Week 5 Lecture Content (Sleep I) Flashcards

1
Q

For the purposes of PSYC317, how do we define sleep? How does this relate to being drowsy?

Source: Lecture 13, Section “Defining Sleep and Drowsiness”

A
  • PSYC317 definition: “A state of diminished sensory responsivity, which follows specific patterns of nervous system activity.”
  • Drowsiness is defined as “a state of heightened desire for sleep,” motivating the behaviour of sleep.
  • Traditional dictionary definitions insufficient, claiming nervous system inactivity or using vague terms like “powers of the body being restored.”
  • PSYC317’s definition focuses on observable changes in sensory responsivity and brain activity during sleep.
  • Sleep involves diminished response to external stimuli, but not a complete shutdown of sensory inputs.

Quote: “Drowsiness prompts you to sleep. So our PSYC317 sleep definition is going to be a state of diminished sensory responsivity, which follows specific patterns of nervous system activity.”
Source: Lecture 13, Section “Defining Sleep and Drowsiness”

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2
Q

Describe the following stages of the sleep cycle in terms of EEG characteristics and any unique outward features: Stage 1, Stage 2, Stage 3/4 (SWS), and REM. Make sure you are familiar with the R&K method, and the later AASA classification.

A

Rechtschaffen and Kales (R&K) Method (1968)

Stage 1:
EEG: Dominated by theta waves (4-8 Hz).
Outward features: Light sleep, reduced muscle tone, and possible hypnic jerks (sudden muscle twitches).
Duration: Shortest stage (~10 minutes).

Stage 2:
EEG: Marked by sleep spindles (bursts of 12-14 Hz activity) and K-complexes (large waveforms).
Outward features: Slightly deeper sleep, reduced responsiveness to external stimuli.
Duration: About 15-20 minutes.

Stage 3 & 4 (Slow Wave Sleep - SWS):
EEG: Transition to delta waves (0.5-4 Hz) in Stage 3, with Stage 4 being predominantly delta activity.
Outward features: Deep sleep, least responsive to external stimuli, difficult to awaken. Grogginess if woken from SWS.
Duration: Longest in the first half of the night, gradually decreasing.
These stages are crucial for brain rest and memory consolidation.

REM Sleep:
EEG: Resembles wakefulness, with theta and beta waves (13-32 Hz).
Outward features: Atonia (muscle paralysis except for the eyes), vivid dreaming, rapid eye movements.
Duration: ~20 minutes, with REM periods lengthening throughout the night.

American Academy of Sleep Medicine (AASM) Classification (2007)

Non-REM Stage 1 (N1):
Similar to R&K Stage 1 with theta waves (~10 minutes), some hypnic jerks, and light sleep.

Non-REM Stage 2 (N2):
Same as R&K Stage 2, marked by K-complexes and sleep spindles. Most of the night is spent in N2 (~50%).

Non-REM Stage 3 (N3):
Combines R&K Stages 3 and 4, referred to as SWS. Dominated by delta waves and important for memory consolidation and physical recovery.

REM Sleep (R):
Same as in the R&K method, with high brain activity resembling wakefulness and muscle paralysis. Dreaming is most vivid during REM.

Key Differences Between R&K and AASM:
The AASM system combined Stage 3 and 4 into a single stage (N3) due to the similarities in delta wave activity between these stages.
The AASM system introduced the more formal designation of NREM (N1, N2, N3) and REM (R) sleep, streamlining the classification system and emphasising the importance of each stage in the sleep cycle.

Quote: “By the time you get to Stage 4… it’s predominantly those slow delta waves that you’re seeing… REM sleep, on the other hand, is a kind of paradox because the brain waves look similar to when you’re awake, but you’re asleep and completely paralysed.”


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3
Q

Describe Stage 1 of the sleep cycle in terms of EEG characteristics and any unique outward features.

Make sure you are familiar with the R&K method, and the later AASA classification.

A

Rechtschaffen and Kales (R&K) Method (1968)
Stage 1:
EEG: Dominated by theta waves (4-8 Hz).
Outward features: Light sleep, reduced muscle tone, and possible hypnic jerks (sudden muscle twitches).
Duration: Shortest stage (~10 minutes).

American Academy of Sleep Medicine (AASM) Classification (2007)
Non-REM Stage 1 (N1):
Similar to R&K Stage 1 with theta waves (~10 minutes), some hypnic jerks, and light sleep.

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4
Q

Describe Stage 2 of the sleep cycle in terms of EEG characteristics and any unique outward features.

Make sure you are familiar with the R&K method, and the later AASA classification.

A

Rechtschaffen and Kales (R&K) Method (1968)
Stage 2:
EEG: Marked by sleep spindles (bursts of 12-14 Hz activity) and K-complexes (large waveforms).
Outward features: Slightly deeper sleep, reduced responsiveness to external stimuli.
Duration: About 15-20 minutes.

American Academy of Sleep Medicine (AASM) Classification (2007)
Non-REM Stage 2 (N2):
Same as R&K Stage 2, marked by K-complexes and sleep spindles. Most of the night is spent in N2 (~50%).

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5
Q

Describe Stage 3/4 (SWS) of the sleep cycle in terms of EEG characteristics and any unique outward features.

Make sure you are familiar with the R&K method, and the later AASA classification.

A

Rechtschaffen and Kales (R&K) Method (1968)
Stage 3 & 4 (Slow Wave Sleep - SWS):
EEG: Transition to delta waves (0.5-4 Hz) in Stage 3, with Stage 4 being predominantly delta activity.
Outward features: Deep sleep, least responsive to external stimuli, difficult to awaken. Grogginess if woken from SWS.
Duration: Longest in the first half of the night, gradually decreasing.
These stages are crucial for brain rest and memory consolidation.

American Academy of Sleep Medicine (AASM) Classification (2007)
Non-REM Stage 3 (N3):
Combines R&K Stages 3 and 4, referred to as SWS. Dominated by delta waves and important for memory consolidation and physical recovery.

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6
Q

Describe REM of the sleep cycle in terms of EEG characteristics and any unique outward features.

Make sure you are familiar with the R&K method, and the later AASA classification.

A

Rechtschaffen and Kales (R&K) Method (1968)
REM Sleep:
EEG: Resembles wakefulness, with theta and beta waves (13-32 Hz).
Outward features: Atonia (muscle paralysis except for the eyes), vivid dreaming, rapid eye movements.
Duration: ~20 minutes, with REM periods lengthening throughout the night.

American Academy of Sleep Medicine (AASM) Classification (2007)
REM Sleep (R):
Same as in the R&K method, with high brain activity resembling wakefulness and muscle paralysis. Dreaming is most vivid during REM.

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7
Q

Describe the key differences Between R&K and AASM:

A

Key Differences Between Rechtschaffen and Kales (R&K) Method (1968) and American Academy of Sleep Medicine (AASM) Classification (2007):

  • The AASM system combined Stage 3 and 4 into a single stage (N3) due to the similarities in delta wave activity between these stages.
  • The AASM system introduced the more formal designation of NREM (N1, N2, N3) and REM (R) sleep, streamlining the classification system and emphasising the importance of each stage in the sleep cycle.
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8
Q

Describe Stage 1 of the sleep cycle in terms of EEG characteristics and any unique outward features.

Stage 1:
EEG: Dominated by _____ waves (__ - __ Hz).
Outward features: _____ sleep, _____ muscle tone, and possible ____ (sudden muscle twitches).
Duration: _____ stage (~___ minutes).

A

theta waves (4-8 Hz).
Light sleep, reduced muscle tone, and possible hypnic jerks
Shortest stage (~10 minutes).

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9
Q

Describe Stage 2 of the sleep cycle in terms of EEG characteristics and any unique outward features.

Stage 2:
EEG: Marked by sleep ______ (bursts of __ - __ Hz activity) and _________ (large waveforms).
Outward features: Slightly _____ sleep, _____ responsiveness to external stimuli.
Duration: About __ - __ minutes.

A

Stage 2:
EEG: Marked by sleep spindles (bursts of 12-14 Hz activity) and K-complexes (large waveforms).
Outward features: Slightly deeper sleep, reduced responsiveness to external stimuli.
Duration: About 15-20 minutes.

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10
Q

Describe Stage 3/4 (SWS) of the sleep cycle in terms of EEG characteristics and any unique outward features.

Stage 3 & 4 (Slow Wave Sleep - SWS):
EEG: Transition to ____ waves (__ - __ Hz) in Stage 3, with Stage 4 being predominantly ____ activity.
Outward features: ___ sleep, ____ responsive to external stimuli, ____ to awaken. ______ if woken from SWS.
Duration: ______ in the first half of the night, gradually _____.
These stages are crucial for ____ ____ and ____ ____.

A

Stage 3 & 4 (Slow Wave Sleep - SWS):
EEG: Transition to delta waves (0.5-4 Hz) in Stage 3, with Stage 4 being predominantly delta activity.
Outward features: Deep sleep, least responsive to external stimuli, difficult to awaken. Grogginess if woken from SWS.
Duration: Longest in the first half of the night, gradually decreasing.
These stages are crucial for brain rest and memory consolidation.

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11
Q

Describe REM of the sleep cycle in terms of EEG characteristics and any unique outward features.

REM Sleep:
EEG: Resembles ______, with ____ and ____ waves (__ - __ Hz).
Outward features: _____ (muscle paralysis except for the eyes), vivid dreaming, rapid eye movements.
Duration: ~__ minutes, with REM periods ______ throughout the night.

A

wakefulness, with theta and beta waves (13-32 Hz).
Atonia
~20 minutes; lengthening

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12
Q

How do K-complexes relate to diminished sensory responsivity? Use sound as an example stimulus, and explain what these EEG events represent in terms of communication between the thalamus and the cortex.

A
  • K-complexes are EEG events in Stage 2 that reflect the brain’s inhibition of sensory inputs.
  • In response to stimuli like sound, inhibitory neurons in the thalamus send signals to the cortex, preventing the sound from waking the sleeper.
  • This activity serves to keep you asleep while also processing and potentially consolidating memories.
  • K-complexes are believed to protect ongoing memory consolidation from being disrupted by external stimuli.

Quote: “K-complexes are being generated by cells projecting from the thalamus to the auditory cortex… They send a signal to the cortex saying, shut up. Stay calm. Don’t wake up.”
Source: Lecture 13, Section “K-complexes”

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13
Q

K-complexes are ___ events in Stage ___ that reflect the brain’s inhibition of sensory inputs.

In response to stimuli like sound, ____ neurons in the ____ send signals to the cortex, preventing the sound from waking the sleeper.

This activity serves to keep you asleep while also processing and potentially consolidating memories.

K-complexes are believed to protect ____ ____ ____ from being disrupted by external stimuli.

A

K-complexes are EEG events in Stage 2 that reflect the brain’s inhibition of sensory inputs.

In response to stimuli like sound, inhibitory neurons in the thalamus send signals to the cortex, preventing the sound from waking the sleeper.

This activity serves to keep you asleep while also processing and potentially consolidating memories.

K-complexes are believed to protect ongoing memory consolidation from being disrupted by external stimuli.

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14
Q

_____ _____ are EEG events in Stage 2 that reflect the brain’s inhibition of sensory inputs.

In response to stimuli like _____, inhibitory neurons in the thalamus send signals to the cortex, preventing the sound from waking the sleeper.

This activity serves to keep you asleep while also processing and potentially consolidating memories.

____ _____ are believed to protect ongoing memory consolidation from being disrupted by external stimuli.

A

K-complexes are EEG events in Stage 2 that reflect the brain’s inhibition of sensory inputs.

In response to stimuli like sound, inhibitory neurons in the thalamus send signals to the cortex, preventing the sound from waking the sleeper.

This activity serves to keep you asleep while also processing and potentially consolidating memories.

K-complexes are believed to protect ongoing memory consolidation from being disrupted by external stimuli.

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15
Q

What are sleep spindles and sharp wave ripples? What are the two theoretical ways in which sleep spindles could aid consolidation?

A
  • Sleep spindles: Short bursts of high-frequency waves (12-14 Hz) that co-occur with sharp wave ripples in the hippocampus during non-REM sleep.
  • Sharp wave ripples: Hippocampal activity representing replayed memories during sleep.
  • Two theories for spindles’ role in memory consolidation:
    1. Cortical reactivation: Sleep spindles reactivate cortical cells involved in encoding the memory, strengthening their connections.
    2. Inhibitory protection: Spindles may inhibit cortical signals, protecting hippocampal replay from interference.

Quote: “The other theory is that we’re talking about something a little bit like the K-complexes, where… sleep spindles reflect just the scrambling of cortical signals that would otherwise interfere with hippocampal replay.”
Source: Lecture 13, Section “Sleep Spindles”

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16
Q

Sleep spindles: Short bursts of ___-frequency waves (__ - __ Hz) that co-occur with sharp wave ripples in the ______ during _____ sleep.

Sharp wave ripples: ________ activity representing replayed memories during sleep.

Two theories for spindles’ role in memory consolidation:

  1. _____ _____: Sleep spindles reactivate cortical cells involved in encoding the memory, strengthening their connections.
  2. _____ _____: Spindles may inhibit cortical signals, protecting hippocampal replay from interference.
A

Sleep spindles: Short bursts of high-frequency waves (12-14 Hz) that co-occur with sharp wave ripples in the hippocampus during non-REM sleep.

Sharp wave ripples: Hippocampal activity representing replayed memories during sleep.

Two theories for spindles’ role in memory consolidation:
1. Cortical reactivation: Sleep spindles reactivate cortical cells involved in encoding the memory, strengthening their connections.
2. Inhibitory protection: Spindles may inhibit cortical signals, protecting hippocampal replay from interference.

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17
Q

How do sleep spindles and delta waves interact and affect our memories? (No need to be detailed with the methods of the study that was presented, just be aware of the specific interactions that were discussed, and their consequences.)

A
  • Delta waves are slow oscillations (0.5-4 Hz) during deep sleep.
  • When sleep spindles occur on top of slow delta waves, they help consolidate memories.
  • If spindles coincide with less pronounced delta waves (not slow oscillations), memories may be weakened instead of strengthened.

Quote: “Consolidation of memories requires very precise timing between spindles and large amplitude, slow delta oscillations.”
Source: Lecture 13, Section “Delta Waves and Spindles in Memory Consolidation”

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18
Q

Delta waves are slow oscillations (__ - __ Hz) during ___ sleep.

When ____ ____ occur on top of slow delta waves, they help consolidate _______.

If _____ coincide with less pronounced delta waves (not slow oscillations), ______ may be weakened instead of strengthened.

A

Delta waves are slow oscillations (0.5-4 Hz) during deep sleep.

When sleep spindles occur on top of slow delta waves, they help consolidate memories.

If spindles coincide with less pronounced delta waves (not slow oscillations), memories may be weakened instead of strengthened.

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19
Q

____ waves are slow oscillations (0.5-4 Hz) during deep sleep.

When sleep spindles occur on top of slow ___ waves, they help consolidate ______.

If spindles coincide with less pronounced ____ waves (not slow oscillations), ______ may be weakened instead of strengthened.

A

Delta

delta; memories.

delta; memories

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20
Q

Is the nervous system “inactive” during sleep? Explain. Be sure to consider the different stages of sleep, as well as consider the CNS and PNS.

A
  • The nervous system is not inactive during sleep; it’s just in different states based on sleep stages.
  • Slow-wave sleep (SWS) features slower neural activity but is crucial for brain “rest” and recovery. Sleep stages differ in EEG activity, from slow oscillations in SWS to high-frequency beta waves during REM.
  • REM sleep has high brain activity, comparable to wakefulness, especially in the motor and visual cortices.
  • Peripheral nervous system (PNS) involvement in sleep can be observed in changes in heart rate and respiration, particularly during REM sleep.
  • REM sleep causes muscle paralysis (except for eye muscles), meaning the body is inactive, but brain activity is high.

Quote: “Slow-wave sleep is critical for what we might call brain rest…and you get this kind of rebound effect where you try to recuperate slow wave sleep the next time you fall asleep.”
Source: Lecture 15, Section “SWS and brain rest”

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21
Q

Is the nervous system “inactive” during sleep?

A

The nervous system is not inactive during sleep; it’s just in different states based on sleep stages.

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22
Q

Explain what happens to the nervous system during Slow-wave sleep (SWS) sleep?

A

Slow-wave sleep (SWS) features slower neural activity but is crucial for brain “rest” and recovery.

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23
Q

Explain what happens to the nervous system during REM sleep?

A

REM sleep has high brain activity, comparable to wakefulness, especially in the motor and visual cortices.

REM sleep causes muscle paralysis (except for eye muscles), meaning the body is inactive, but brain activity is high.

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24
Q

How can the peripheral nervous system (PNS) involvement in sleep be observed?

A

Peripheral nervous system (PNS) involvement in sleep can be observed in changes in heart rate and respiration, particularly during REM sleep.

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25
Q

Peripheral nervous system (PNS) involvement in sleep can be observed in changes in ________ and _______, particularly during REM sleep.

A

Peripheral nervous system (PNS) involvement in sleep can be observed in changes in heart rate and respiration, particularly during REM sleep.

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26
Q

Compare and contrast the recuperation theory of sleep vs. the adaptation theory of sleep.

A
  • Recuperation theory: Proposes that sleep is necessary to restore some physiological or neurological function depleted during wakefulness. This could be related to brain homeostasis, energy, or learning.
  • Adaptation theory: Suggests sleep is an evolutionary adaptation to conserve energy and avoid dangers, such as predation. Sleep is seen as a protective mechanism rather than restorative.
  • Criticism of adaptation theory: Sleep isn’t merely about energy conservation because different sleep stages (e.g., REM) have distinct functions not explained by the need for energy conservation.
  • In both theories, slow-wave sleep is highlighted for its homeostatic function, particularly in restoring brain activity.

Quote: “If it was just trying to conserve energy, then that doesn’t really make sense. You’d have these different sleep stages, for example.”
Source: Lecture 14, Section “Recuperation and adaptation theories”

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27
Q

________ theory proposes that sleep is necessary to restore some physiological or neurological function depleted during wakefulness. This could be related to brain homeostasis, energy, or learning.

A

Recuperation theory

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28
Q

________ theory suggests sleep is an evolutionary adaptation to conserve energy and avoid dangers, such as predation. Sleep is seen as a protective mechanism rather than restorative.

A

Adaptation theory

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29
Q

Recuperation theory of sleep vs. the adaptation theory of sleep - In both theories, _____ sleep is highlighted for its homeostatic function, particularly in restoring brain activity.

A

Recuperation theory of sleep vs. the adaptation theory of sleep - In both theories, slow-wave sleep is highlighted for its homeostatic function, particularly in restoring brain activity.

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30
Q

Criticism of adaptation theory of sleep?

A

Sleep isn’t merely about energy conservation because different sleep stages (e.g., REM) have distinct functions not explained by the need for energy conservation.

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31
Q

What is the SHY (Synaptic Homeostasis Hypothesis)? What evidence was discussed in favour of/against this hypothesis?

A
  • SHY hypothesis (Tononi & Cirelli, 2006): Suggests that synapses grow stronger during wakefulness due to learning and experience. During sleep, especially slow-wave sleep, synaptic strength is “downscaled” to prevent saturation.
  • Synaptic downscaling: Ensures that there’s enough capacity for learning the next day by reducing synaptic strength during SWS.
  • Evidence: Delta wave power reduces over the course of SWS as synapses weaken. Experiments show a reduction in the size of dendritic spines during sleep.
  • Some contradictory evidence suggests that not all synapses weaken during sleep. Certain neurons, such as those in the thalamus, might actually increase their synaptic strength during sleep.

Quote: “Sleep is the price we pay for plasticity. As synapses strengthen during the day, they weaken during sleep to free up space for learning the next day.”
Source: Lecture 14, Section “SHY Hypothesis”

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32
Q

The ____ hypothesis suggests that synapses grow stronger during wakefulness due to learning and experience. During sleep, especially slow-wave sleep, synaptic strength is “downscaled” to prevent saturation.

A

SHY hypothesis (Tononi & Cirelli, 2006) suggests that synapses grow stronger during wakefulness due to learning and experience. During sleep, especially slow-wave sleep, synaptic strength is “downscaled” to prevent saturation.

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33
Q

SHY hypothesis (Tononi & Cirelli, 2006) suggests that synapses grow _____ during wakefulness due to learning and experience. During sleep, especially ____ sleep, synaptic strength is “downscaled” to prevent saturation.

A

SHY hypothesis (Tononi & Cirelli, 2006) suggests that synapses grow stronger during wakefulness due to learning and experience. During sleep, especially slow-wave sleep, synaptic strength is “downscaled” to prevent saturation.

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34
Q

What is synaptic downscaling?

A

Synaptic downscaling ensures that there’s enough capacity for learning the next day by reducing synaptic strength during SWS.

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35
Q

What is the contradictory evidence to the SHY (Synaptic Homeostasis Hypothesis)?

A

Some contradictory evidence suggests that not all synapses weaken during sleep. Certain neurons, such as those in the thalamus, might actually increase their synaptic strength during sleep.

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36
Q

Some contradictory evidence to the SHY (Synaptic Homeostasis Hypothesis) suggests that _____________. Certain neurons, such as those in the thalamus, might actually _____ their synaptic strength during sleep.

A

Some contradictory evidence to the SHY (Synaptic Homeostasis Hypothesis) suggests that not all synapses weaken during sleep. Certain neurons, such as those in the thalamus, might actually increase their synaptic strength during sleep.

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37
Q

What is the evidence to support the SHY (Synaptic Homeostasis Hypothesis)?

A

Delta wave power reduces over the course of SWS as synapses weaken. Experiments show a reduction in the size of dendritic spines during sleep.

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38
Q

The evidence to support the ___ hypothesis states that delta wave power reduces over the course of SWS as synapses weaken. Experiments show a reduction in the size of dendritic spines during sleep.

A

The evidence to support the SHY hypothesis (Synaptic Homeostasis Hypothesis) states that delta wave power reduces over the course of SWS as synapses weaken. Experiments show a reduction in the size of dendritic spines during sleep.

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39
Q

The evidence to support the SHY hypothesis (Synaptic Homeostasis Hypothesis) states that ____ wave power reduces over the course of SWS as synapses weaken. Experiments show a _____ in the size of dendritic spines during sleep.

A

The evidence to support the SHY hypothesis (Synaptic Homeostasis Hypothesis) states that delta wave power reduces over the course of SWS as synapses weaken. Experiments show a reduction in the size of dendritic spines during sleep.

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40
Q

The evidence to support the SHY hypothesis (Synaptic Homeostasis Hypothesis) states that delta wave power reduces over the course of ___________ sleep as synapses weaken. Experiments show a reduction in the size of dendritic spines during sleep.

A

slow wave sleep

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41
Q

What is the Glymphatic Drainage hypothesis? What evidence was discussed in favour of/against this hypothesis?

A
  • Glymphatic Drainage Hypothesis: Proposes that sleep allows the brain to “wash away” metabolic waste products, including toxins like beta-amyloid, through a specialised system involving cerebrospinal fluid (CSF).
  • This system, discovered by Nedergaard’s lab, increases efficiency during sleep, particularly during SWS. Astrocytes facilitate the process by shrinking to allow more space for fluid flow.
  • Evidence: During sleep, greater flow of tracer dyes through paravascular spaces is observed, as well as faster clearance of toxins.
  • Criticism: Some studies have shown contradictory results, where waste clearance can also occur during wakefulness in certain conditions.

Quote: “There’s a one-way plumbing system in the brain that washes away metabolic waste, and this is facilitated by sleep.”
Source: Lecture 14, Section “Glymphatic Drainage”

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42
Q

What is the Glymphatic Drainage hypothesis?

A

Glymphatic Drainage Hypothesis proposes that sleep allows the brain to “wash away” metabolic waste products, including toxins like beta-amyloid, through a specialised system involving cerebrospinal fluid (CSF).

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43
Q

________ ______ hypothesis proposes that sleep allows the brain to “wash away” metabolic waste products, including toxins like beta-amyloid, through a specialised system involving cerebrospinal fluid (CSF).

A

Glymphatic Drainage hypothesis proposes that sleep allows the brain to “wash away” metabolic waste products, including toxins like beta-amyloid, through a specialised system involving cerebrospinal fluid (CSF).

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44
Q

Glymphatic Drainage hypothesis proposes that sleep allows the brain to “wash away” metabolic waste products, including toxins like beta-amyloid, through a specialised system involving ______ ______.

A

cerebrospinal fluid (CSF).

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45
Q

Glymphatic Drainage hypothesis proposes that sleep allows the brain to “wash away” metabolic waste products, including toxins like beta-amyloid, through a specialised system involving cerebrospinal fluid (CSF).

This system, discovered by __________’s lab, increases efficiency during sleep, particularly during SWS. Astrocytes facilitate the process by shrinking to allow more space for fluid flow.

A

Glymphatic Drainage hypothesis proposes that sleep allows the brain to “wash away” metabolic waste products, including toxins like beta-amyloid, through a specialised system involving cerebrospinal fluid (CSF).

This system, discovered by Nedergaard’s lab, increases efficiency during sleep, particularly during SWS. Astrocytes facilitate the process by shrinking to allow more space for fluid flow.

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46
Q

Glymphatic Drainage hypothesis proposes that sleep allows the brain to “wash away” metabolic waste products, including toxins like beta-amyloid, through a specialised system involving cerebrospinal fluid (CSF).

This system, discovered by Nedergaard’s lab, increases efficiency during sleep, particularly during ___. Astrocytes facilitate the process by shrinking to allow more space for fluid flow.

A

Glymphatic Drainage hypothesis proposes that sleep allows the brain to “wash away” metabolic waste products, including toxins like beta-amyloid, through a specialised system involving cerebrospinal fluid (CSF).

This system, discovered by Nedergaard’s lab, increases efficiency during sleep, particularly during SWS. Astrocytes facilitate the process by shrinking to allow more space for fluid flow.

47
Q

Glymphatic Drainage hypothesis proposes that sleep allows the brain to “wash away” metabolic waste products, including toxins like beta-amyloid, through a specialised system involving cerebrospinal fluid (CSF).

This system, discovered by Nedergaard’s lab, increases efficiency during sleep, particularly during SWS. _______ facilitate the process by shrinking to allow more space for fluid flow.

A

Glymphatic Drainage hypothesis proposes that sleep allows the brain to “wash away” metabolic waste products, including toxins like beta-amyloid, through a specialised system involving cerebrospinal fluid (CSF).

This system, discovered by Nedergaard’s lab, increases efficiency during sleep, particularly during SWS. Astrocytes facilitate the process by shrinking to allow more space for fluid flow.

48
Q

What is the evidence for the Glymphatic Drainage hypothesis?

A

Evidence: During sleep, greater flow of tracer dyes through paravascular spaces is observed, as well as faster clearance of toxins.

49
Q

What is the criticism for the Glymphatic Drainage hypothesis?

A

Criticism: Some studies have shown contradictory results, where waste clearance can also occur during wakefulness in certain conditions.

50
Q

What happens when you deprive someone of Stage 1 sleep?

A

Stage 1: Little consequence if deprived, as it’s a very light sleep phase. Most people do not report significant cognitive or physiological deficits.

51
Q

What happens when you deprive someone of Stage 2 sleep?

A

Stage 2: K-complexes and sleep spindles are important for memory consolidation, so long-term deprivation could result in memory issues.

52
Q

What happens when you deprive someone of Stage 3/4 slow wave sleep?

A

SWS (Stage 3/4): Critical for memory retention and cognitive functions. Deprivation leads to attention deficits, irritability, and attempts to rebound by prioritising SWS in subsequent sleep.

53
Q

What happens when you deprive someone of REM sleep?

A

REM sleep: Memory consolidation, particularly of emotional and complex memories, is impacted. There is a REM rebound effect after deprivation, indicating its importance. Interestingly, REM deprivation can increase sensitivity to pain.

54
Q

What happens when you deprive someone of [____] sleep?

Little consequence if deprived, as it’s a very light sleep phase. Most people do not report significant cognitive or physiological deficits.

A

What happens when you deprive someone of Stage 1 sleep

55
Q

What happens when you deprive someone of [____] sleep?

K-complexes and sleep spindles are important for memory consolidation, so long-term deprivation could result in memory issues.

A

Stage 2 sleep

56
Q

What happens when you deprive someone of [____] sleep?

Critical for memory retention and cognitive functions. Deprivation leads to attention deficits, irritability, and attempts to rebound by prioritising SWS in subsequent sleep.

A

What happens when you deprive someone of SWS (Stage 3/4) sleep

57
Q

What happens when you deprive someone of [____] sleep?

Memory consolidation, particularly of emotional and complex memories, is impacted. There is a rebound effect after deprivation, indicating its importance. Interestingly, deprivation can increase sensitivity to pain.

A

What happens when you deprive someone of REM sleep

58
Q

Identify the major nuclei and arousal/sleep effects associated with Acetylcholine (ACh)

A

Acetylcholine (ACh): Major nuclei are the pontine and tegmental nuclei in the brainstem and the nucleus basalis in the basal forebrain.
- Effects: Increases cortical activation, associated with wakefulness and REM sleep.
- Levels: High during wakefulness, medium during REM, low during SWS.

59
Q

Identify the major nuclei and arousal/sleep effects associated with Norepinephrine (NE)

A

Norepinephrine (NE): Major nucleus is the locus coeruleus (LC) in the pons.
- Effects: Associated with vigilance and attention.
- Levels: High during wakefulness, low during SWS, zero during REM.

60
Q

Identify the major nuclei and arousal/sleep effects associated with Serotonin (5-HT)

A

Serotonin (5-HT): Major nuclei are the raphe nuclei in the reticular formation.
- Effects: Facilitates cortical arousal and automatic movements.
- Levels: High during wakefulness, low during SWS and REM (with brief bursts post-REM).

61
Q

Identify the major nuclei and arousal/sleep effects associated with Histamine

A

Histamine: Major nucleus is the tuberomammillary nucleus (TMN) in the posterior hypothalamus.
- Effects: Increases arousal and is associated with attention and alertness.
- Levels: High during wakefulness, low during SWS and REM.

62
Q

Identify the major nuclei and arousal/sleep effects associated with Histamine

A

Histamine: Major nucleus is the tuberomammillary nucleus (TMN) in the posterior hypothalamus.
- Effects: Increases arousal and is associated with attention and alertness.
- Levels: High during wakefulness, low during SWS and REM.

63
Q

Identify the major nuclei and arousal/sleep effects associated with Orexin?

A

Orexin: Major nuclei are the lateral and posterior hypothalamus.
- Effects: Stimulates arousal centres like LC, raphe, TMN, and others; critical for staying awake, especially when hungry or needing to focus.
- Levels: High during wakefulness, low during SWS and REM.

64
Q

___________: Major nuclei are the pontine and tegmental nuclei in the brainstem and the nucleus basalis in the basal forebrain.
- Effects: Increases cortical activation, associated with wakefulness and REM sleep.
- Levels: High during wakefulness, medium during REM, low during SWS.

A

Acetylcholine (ACh): Major nuclei are the pontine and tegmental nuclei in the brainstem and the nucleus basalis in the basal forebrain.
- Effects: Increases cortical activation, associated with wakefulness and REM sleep.
- Levels: High during wakefulness, medium during REM, low during SWS.

65
Q

Acetylcholine (ACh): Major nuclei are the _______ and _________ nuclei in the brainstem and the nucleus _______ in the basal forebrain.

A

pontine and tegmental nuclei; nucleus basalis

66
Q

Acetylcholine (ACh):
- Effects: ______ cortical activation, associated with _______ and _____ sleep.
- Levels: ____ during wakefulness, _____ during REM, ____ during SWS.

A

Acetylcholine (ACh):
- Effects: Increases cortical activation, associated with wakefulness and REM sleep.
- Levels: High during wakefulness, medium during REM, low during SWS.

67
Q

____________: Major nucleus is the locus coeruleus (LC) in the pons.
Effects: Associated with vigilance and attention.
Levels: High during wakefulness, low during SWS, zero during REM.

A

Norepinephrine (NE): Major nucleus is the locus coeruleus (LC) in the pons.
Effects: Associated with vigilance and attention.
Levels: High during wakefulness, low during SWS, zero during REM.

68
Q

Norepinephrine (NE): Major nucleus is the _______ _______ in the _______.

A

Norepinephrine (NE): Major nucleus is the locus coeruleus (LC) in the pons.

69
Q

Norepinephrine (NE):
Effects: Associated with _____ and ______.
Levels: _____ during wakefulness, ____ during SWS, ____ during REM.

A

Norepinephrine (NE):
Effects: Associated with vigilance and attention.
Levels: High during wakefulness, low during SWS, zero during REM.

70
Q

_________: Major nuclei are the raphe nuclei in the reticular formation.
Effects: Facilitates cortical arousal and automatic movements.
Levels: High during wakefulness, low during SWS and REM (with brief bursts post-REM).

A

Serotonin (5-HT): Major nuclei are the raphe nuclei in the reticular formation.
Effects: Facilitates cortical arousal and automatic movements.
Levels: High during wakefulness, low during SWS and REM (with brief bursts post-REM).

71
Q

Serotonin (5-HT): Major nuclei are the _____ nuclei in the _____ _____.

A

Serotonin (5-HT): Major nuclei are the raphe nuclei in the reticular formation.

72
Q

Serotonin (5-HT):
Effects: Facilitates _____ and _____ _____.
Levels: ___ during wakefulness, ____ during SWS and REM (with brief bursts post-REM).

A

Serotonin (5-HT):
Effects: Facilitates cortical arousal and automatic movements.
Levels: High during wakefulness, low during SWS and REM (with brief bursts post-REM).

73
Q

_______: Major nucleus is the tuberomammillary nucleus (TMN) in the posterior hypothalamus.
Effects: Increases arousal and is associated with attention and alertness.
Levels: High during wakefulness, low during SWS and REM.

A

Histamine

74
Q

Histamine: Major nucleus is the ________ nucleus in the _______ _______.

A

tuberomammillary nucleus (TMN); posterior hypothalamus.

75
Q

Histamine:
Effects: Increases arousal and is associated with attention and alertness.
Levels: High during wakefulness, low during SWS and REM.

A

Histamine:
Effects: Increases _____ and is associated with ______ and ______.
Levels: ___ during wakefulness, ___ during SWS and REM.

76
Q

_____: Major nuclei are the lateral and posterior hypothalamus.
Effects: Stimulates arousal centres like LC, raphe, TMN, and others; critical for staying awake, especially when hungry or needing to focus.
Levels: High during wakefulness, low during SWS and REM.

A

Orexin: Major nuclei are the lateral and posterior hypothalamus.
Effects: Stimulates arousal centres like LC, raphe, TMN, and others; critical for staying awake, especially when hungry or needing to focus.
Levels: High during wakefulness, low during SWS and REM.

77
Q

Orexin: Major nuclei are the _____ and ______ ________.

A

lateral and posterior hypothalamus.

78
Q

Orexin:
Effects: Stimulates arousal centres like ___, ____, ____, and others; critical for staying awake especially when hungry or needing to focus.
Levels: ___ during wakefulness, ___ during SWS and REM.

A

LC, raphe, TMN,
High; low

79
Q

Be familiar with von Economo’s contributions to understanding sleep mechanisms. Put his hypothalamic findings into modern day context regarding the sleep-wake flip-flop circuit.

A
  • Von Economo’s findings: Damage to the posterior hypothalamus caused excessive sleepiness, while damage to the anterior hypothalamus caused insomnia.
  • This led to the hypothesis that the anterior hypothalamus is a sleep centre, and the posterior hypothalamus is a wakefulness centre.
  • This work paved the way for understanding the sleep-wake flip-flop circuit, where these two regions inhibit one another, stabilising sleep or wakefulness.
  • Modern context: The preoptic area (POA) in the anterior hypothalamus sends inhibitory signals to arousal centres like the LC, raphe nuclei, TMN, and orexin neurons, switching off arousal during sleep.

Quote: “Von Economo found that… damage to the posterior hypothalamus caused excessive sleepiness… anterior hypothalamus caused insomnia.”
Source: Lecture 15, Section “von Economo and Sleep-Wake Centres”

80
Q

What were Von Economo’s findings?

A

Von Economo’s findings: Damage to the posterior hypothalamus caused excessive sleepiness, while damage to the anterior hypothalamus caused insomnia.

81
Q

Von Economo’s findings: Damage to the ______ hypothalamus caused excessive sleepiness, while damage to the _____ hypothalamus caused insomnia.

A

Von Economo’s findings: Damage to the posterior hypothalamus caused excessive sleepiness, while damage to the anterior hypothalamus caused insomnia.

82
Q

Von Economo’s findings: Damage to the posterior hypothalamus caused ______ ______, while damage to the anterior hypothalamus caused ______.

A

Von Economo’s findings: Damage to the posterior hypothalamus caused excessive sleepiness, while damage to the anterior hypothalamus caused insomnia.

83
Q

Von Economo’s findings led to the hypothesis that the _____ hypothalamus is a sleep centre, and the _____ hypothalamus is a wakefulness centre.

A

Von Economo’s findings led to the hypothesis that the anterior hypothalamus is a sleep centre, and the posterior hypothalamus is a wakefulness centre.

84
Q

Von Economo’s findings led to the hypothesis that the anterior hypothalamus is a _____ centre, and the posterior hypothalamus is a ______ centre.

A

sleep centre, wakefulness centre.

85
Q

Von Economo’s findings paved the way for understanding the ___ - ___ ___ - ___ circuit, where these two regions inhibit one another, stabilising sleep or wakefulness.

A

Von Economo’s findings paved the way for understanding the sleep-wake flip-flop circuit, where these two regions inhibit one another, stabilising sleep or wakefulness.

86
Q

Von Economo’s findings modern context: The ____ ____ in the anterior hypothalamus sends _____ signals to arousal centres like the LC, raphe nuclei, TMN, and orexin neurons, switching off arousal during sleep.

A

Von Economo’s findings modern context: The preoptic area (POA) in the anterior hypothalamus sends inhibitory signals to arousal centres like the LC, raphe nuclei, TMN, and orexin neurons, switching off arousal during sleep.

87
Q

Von Economo’s findings modern context: The preoptic area (POA) in the anterior hypothalamus sends inhibitory signals to arousal centres like the ___, ____ nuclei, ____, and _____ neurons, switching off arousal during sleep.

A

LC, raphe nuclei, TMN, and orexin neurons

88
Q

Be able to link Weeks 2-3 hunger lectures with Week 4 sleep circuit lectures, e.g., why might hunger keep us awake?

A
  • Orexin is a key link between hunger and arousal. It is released from the lateral hypothalamus, where it is involved in both promoting feeding behaviours and arousal.
  • When you are hungry, orexin release increases, promoting wakefulness to motivate food-seeking behaviours.
  • This reflects an allostatic mechanism where the need for food can override sleep, keeping you awake to ensure survival.
  • Arousal centres like the LC, raphe nuclei, and TMN are all activated by orexin during hunger, making it harder to fall asleep.

Quote: “Orexin… would be a compelling trigger of hunger… and also make you awake and vigilant.”
Source: Lecture 15, Section “Orexin and Hunger”

89
Q

_____ is a key link between hunger and arousal. It is released from the lateral hypothalamus, where it is involved in both promoting feeding behaviours and arousal.

A

Orexin is a key link between hunger and arousal. It is released from the lateral hypothalamus, where it is involved in both promoting feeding behaviours and arousal.

90
Q

Orexin is a key link between hunger and arousal. It is released from the ______ _______, where it is involved in both promoting feeding behaviours and arousal.

A

Orexin is a key link between hunger and arousal. It is released from the lateral hypothalamus, where it is involved in both promoting feeding behaviours and arousal.

91
Q

Orexin is a key link between _____ and ____. It is released from the lateral hypothalamus, where it is involved in both promoting _____ behaviours and _____.

A

Orexin is a key link between hunger and arousal. It is released from the lateral hypothalamus, where it is involved in both promoting feeding behaviours and arousal.

92
Q

When you are hungry, _____ release increases, promoting wakefulness to motivate food-seeking behaviours.

A

orexin

93
Q

Arousal centres like the LC, raphe nuclei, and TMN are all activated by _____ during hunger, making it harder to fall asleep.

A

Arousal centres like the LC, raphe nuclei, and TMN are all activated by orexin during hunger, making it harder to fall asleep.

94
Q

Arousal centres like the ____, ____ nuclei, and ____ are all activated by orexin during hunger, making it harder to fall asleep.

A

Arousal centres like the LC, raphe nuclei, and TMN are all activated by orexin during hunger, making it harder to fall asleep.

95
Q

Does a strong coffee help keep you awake? In theory it should…. why?

A
  • Caffeine acts as an adenosine receptor antagonist, specifically blocking the A1 receptor.
  • Adenosine accumulates during wakefulness, promoting sleep by inhibiting neural activity. Caffeine blocks this inhibitory effect, thus maintaining wakefulness.
  • Caffeine’s effects are both psychological (alertness, focus) and physiological (mimicking the sympathetic nervous system and promoting fight-or-flight responses).
  • The blocking of adenosine receptors reduces sleep pressure, helping you stay awake for longer.

Quote: “Caffeine blocks the A1 adenosine receptor… blocking the inhibitory effects of adenosine.”
Source: Lecture 14, Section “Caffeine and Adenosine”

96
Q

Caffeine acts as an ______ receptor antagonist, specifically blocking the A1 receptor.

A

adenosine

97
Q

Caffeine acts as an adenosine receptor ______, specifically _____ the A1 receptor.

A

antagonist; blocking

98
Q

________ accumulates during wakefulness, promoting sleep by inhibiting neural activity. Caffeine blocks this inhibitory effect, thus maintaining wakefulness.

A

Adenosine accumulates during wakefulness, promoting sleep by inhibiting neural activity. Caffeine blocks this inhibitory effect, thus maintaining wakefulness.

99
Q

Adenosine accumulates during wakefulness, promoting sleep by inhibiting neural activity. ______ blocks this inhibitory effect, thus maintaining wakefulness.

A

Caffeine

100
Q

For the purposes of PSYC317, sleep is defined as a state of diminished ___________, which follows specific patterns of ___________ activity.

A

sensory responsivity, nervous system

101
Q

Drowsiness is defined as a heightened ___________ for sleep and serves as a ___________ to prompt sleep behavior.

A

desire, motivator

102
Q

In the R&K method, Stage 1 is characterised by ___________ waves, while Stage 2 includes both ___________ and ___________ on the EEG.

A

theta, K-complexes, sleep spindles

103
Q

In the AASM classification, Stages 3 and 4 from the R&K method are combined into a single stage called ___________, which is dominated by ___________ waves.

A

N3, delta

104
Q

REM sleep is marked by an EEG pattern that resembles ___________ with the presence of ___________ and muscle ___________.

A

wakefulness, rapid eye movements, paralysis

105
Q

K-complexes are generated by inhibitory neurons in the ___________, which project to the ___________ and help maintain sleep by reducing ___________ to external stimuli.

A

thalamus, cortex, responsiveness

106
Q

Sleep spindles are bursts of high-frequency activity that co-occur with ___________ in the ___________ during non-REM sleep and may aid in ___________ consolidation.

A

sharp wave ripples, hippocampus, memory

107
Q

The ___________ hypothesis suggests that synapses weaken during sleep to prevent saturation, allowing for more learning the next day.

A

Synaptic Homeostasis (SHY)

108
Q

The ___________ hypothesis proposes that sleep allows the brain to clear out metabolic waste via the flow of ___________ fluid through paravascular spaces.

A

Glymphatic Drainage, cerebrospinal

109
Q

Deprivation of ___________ sleep leads to significant deficits in attention and memory, while deprivation of ___________ sleep leads to impairments in complex memory consolidation and a ___________ effect.

A

slow wave, REM, REM rebound

110
Q

The neurotransmitter ___________ is released from the locus coeruleus and is associated with vigilance and ___________, while serotonin (5-HT) from the ___________ nuclei promotes cortical arousal and automatic movements.

A

norepinephrine (NE), attention, raphe

111
Q

According to von Economo’s findings, damage to the ___________ hypothalamus causes excessive sleep, while damage to the ___________ hypothalamus results in insomnia.

A

posterior, anterior

112
Q

The lateral hypothalamus releases the neurotransmitter ___________, which promotes both wakefulness and ___________ behavior.

A

orexin, feeding

113
Q

Caffeine promotes wakefulness by blocking the ___________ receptor, thereby preventing the inhibitory effects of ___________.

A

A1 adenosine, adenosine

114
Q

Acetylcholine (ACh): Major nuclei are the pontine and tegmental nuclei in the _________ and the nucleus basalis in the ______ _____.

A

brainstem; basal forebrain