Learning & Memory

Learning & Memory

1. Learning = The acquisition of information (Encoding)

   • Classical Conditioning
     • Involves the association between TWO STIMULI and an AUTOMATIC RESPONSE
       • An unconditioned stimulus (US) causes an unconditioned response (UR)
         • If the US is paired with a neutral stimulus, the neutral stimulus can begin to elicit the , now conditioned, response (CR)
           • E.g. Pavlov's dogs - sound of bell - salivate
   • Operant conditioning
     • Association between a LEARNED RESPONSE and a STIMULUS
       • Changing behaviour by means of reinforcement. Behaviour that is reinforced is more likely to be repeated (strengthened) whereas if behaviour is not reinforced, it tends to be extinguished
         • Associations are between a stimulus and response are STRENGTHENED
           • E.G. Skinner and rats
   • Learning & the Brain
     • HEBB'S RULE
       • A SYNAPSE that is REPEATEDLY ACTIVE when the POST SYNAPTIC NEURON is firing will become STRENGTHENED
         • Classical Conditioning
           • US (puff of air to eye) - UR via strong synapse
             • Pairing of TONE with US strengthens weak synapse, leading to tone becoming a CONDITIONED STIMULUS (CS)
               • Will now blink to the sound of TONE
         • Operant Conditioning
           • Reinforcement system STRENGTHENS an ASSOCIATION between a perception (lever) and a behaviour (pressing)
             • BASAL GANGLIA integrates PERCEPTON and ACTION PLANNING.
               • Destruction of the BG leads to FAILURE OF OPERANT CONDITIONING
             • Reinforcement strengthens the link between the perceptual system and the motor system

2. Memory = The retention of information (Storage & Retrieval)

   • Memory in the Brain
     • Cajal proposed that synaptic connections between neuons mediate behaviour - they become modified by learning which may serve as memory.
       • Non-declarative memories may be stored in the neural circuit that produces the behaviour - e.g. unconscious memories e.g. skills
   • Hippocampus and Memory Consolidation
     • Damage to the hippocampus causes issues with declarative memory
       • Amnesia - disorder of memory
         • Anterograde and Retrograde
     • Patient H.M
       • Bilateral temporal lobe resection
         • Normal WM (digit span), perceptual leaning, operant and classical conditioning
           • Hippocampus is not necessary for STM
             • Previous declarative memory still intact thus HIPPOCAMPUS is not where LTM is stored.
               • Hippocampus is CRITICAL for CONSOLIDATION for new memories

3. Reinforcement

   • The brain region known as the VENTRAL TEGMENTUM (VT) and the neurotransmitter system DOPAMINE has been identified with reward
     • Electrical microstimulation of VT (lower midbrain) can have reinforcing effects on behaviours, similar to natural reinforcers (food / sex)
       • VT projects to the LIMBIC SYSTEM - the MESOLIMBIC DOPAMINERGIC SYSTEM
         • Extracellular dopamine concentration (rats) and fMRI activation (humans) in NUCLEUS ACCUMBENS (in limbic system)
           • VT stimulation - rats; Money reward - humans
   • Unexpected reward (novel food) - strong POSITIVE DOPAMINE SIGNAL
     • Declines with REPEATED PRESENTATION and learning
       • Eventually, the presentation of the a predicted reward = dopamine stops firing
         • BUT dopamine in the Nucleus Accumbens surged in response to the PREDICTIVE STIMULUS (e.g. tone)
           • Dopamine plays an important role in learning, particularly associative learning
   • Dopamine ANTAGONISTS (reduce DA activation) block reinforcement learning
     • D1 receptor activation enhances the activity of neurons receiving strong excitatory input from other sources, and reduces activity of neurons that are weakly activated
       • This helps because they increase the contrast between the important things and the not so important things. Dopamine is a MODULATOR OF LEARNING
         • FOCUS on what really matters

4. Cortico-Hippocampal Networks for Memory - Evidence for Animals

   • Hippocampal lesions impaired monkey performance on a delayed non-matching task
     • More selective lesions that spares cortex and amygdala had no effect.
       • Parahippocampal lesions affect memory
         • The hippocampus

5. LONG-TERM POTENTIATION (LTP)

   • Use-dependent strengthening of synaptic connections (LTP)
     • In agreement with Hebb's rule
     • Principle: If a weak and a strong input act on a neuron at the same time, the weak synapse becomes stronger (HEBBIAN LEARNING)
       • When the weak input occurs again, the response to the weak input will increase (strengthening of that input)
         • For LTP to be induced, 2 things MUST be in place:
           • The POST-SYNAPTIC CELL must be DEPOLARIZED (must be excited)
             • The POST-SYNAPTIC CELL must RECEIVE ADDITIONAL INPUT (weak input)
     • Actual cellular mechanism
   • LTP: Synaptic mechanisms
     • Excitatory neurotransmitter - GLUTAMATE
       • Glutamate binds to NMDA receptors, Ca2+ activates enzymes in the post synaptic cell. The calcium causes new AMPA receptors to be created.
         • NO is also synthesised - used by brain- goes back to pre-synaptic cell and causes more glutamate to be released.
           • Strengthens the synapse in 2 ways - more receptors on the post-synaptic cell and more neurotransmitter on the pre-synaptic cell
             • Long Term Depression
               • Need this so we can UNLEARN (weakening of synapses)
                 • Harder to induce - inputs that do not contribute to postsynaptic firing are weakened
                   • THUS, learning represented in the brain - as memory

6. THE HIPPOCAMPUS

   • 2 way connections with cortical association areas
     • Direct and indirect connections with limbic areas (strong emotions)
       • All links are EXCITATORY