Lecture 10 - learning Flashcards
Example of sequence learning
- Asked to follow sequence
- If sequence random harder to learning = RT longer
- If sequence predictable can learn motor associations and sequencing needed to produced response = faster RT
- Gives important info about learning and memory:
- -> Interaction between implicit (procedural) and explicit (declarative) process
- -> Role of sleep
- -> Interference
- -> Consolidation
- -> Probabilistic learning
Motor consolidation
- Memories consolidate in around 4-6 hours
- Offline learning:
- -> Skills improve between practice sessions
- -> Performance of task improved after sleep
- New memories = fragile
- Old memories = robust
- If learn skill and then learn interfering task –> motor memories of first task disrupted
Primary somatosensory cortex (S1)
- M1 and S1 sit either side of central sulcus
- Send and receive signals from contralateral side of body
- If born with missing limb initial map already reformed and if injury remapping occurs and that area of cortex responding to touch will re-map into neighbouring area which is no longer being activated
- Phantom limb pain with injury group = brain receives signals from limb not there, depending on how mapping occurs can produce pain
Non-associative learning
- Relatively permanent change in strength of respond to single stimulus due to repeated exposure to stimulus
- Habituation = reduction in response
- Sensitisation = increase in response
- Both short term and reversible
- Perceptual learning = increasing sensory discrimination with experience
Associative learning
- Process by which association between 2 stimuli or a behaviour and a stimulus is learnt
- Classical conditioning = S-S association
- Motor learning in some forms e.g. cerebellum
- Instrumental/operant conditioning e.g. basal ganglia
Relational learning
- Learning relationships between stimuli
- Spatial processing (maps)
- Declarative memory = constructing episodic memories
Learning-based neural changes: synapse efficacy
Pre-synaptic:
- Increase vesicle volume
- Increase availability of vesicles
- Increase release probability
Synaptic cleft:
- Reduce re-uptake mechanisms
- Reduce gap dimensions
Post-synaptic:
-Increase receptor density/area
Growth – new synapse
-Make new synapses
Spinal flexion reflex
- Withdrawal from cutaneous inputs (heat) rapidly habituates
- Complex pathway
Aplysia (sea slug) gill withdrawal
- Simple nerve system
- Habituation to repeated tactile stimuli = functionally relevant to living in sea weed
- Sensitization preceding electric shock on the tail leads to enhanced gill withdrawal with light touch
Habituation
Synaptic depression: down-regulation of synapse:
- Reduction in neurotransmitters released by synaptic terminals
- Fewer synapses
- Both lead to reduced strength of sensory neuron on motor neuron
Sensitisation
- Synaptic facilitation: up regulation of synapse
- Increase in neurotransmitters released by synaptic terminals
- More synapses
- Both lead to increased strength of sensory neuron on motor neuron
Hebbs rule
- Associative learning
- When neuron A repeatedly participates in firing neuron B, the strength of the action of A onto B increases
Somatosensory remapping
- Rapid changes in somatosensory (or motor maps) evident after change in inputs
- Denervation = if remove input then neighbouring areas will encroach = through amputation of fingers, short term through nerve blockages, if cortex blocked
Chances in map reflect…
- Long term changes in functional connectivity e.g. growth of neurons
- Branching (or pruning) of dendritic connections
- Neurons appear to compete for space in the cortex – unused cortex gets taken over by other inputs
- Imaging of the living mouse brain shows changes (growth and pruning) in dendritic branches in the mouse within hours or days of a new task
Long-term synaptic plasticity
LTP:
- Activity-dependent persistent strengthening of synapses
- These produce a long-lasting increase in signal transmission between 2 neurons
LTD:
- Activity-dependent reduction in the efficacy of neuronal synapses
- Produce long-lasting decreases in signal transmission between 2 neurons
Associative LTP induction
- Before learning have pre-synaptic state = vesicles of glutamate
- AP causes glutamate to diffuse across cleft
- Glutamate binds to AMPA and NMDA receptors
- AMPA = activated and produces response
- To increase strength of association want more AMPA receptors
- Processing in cell that allow AMPA to by synthesised and will placed on membrane = but need calcium
- Get calcium into cell = triggers cascade of responses
- Next time glutamate in cleft = get a stronger response
- NMDA doesn’t respond to glutamate = blocked by Mg ion
- When post synaptic cells sufficiently activated, electoral potential will expel Mg from NMDA
- Can fake this by stimulating cell with electricity
- When glutamate enters cleft = both AMPA and NMDA receptors open and allow usual sodium ions into cell
- NMDA also allows calcium into cell
- Calcium triggers process that manufactures more AMPA and plugs into membrane = more receptors
Key principles of LTP
- Cooperatively = LTP requires simultaneous activation of large number of axons (due to large depolarisation)
- Associative: When weak synaptic input is paired with strong, then large depolarisation can propagate and cause LTP at synapse with weak input
- Synapse-specific: If particular synapse is not activated then LTP will not occur even with strong post synaptic depolarisation
Importance of learning and memory
- Cooperatively: ensure that only event of a high degree of significant (that activate sufficient inputs) will result in memory storage
- Associative: allows even with little significant (CS) to be endowed with a higher degree of meaning, if associated with a significant event (US)
- Synapse specific: Inputs that convey info not related to a particular even will not be strengthened to participate in a given memory
Long term depression
- First identified in hippocampus, thought to be major component of motor learning in cerebellum
- Cerebellar LTD involves decrease in AMPA receptors however not NDMA-dependent
Measuring LTD in humans: TMS
- Sensors put on skin record muscle activity
- Electricity through coil that produces magnetic pulse = magnetic field applied
- Causes brief electric pulse –> twitch of muscle
- If done over motor cortex can activate betz cells = cause movement
- Measure time taken between pulse and response = distance signal travelled
- EMG records response = senses you place on skin that record muscle activity
- Can measure height of responses
LTP and LTD like mechanisms in humans
- Can use TMS to measure LTD and LTP
- Can apply drugs that block receptors e.g. MDMA antagonist blocks LTP
- LTD not blocked by NMDA antagonist