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Dreams For No Reason Flashcards

1
Q

Glial cells

A

Extra cellular physical support
Provision on nutrients
Maintenance of extra cellular fluid around synapses
Types; oliogodendrocytes, asteocytes, microglia

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2
Q

Cerebrospinal fluid

A

Clears waste

Maintains homeostasis

125ml at any point & 500ml generated every day

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3
Q

Brain is richly supplied with blood

A

Dense capillary system in brain

20% of all blood pumped to brain

60% of all glucose used by brain when at rest

Comprises only 2% of body’s mass

85 billion cells, 1,000-10,000 connections

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4
Q

Lymphatic system of brain

A

Drains fluid back into heart from lymphatic nodes

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5
Q

Ventricles of brain

A

Cerebrospinal fluid

Fluid washes the brain, removing by-products

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6
Q

Thalamus: specific relay nuclei

A

Vision: lateral geniculate nucleus

Hearing: medial geniculate nucleus

Sensation: central posterior nucleus

PGO (pons, LGN, occipital cortex) waves frequently referred to in discussion of sleep REM & are invoked to explain source of dreaming

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7
Q

Thalamus; non-specific

A

Intralaminar nuclei & midline nuclei- diffuse projections to the cortex, general altering system

Reticular nucleus of the thalamus- coat over the thalamus, involved in sleep & wakeness

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8
Q

Why do non-specific neurone matter?

A

Input from the senses pass through this layer before reaching their specialised processing sections of the thalamus & been passed to specialised processing sections of the cortex

Activity here has the ability to greatly waken all external input- ability to fall asleep & not be woken by external stimulation

Activity here has the ability to amplify input from specific senses or all- arousal/wakefulness

Changes the balance of cortical input from external to internal sources- dreaming

Neurons exist in tonic mode or burst mode

During sleep most are in burst mode (many during wakefulness)

No info can be transferred when rhymic bursts happen

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9
Q

Thalamus: association neurons

A

Pulvinar- visual info & eye movement, probably attention

Input from distributed cortex & eye movement area

Output to secondary visual cortex in parietal/temporal area

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10
Q

Neurotransmitters involved in sleep & dreaming

A

Release neurotransmitter wide, extremely long axons which terminate all over cortex

Acetylcholine- involved in muscles, released during sleep before REM initiated

Norepinephrine

Serotonin

Neurotransmitters manufactures & stored in axon terminals, then bind to receptor sites, opens/closes channels

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11
Q

Synthesis, packaging & transport of neurotransmitters

A

Calcium influx causes vesicles to blend with membrane

Small molecule neurotransmitters- very important in sleep, in the terminal button by the Golgi complex

Large molecule neurotransmitters- in the cell body & transportes down to the terminals

Some neurotransmitters manufactured in axon terminal, some in cell body packaged & actively transported down axon terminal via micro tubules

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12
Q

Metabotropic receptors

A

Can open ion channels from inside the cell

Slow developing, long lasting, varied in kind

Typical type for neurotransmitters involved in sleep

Can activate a cascade of enzyme production

Metabolic receptors work differently

Diffused vs localised release- localised release is very specific but general is diffuse so can affect more cells

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13
Q

Neurotransmission

A

Local

Specific

Brief

Fine control

E.g. switching off wakefulness

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14
Q

Neuromodulation

A

Widespread

Non-specific

Long-lasting

Increase of cortical stimulation

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15
Q

Computational unit

A

Electrical charge inside next neuron will significantly change if the effect of many post-synaptic intervals are added

This will be most effective if they arrive about the same time in same part of next neuron

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16
Q

Excitatory neurotransmitters & inhibitory effects

A

Effect of summing the inputs to give a cell body of neuron is that it either produces AP’s or doesn’t

If it produces AP’s this can lead to release of excitatory or inhibitory neurotransmitters

If it releases inhibitory neurotransmitters then the cells it contacts with become less & less likely to produce nerve impulses

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17
Q

Neurotransmitters

A

Amino acids- glutamate (dominant excitatory neurotransmitter), GABA (inhibitory)

Monoamine neurotransmitters- serotonin, dopamine, norepinephrine (control sleep, brain stem neurona with diffuse branching)

Acetylcholine- involved in sleep & transmission to REM (dreaming?)

Neuropeptides- look & act like neurotransmitters, orexin (sleep control)

18
Q

Recycling of neurotransmitters

A

After the neurotransmitters have had their effect they are typically reabsorbed back into the neuron that released them (pre-synaptic cell)

19
Q

Theories from REM observation

A

A perspective that studies REM sleep & makes inferences about dreaming

Many variants but share a conclusion

Dreams are a by-product of brain activity, they have no meaning or purpose

Brain is active, sometimes more active than wakeness

No perfect correspondence between dream & REM, perception cannot be equated to brain activity, some other property of consciousness, dreams not reducible to physiology

Seems to be random, chaotic activity from pons & medulla

Brain still working so still get some experience but doesn’t mean anything

Most popular explanation

20
Q

Aserinsky & Kleitman (1955)

A

Only in 20/27 cases when people were woken from REM did they report having dreaming

21
Q

Vertes & Eastman (2000)

A

Slow wave sleep (deep sleep)- brain activity is very different from wakefulness

REM sleep- the brain activity is more similar to wakefulness

Theory; REM maintains CNS activity throughout sleep- keeps it active so when wake up brain can function

REM eases sleeper back to wakefulness

Implication- dreams are a by-product of this biological necessity as activity approaches that of consciousness

22
Q

Sleep cleans the brain

A

Xie et al (2013)

Cerebrospinal fluid flows through the brain & clears out toxins through a series of channels that expand during sleep

Distorted processing occurs (dreaming)

23
Q

Reverse learning

A

Crick & Mitchinson (1983)

No function of dreaming (by-product of cognitive neural change)

In order for brain to function when awake, neurons have to be in autonomous state, in sleep neurons out in this state so when wake up neurons can respond

24
Q

Purpose of REM sleep

A

Dreams are still meaningless

You are the passive observer as memories are unlearned

Experience old memories being discarded (rubbish in the brain, stupid connections being broken)

Undesirable links broken, the irrelevant eliminated

Not just random, a function & purpose

25
Q

Neural networks

A

Theoretical influence

Network of cells linked together= 1 event

Distributed, robust & superimposed (some nerve cells might encode different things)

Different stimuli activates different cells, pattern of activation= experience

When such networks become overloaded, distant associations activated, responses from weak stimuli (want strong stimuli activating its representation)

26
Q

Reverse learning- how to fix an overloaded network

A

How to eliminate the parasitic connection

1) switch off external input
2) bombard with random signals
3) weaken any association that fires

27
Q

Brain stem mechanisms

A

Random firing in brain stem effects cortex

PGO waves first sign of REM sleep in animals

Weak signals activated are experienced in dream- want to break these links so brain isn’t overloaded (ensures appropriate connections)

PGO waves send weak signals

If weak signal can activate a memory, that link must be broken

Reverse learning is this process that weakens the links

Dreams are the experience of the activation of memories by weak random input

If they were important, you’d remember them

Dream for 1.5-2 hrs every night & little remembered

During dreaming we get rid of memories we don’t need- dream in order to forget

28
Q

Synaptic homoeostasis hypothesis

A

You get a glimpse at the neural free for all in dreams

Tonnoni (2013)

Fruit flies- control flies left in boring 1 fly per tube, experimental flies unleaded for 12 hrs to a fly mall with hundreds of other flies

Number of connections fell back to normal levels after sleep, showing correlating cycle of neuronal connections after waking activities & declines after sleep

Rapidly create dendrites (connections) throughout the day, simplified during sleep (get rid of irrelevant stuff)

29
Q

Activation- synthesis

A

Hobson & McCarley (1977)

Random signals sent from brain stem to visual cortex & other areas

Memories, emotions etc are randomly activated

External signals attenuated

Internal signals relatively strong

Hypothesis- cortex tries to make sense of input, that is experienced as dreaming

30
Q

Brain stem activity- the signal starts

A

PGO waves

Brain getting input it needs to make sense of

31
Q

The input to be understood

A

Brain is living in virtual reality world, constructing it

Analogous to a Rorscach ink blob- brain makes sense of things with no meaning

Dream seems real as same neural structures used that create your reality when awake

32
Q

AIM model

A

Extension of activation-synthesis theory

Accommodates all conscious states, including the dream state

33
Q

Activation element of AIM

A

Activation- low= no consciousness, high= consciousness

In REM sleep activation is high, in NREM activation is low

34
Q

Physiological mechanism

A

A brain stem mechanism

Reticular activating system

Long axons to many parts of the brain

Neuromodulators- widespread effects

35
Q

Internal element of AIM

A

Where does input come from?

External- when awake

Internal- REM & NREM sleep

Random brain stem signals to many cortical areas (see & hear) & limbic areas (emotions)

36
Q

External attenuation

A

Shell of the thalamus (reticular nucleus)

37
Q

Modulation element of AIM

A

Neuro-modulators balance shifts

Awake & NREM- acetylcholine (inhibited)

REM- acetylcholine released

38
Q

Key neurotransmitter systems

A

Serotoninergic- raphe nuclei

Noradrenergic- locus coerulus

Acetylcholinergic- dorsal brainstem (peribrachial area)

39
Q

Shift in neurotransmitter balance

A

Relative balance of neurotransmitters change during sleep

Activated limbic structures, deactivated dorsolateral prefrontal lobe structures, can’t judge, remember, plan, reason etc

Deactivated posterior cingulated- poor episodic memory

40
Q

Dream features accounted for

A

Dreams seem very real (sensory character)

Planning & memory is weak e.g. why are you there, what you are trying to do

Often a strong, typically negative tone

Sleep (8 decks)

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