Sleep and memory 04/05 Flashcards

1
Q

What is the role of the previous nights sleep in learning and memory?

A

Preceding sleep improves the acquisition of memories in the subsequent wake period

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2
Q

What is the role of sleep after learning and memory

A

Subsequent sleep improves consolidation of newly encoded memories

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3
Q

Define sleep

A

a reversible state of disconnection from the environment, often with reduced mobility.

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4
Q

How is sleep measured?

A

Electroencephalogram (EEG).

Due to the highly organised structure of the cortex (layers of cells with the same direction) the net effects of local field potentials add up into something coherent, that can be measured as deflections in the potential of the scalp.

EEG is used alongside EMG to distinguish different stages of sleep.

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5
Q

How is REM sleep distinguished from wakeful states?

A

The EEG of REM and wake states is similar - very high frequency oscillations (theta waves)
However, the EEG is combined with an EMG - electromyogram. REM is differentiated from wake state by the low level of muscular tone.

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6
Q

How is non-rem sleep distinguished?

A

There are three levels of non-rem sleep.

There are two brief transitional stages - nonrem-1 and nonrem-2. They are characterised by the appearance of spindles, especially in non-rem2.

High amplitude low frequency oscillations on an EEG is deep slow wave sleep (non-rem3). Spindles also occur here too.

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7
Q

What is the order of the sleep stages?

A

Wake

Non-rem1
Non-rem2

Non-rem3

Non-rem2
Non-rem1

REM

This can be visualised on a hypogram. In humans this lasts 90 minutes. Rodent cycle is much shorter and fragmented.

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8
Q

What are the types and locations of non-REM EEG signatures?

A

Slow oscillation (cortical)

Spindle (thalamo-cortical system)

Sharp wave ripple (hippocampus)

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9
Q

How do sleep patterns change throughout the night?

A

Early sleep is dominated by deep non-REM sleep.
Late sleep is dominated by REM sleep.

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10
Q

How do neuromodulatory transmitters contribute to REM.

A

Increase in Ach, Decrease in NA and 5HT and Increase in cortisol.

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11
Q

How do neuromodulatory transmitters contribute to SWS/non-REM.

A

The cortical regions are under control of neuromodulatory afferents from subcortical areas.
SWS is associated with decreases in cortisol, 5HT and NA changes and decreases in ACh.

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12
Q

The dual process hypothesis

A

Hippocampal declarative memory consolidation is dependent on slow wave sleep, whereas REM sleep facilitates non-declarative (procedural, emotional), hippocampus independent memory

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13
Q

What is the sequential processes hypothesis?

A

The optimum benefit of sleep on declarative and non-declarative memory occurs when SWS is followed by REM sleep. Evidence in support of this is that even short naps improve results on training tests if SWS is followed by REM.

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14
Q

What are the effects of disrupting hippocampal REM sleep on memory?

A

Optogenetic experiments now allow manipulation of REM sleep, which was very difficult before due to short length of REM and the confounding nature of waking the animal up. An experiment by Boyce et al 2016 used optogenetic inhibition of medial septum GABAergic projection neurons to prevent them from generating theta oscillations, effectively disrupting REM sleep.

This destroyed memory in novel object recognition test.
During fear conditioning, it impaired memory of the context of the shock but not of the auditory tone associated with the shock.

These may give some insights as to the function of REM sleep.

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15
Q

What is the impact of sleep deprivation on LTP?

A

A common molecular marker of LTP is cAMP - it is required for long lasting changes in synaptic plasticity. There is evidence that LTP occurs during REM sleep, as there is an increase of cAMP.
Sleep deprivation lowers levels of cAMP and increases levels of cAMP-degrading phosphodiesterase (PDE4). Blocking PDE4 reverses the effect of sleep deprivation on LTP.

Sleep deprivation does not alter non-cAMP dependent LTP.

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16
Q

Evidence as to how sleep may allow for memory consolidation of episodic spatial memories?

A

Ca2+ photon microscopy*** allows imaging of neurons and even synpases that are activated during a running task in mice. Specific populations of cells are activated in sequence as the mouse runs along the track (place cells). The same neurons are activated during sleep in a temporally conserved but compressed manner.

17
Q

What is the active systems consolidation hypothesis?

A

The SWS synchronize spindles and sharp wave – ripples.

This facilitates reactivation of hippocampal memories and transfer to neocortex.

Up states in the SWS maintain plasticity at synapses.

These plasticity events remain supported during replay in REM (LTP) which follows the SWS.

-Essentially, the information is transfer to the neocortex during SWS and then these new configuraitons are strengthened by LTP in REM.-

18
Q

What is the evidence for the hypothesis that sleep serves to restore functionality due to the ‘cost of learning’?

A

It is found that if rats are trained in a motor task when they are awake with a low sleep pressure, then their performance errors are low. If they are forced to stay awake, then the sleep pressure becomes high and there are many more performance errors. Not only this, but it is found that even though the rat is awake, subpopulations of cortical neurons will go offline - a phenomenon known as local sleep.

There is a correlation between the presence of ‘off’ periods of neurons and missing in a pellet reaching task.

19
Q

What is the evidence that sleep is required for clearing of metabolites?

A

diffusion of CSF through the extracellular space clears waste products.

  • Sleep leads to a 60% increase in extracellular space
  • CSF’s flow during wake is only 5% of flow observed during sleep
20
Q

What is the synpatic homeostasis hypothesis?

A

One of the functions of sleep is to restore synapses to their optimum functionality.

Wakefulness results in a saturation of plastic potential of the brain.

Sleep allows for ‘synaptic downscaling’ = net reduction of synaptic strength. levels of LTP associated proteins such as AMPAR, NMDAR decrease during sleep.

This allows for elimination of irrelevant information.

This is contradiction with the active systems consolidation theory. They may occur simultaneously in different networks within the same cortical region.

21
Q

What are the cellular costs of learning?

A
  • energy consumption
  • increased noise to signal ratio
  • reduced selectivity of firing
  • saturation of plastic potential