Dreams For No Reason Flashcards
Glial cells
Extra cellular physical support
Provision on nutrients
Maintenance of extra cellular fluid around synapses
Types; oliogodendrocytes, asteocytes, microglia
Cerebrospinal fluid
Clears waste
Maintains homeostasis
125ml at any point & 500ml generated every day
Brain is richly supplied with blood
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
Lymphatic system of brain
Drains fluid back into heart from lymphatic nodes
Ventricles of brain
Cerebrospinal fluid
Fluid washes the brain, removing by-products
Thalamus: specific relay nuclei
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
Thalamus; non-specific
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
Why do non-specific neurone matter?
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
Thalamus: association neurons
Pulvinar- visual info & eye movement, probably attention
Input from distributed cortex & eye movement area
Output to secondary visual cortex in parietal/temporal area
Neurotransmitters involved in sleep & dreaming
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
Synthesis, packaging & transport of neurotransmitters
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
Metabotropic receptors
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
Neurotransmission
Local
Specific
Brief
Fine control
E.g. switching off wakefulness
Neuromodulation
Widespread
Non-specific
Long-lasting
Increase of cortical stimulation
Computational unit
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
Excitatory neurotransmitters & inhibitory effects
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
Neurotransmitters
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)
Recycling of neurotransmitters
After the neurotransmitters have had their effect they are typically reabsorbed back into the neuron that released them (pre-synaptic cell)
Theories from REM observation
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
Aserinsky & Kleitman (1955)
Only in 20/27 cases when people were woken from REM did they report having dreaming
Vertes & Eastman (2000)
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
Sleep cleans the brain
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)
Reverse learning
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
Purpose of REM sleep
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
Neural networks
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)
Reverse learning- how to fix an overloaded network
How to eliminate the parasitic connection
1) switch off external input
2) bombard with random signals
3) weaken any association that fires
Brain stem mechanisms
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
Synaptic homoeostasis hypothesis
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)
Activation- synthesis
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
Brain stem activity- the signal starts
PGO waves
Brain getting input it needs to make sense of
The input to be understood
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
AIM model
Extension of activation-synthesis theory
Accommodates all conscious states, including the dream state
Activation element of AIM
Activation- low= no consciousness, high= consciousness
In REM sleep activation is high, in NREM activation is low
Physiological mechanism
A brain stem mechanism
Reticular activating system
Long axons to many parts of the brain
Neuromodulators- widespread effects
Internal element of AIM
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)
External attenuation
Shell of the thalamus (reticular nucleus)
Modulation element of AIM
Neuro-modulators balance shifts
Awake & NREM- acetylcholine (inhibited)
REM- acetylcholine released
Key neurotransmitter systems
Serotoninergic- raphe nuclei
Noradrenergic- locus coerulus
Acetylcholinergic- dorsal brainstem (peribrachial area)
Shift in neurotransmitter balance
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
Dream features accounted for
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
