Learning_1

Learning_1

1. Scoville & Milner 1957 patient HM no new declarative (episodic, spatial) LTM

   • Important for spatial learning (type of relational learning) (Morris water maze, 1982), (Kolb & Whishaw, 1996)
     • O'Keefe &Dostrovsky (1971) Cognitive mapping pyramidal cells in hippocampus make up map fire in familiar enviroment
       • Oltons & Samuelsons radial arms maze test- remove cues and they remember where they are
         • Sherry et al, hippocampus lesioned spatial task distrupted, MAguire taxi drivers larger hippocampus
           • Hippocampus important for spatial learning evidence its consolidated to LTM by hippocampus

2. Amygdala

   • Intergrates components of fear as an emotional response: behavioural, autonomic and hormonal
     • Monkeys w/ damage to medial temporal lobe cease to show normal aggression or fear responses (Kluver & Bucy 1939) MTL damage affects our ability to feel emotion
       • Lesion just amygdala in rhesus monkeys no fear response (Dicks,1969)
   • Fear: Darwin (1872) innate, involuntary action, survival
     • Born deaf and blind can still laugh and cry
       • Elkman & Fruesen (1971) remote new guinea tribe able to recognise facial expressions
   • Shown to have primary role in memory and emotional (fear, aggression) reaction. Part of limbic system. Located in medial temporal lobe.
   • Role of amygdala in fear conditioning to study learning, you can LEARN a particular stimulus is threatening. Occurs quickly, long lasting
     • Conditioned stimulus in mice eg tone on its own no responses, unconditioned stimulus eg shock paired with CS, when CS presented alone fear response. learnt to fear tone. Philips and Le Doux (1992)
       • Galili et al (2011) even in drosophila they voluntairly go to less appealing odor not associated with shock, shows it has learnt lesson about odor conditioned with shocked
         • Can habituate fear conditioning, go back to no fear is CS keeps appearing with no shock (extinction). Can also just fear a context where US happened.
     • Philips and Le Doux (1992) if lesion hippocapmus normal fear conditioning but less fear in contextual. If lesion amygdala no learning, important for conditioning

3. Hippocampus

   • LTP mainly produced in CA1 region, on the dendritic spines of many pyramidal cells which contain high numbers of NMDA and AMPA receptors
     • Ca ion entering NMDA receptor activates CAMKII in dendrite which migrates to synapse resulting in more AMPA receptors. More AMPA receptors increase reponse to glutamate = larger EPSP's = stronger synapse.
       • CAMKII critical for LTP. Silvia et al (1992), No LTP in CA1 field of mice with mutation of gene responsible for CAMKII
   • Role in memory. Part of limbic system. Located in medial temporal lobe.

4. Neurobiology of learning

   • Synaptic plasticity hypothesis: Strength of synaptic connections is modifiable by neural activity and learning may make use of this synaptic change
     • Hebb: cells associate over large brain areas to represent info/memory, caused by strengthtening of connections between neurons
       • Synaptic plasticity is foundation of learning
         • Alpysia 20,000 neurons. Kandel & Schwartz (1982) sensitization and habituation condition (learning) also change in synapse
           • Lomo (1966) intense stimulation of axons caused a long-term increase in strength of EPSP's in post-synaptic neuron. EPSP's must summate to depolarise the dendtrite spine. Synaptic strengthening/LTP occurs only when synapses are active while the post-synaptic cell is depolarised, Kelso et al (1986)
             • This is LTP, which appears to underlie synaptic plasticity, esp as a weak synapse is strengthened by a strong one if they are activated stimultaneously.
               • (1973) Bliss & Lomo LTP formed in hippocampus and other parts of brain

5. LTP learning?

   • Zola-morgan et al (1986) patient RB had missing CA1 hippocampal region, no to ability to form LTM (couldn't learn) is this because LTP couldn't happen?
     • Hippocampus dependent task (Morris water maze 1989) rats with D-AP5 NMDA receptor agonist (prevents some forms of LTP by blocking Ca ion passage) learned more slowly, may have relied on procedural learning rather than spatial (still learning). If LTP was neuro basis of learning no learning could occur here.
       • Complexity of hippocampal based learning has been unable to demonstrate directly that learning causes change in synaptic connections as a result of LTP. Move to simplier form of learning to test LTP fear conditioning