists (e.g., caffeine) inhibit sleep

Adenosine activates the VLPO (sleep promoting) neurons.

50
Q

What are the two pathways of the Ascending Reticular Activating System (ARAS)?

A

Dorsal and Ventral.

51
Q

What is the dorsal pathway of the ARAS? Include its route, neurotransmitters, and roles in wakefulness and sleep.

A

Route: Brainstem → Thalamus → Cerebral Cortex

Neurotransmitters: Acetylcholine (ACh)

Role in Wakefulness: Maintains arousal by enhancing sensory relay through the thalamus.

Role in Sleep: Active during REM sleep, facilitating sensory experiences in dreams.

52
Q

What is the ventral pathway of the ARAS? Include its route, neurotransmitters, and roles in wakefulness and sleep.

A

Route: Brainstem → Hypothalamus → Basal Forebrain → Cerebral Cortex

Neurotransmitters: Monoamines (Norepinephrine, Serotonin, Histamine, Dopamine), Orexin

Role in Wakefulness: Stabilizes wakefulness by promoting cortical activation and preventing transitions to sleep.

53
Q

What is the source and role of noradrenaline in arousal and wakefulness?

A

Source: Locus Coeruleus

Role: Promotes wakefulness

Targets: Neocortex, Hippocampus, Thalamus, Hypothalamus, Cerebellum, Brainstem

Drugs: Amphetamines (+) arousal/wakefulness

54
Q

What is the source and role of serotonin in arousal and wakefulness?

A

Source: Raphe Nuclei

Role: Promotes wakefulness

Targets: Neocortex, Hippocampus, Thalamus, Basal Ganglia, Hypothalamus

Drugs: MDMA (+) arousal/wakefulness

55
Q

What is the source and role of histamine in arousal and wakefulness?

A

Source: Tuberomammillary Nucleus

Role: Promotes wakefulness

Targets: Neocortex, Hippocampus, Thalamus, Basal Ganglia, Hypothalamus

Drugs: Antihistamines (-) drowsiness/sleep (Note: newer versions that do not cross the blood-brain barrier lack this effect)

56
Q

Describe the relationship between the spikes/second of Noradrenaline cells and the sleep/wake of a rat.

A

The activity in the cell is high when the animal is awake and then it declines.

As the cell starts to switch off, it begins to shift into SWS.

It continues to taper off until REM sleep where there is almost NO activity.

57
Q

What is the source and role of acetylcholine in arousal and wakefulness?

A

Source: Pedunculopontine Tegmental Nucleus (PPTN) and Laterodorsal Tegmental Nucleus (LDTN)

Role: Promotes wakefulness

Targets: Thalamus, Cortex, Basal Ganglia, and Basal Forebrain

Drugs:
Cholinesterase inhibitors (+): Enhance ACh availability (used in Alzheimer’s to improve cognition).

Anticholinergics (-): Reduce ACh activity (cause sedation or impair wakefulness).

58
Q

What happens if you stimulate cholinergic neurons in the ascending reticular activating system?

A

It produces arousal and wakes the animal up (if it was sleeping ofc).

59
Q

What is the relation to ACh cells and wake, REM and SWS?

A

High firing during wake and REM

Low firing during SWS.

60
Q

What causes changes in mental states revealed by EEG during sleep?

A

Changes in mental states revealed by EEG result from changes in communication between the thalamus and cortex.

61
Q

What brainstem inputs do thalamocortical cells receive?

A

Thalamocortical cells receive brainstem inputs from:

Locus coeruleus (noradrenaline)
Raphe nuclei (serotonin)
Pontine nuclei (cholinergic)

62
Q

What happens when activity in brainstem afferents decreases?

A

When activity in brainstem afferents decreases:

Thalamic rhythmic bursting occurs.
There is increased synchrony of cortical targets.

63
Q

What does EEG show during sleep (stage 4) and wakefulness?

A

During sleep (Stage 4):

Synchronous activity of many thalamic and cortical neurons.

Appears as high amplitude slow waves (delta activity).

During wakefulness:

Asynchronous activity across thalamic and cortical neurons.

Appears as alpha and beta activity.

64
Q

What does EEG measure (during sleep research) and how does it differ during sleep and wakefulness?

A

EEG measures: Communication from the thalamus to the cortex, recording groups of cortical cells switching on or off.

During sleep: Thalamic cells rhythmically switch on and off, creating synchronous slow waves.

During wakefulness: Thalamic cells stop rhythmic switching and instead respond to sensory information they are tuned to, resulting in asynchronous activity.

Clocks, Sleep & Rhythms Of Life (6 decks)

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