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What are the two types of long term memory in mammals?
- Declarative (explicit)
- Non-declarative (non-explicit)
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Which systems control declarative memory, and what do these memories entail?
- Medial Temporal Lobe
- Diencephalon
- Facts and events
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Which systems control declarative memory, and what do these memories entail?
- Skills and habits (Striatum)
- Priming (Neocortex)
- Associative memories- conditioning (cerebellum & amygdala)
- Non associative- habituation and sensitisation (reflex pathways)
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What was Cajal's theory of memory?
Memory is stored in the brain by anatomical changes in neural connections.
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What was Hebb's theory?
- The strength of connection between 2 neurons is increased when firing of pre-synaptic and post-synaptic neurons are close in time
- This is known as Hebb's 'cell assembly'
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What was Hyden's theory?
- If memory involves synaptic growth, it requires proteins and RNA.
- If we selectively exercise synapses, we should be able to see corresponding RNA changes
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What are the levels at which memory can be studied (from cause to effect)?
- Cellular machinery
- Ion channel activity
- Neuronal activity
- Neural network formation
- Biomechanics/kinematics
- Overt behaviour
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Why are invertebrates good for study?
- Have fewer neurons; C. elegens has 302 vs our 10^10!
- Axons are larger and more accessible due to a lack of skull.
- Cells are clustered in ganglia; individual ganglia might control certain behaviours.
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What did Benzer look at?
- Drosophila (fruit flies)
- Test tubes with electrical grids with smelly chemicals inside.
- Flies in this tube don't like getting zapped and so stay away from the grids.
- He then puts them into the new environment, with two non-electric grids on each side. One smells smelly, the other is neutral.
- The flies fly away from the smelly one suggesting that they remember!
- Mushroom bodies in droso brain discovered, and damage or removal impairs memory.
- He genetically modified the flies and looked at it's effect on learning
- Worse (or lack) of memory when signal transduction cascade was inhibited (control enzyme activity, protein channels etc)
- Suggests that learning depends on the normal functioning of a signal transduction cascade in some cells, and that the function of the signal transduction cascade is to tell a cell’s nucleus that something memorable has happened
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What are the 3 characteristics outlined in Hebb's theory?
- Homosynaptic plasticity: events responsible for triggering synaptic strengthening occur at same synapse that's being strengthened
- Associative: it associates firing of post-synaptic neuron with that of presynaptic neuron.
- Input specificity: each cell on average is connected to 50,000 other cells. For learning, you need specificity of 2 cells in question.
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What are the 3 simple forms of learning in Kandel's reductionist model?
- Studied these in California sea snails
- Habituation: Non-associative, decrease in behviour in response to repeated stimulus
- Sensitization: Non-associative, strengthening of response to variety of neutral stimuli after an intense noxious stimuli
- Classical conditioning: Associative
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Why did Kandel look at California sea snails?
- If disturbed it retracts it's gill
- He measured the activity of motor neuron and sensory neuron as he poked at the snail.
- Sensory neuron makes motor neuron fire action potentials, leading to gill retraction
- He looked at the effect of the three learning models on this process
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How did Kandel predict the learning models would effect the California sea snail behaviour?
- Habituation (repeatedly poking): Decrease withdrawal reflex (due to depression of synaptic transmission between sensory and motor neurons causing reduced glutamate release). This is a homosynaptic process, as change happens at site of stimulation.
- Sensitization (shocking the tail): Increase motor neuron response, no change in sensory response. This is a heterosynaptic facilitation, as the synapse where cause of increased response happens (the tail), is not the same as the synapse where the increase occurs (sensory-motor neuron).
- This all happened using enzyme activity (no new proteins need to be produced)
- Classical conditioning: Siphon is touched whenever the tail is shocked. This touch leads to quicker gill retraction
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Describe the molecular process behind short term memory in stages
- 1) Serotonin is released by a facilitator neurone
- 2) Serotonin binds to the G-protein receptor
- 3) This leads to the activation of adenylate cyclase, and an increase in cAMP (Cyclic adenosine monophosphate)
- 4) cAMP leads to the phosphorylation (add phosphate to turn on) of kinase proteins (that alter other proteins)
- 5) This prevents K+ channels from opening, meaning the sensory neurone is depolarised for longer
- 6) This also means there are more calcium ions present, so more vesicles can fuse with the cellular membrane
- 7) This means more Glutamate neurotransmitter is released
- 8) This excites the motor neurone
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Describe the molecular process behind long term memory
- Occurs due to repeated serotonin release
- Same steps as short term initially: more cAMP, protein kinase A
- Then some PKA goes to nucleus and it's binding catalytic subunit passes through the nuclear membrane where the DNA's resides, and stimulates gene transcription via cAMP response element-binding (CREB)
- CREB-1 binds to cAMP response element - a DNA sequence in prompters of many genes whose transcription and translation produce proteins needed for new synapse connections between sensory and motor neurons in siphon-gill pathway.
- This DOES require protein formation (CREB-1)
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