Lecture 10 - Learning and memory

And adaptive process in which the tendency to perform a particular behaviour is changed by experience - system tries to adapt to changes in environment Experiences causes change physiological changes to nervous sytem - circuits involved in perceiving, performing, thinking and planning are modified

Involved in synpatic plasticity - makes synapses more potent/ strengthens connections - requires a combination of : • membrane depolarisation • activation of NMDA receptors (Ca2+ calcium(

focus on acquisition processes • how infor gets into the system • influenced by distraction • once info is in, we retrieve it

focus on retention and retrieval processes, consolidation of info - how we get info back

• S-R learning • motor learning • perceptual learning • Relational learning - all linked to different areas of the brain

Connects perception/ stimulus to movement/ response, to anticipate stimulus • can be automatic (reflex) or a complicated movement • CC must regularly offuc prior to presentation of UCS and CS shouldnt regularly occur without UCS • operant: Thorndike/ skinner, fruit loops maze thing - we learn via operating on our environment

he added a physiological basis to SR learning, argued learning involves: • synaptic plasticity - changes in structure/ biochemicstry that changes how they effect post-synaptic neurons WHAT FIRES TOGETHER, WIRES TOGETHER

If neuron A is active and trying to fire on neuron B, the connection could be strengthened via a plastic change. If Neuron B is receiving strong input from elsewhere (AP’s), it forms a better connection with neuron A as Neuron A is constantly there - This explains condition/associative learning as neuron A becomes associated with the AP’s of Neuron B

Change in synaptic strength/weight

CC reflected a strengthened connection between a brain area that represented cs and a brain area that represented UCS

Wanted to investigate CC in the brain, removed portions of rat brains. He found: • More brain removed = more problems with learning • Doesnt matter where ,always worse at learning • cut through connecting fibers = gneralised locatlisation about which areas do what Falsely concluded that: - memories were widely/ evenly distributed across the brain

Damage to Amygdala = no reinforcement/ conditioning Damate to PFC = differences in goal directed behaviour which leads to reinforcement - struggle with behaviour that brins us towards a goal

it Induces synpatic plasticity by facilitating LTP - does this in the nuclues accumbens, amygdala and PFC - important for memory consolidation - expecting a reward Amygdala is important for LTP - it is the physiological version of wiring then firing together

Result of changes in synaptic connections within SENSORY ASSOCIATION CORTEX • connections are reinforced, so we know which 2 stimuli go together • fMRI shows that memories of pictures, sounds, movements or spatial locations activate the appropriate areas of SAC • sounds are in occiptal love - which then goes to inferior temporal and parietal lobe

Problems in visual discrimination

Info between CS and UCS converges in LATERAL AMYGDALA • high frequency stimulation to lateral amygdala leads to LTP • blocking NMDA receptors here prevents CC

• Supplementary motor area (learning sequences of movements) • Pre motor area - selecting movements to make in response to stimli • Basal Ganglia - involved in automated responses - why there is no automated responses in parkinsons • ventral Tegmental area - lots of dopamine here

• Amygdala/ lateral hypothalamus - Neurons fire in response to stimuli capable of reinforcing behaviour or pleasurable things • PFC - plans for movement, select movement/sequence/bodypart • Nucleus accumbens - reinforces behaviour - addiction

Argues that perceptual learning involves changes in brain chemistry. Found that when animals were trained: • INcreased productino of chemicals (RNA) • increased production of proteins

Info -> visual cortex -> prestriate cortex -> inferior temporal cortex

Extreme ANTEROGRADE amnesia (alcohol amnestic syndrome) - Fixed n time, cant learn anything new, think youre still young - OFten caused by alcohol (vitamin B1, Thiamine deficiency) Caused by damage to: • thalamus and mamillary bodies (hypothalamus - gets input from hippocampus via fornix) - areas crucial for learning and memory

• Apathy, lack of insight, confusion, confabulation * Disruption to front lobe functioning (reality checks)

had Severa anterograde amnesia - due to a bilateral removal of temporal lobes to treat epilepsy (including hippocampus) • couldnt form new, but could remember old, like korsakoff

argued that no one mechanism could be rapid enough for immediate memory, but stable enough for permanent memory, argued there must be two things