Title: Chapter Thirteen The Biology of Learning and Memory
1Chapter ThirteenThe Biology of Learning and
Memory
2Lashleys Engram
- Engram-the physical representation of what has
been learned - Trained rats on mazes and observed what happened
when he disrupted connections between two brain
areas or removed part of the brain - Results
- Disrupted connections did not affect maze
performance - Maze performance was only decreased when large
amounts of brain were removed
3Figure 13.3 Cuts that Lashley made in the brains
of various ratsHe found that no cut or
combination of cuts interfered with a rats
memory of a maze.
4Figure 13.1 Procedures for classical
conditioning In classical conditioning two
stimuli (CS and UCS) are presented at certain
times regardless of what the learner does.
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6Modern Search for the Engram
- Simple classical conditioning procedures take
place in the lateral interpositus nucleus - More complex learning paradigms depend on areas
outside of the cerebellum
7Short-term and Long-term Memory
- Short-term-events that have just occurred
- Long-term-events from previous times
- Memories that stay in short-term memory long
enough are consolidated into long-term memory - Emotional responses can enhance consolidation by
stimulating the amygdala
8Hippocampus and Amnesia
- Anterograde Amnesia-loss of memories for events
that happen after brain damage - Retrograde Amnesia-loss of memories that occurred
shortly before brain damage
9H.M.
10Brain Damage and Amnesia
- Korsakoffs Syndrome-brain damage caused by
long-term thiamine deficiency (both retrograde
and anterograde amnesia) - Alzheimers Disease-severe memory loss associated
with aging - Amyloid beta protein 42-accumulates in the brain
and impairs neuron function - Plaques
- Tangles
11A Common Model for Studying Learning
- Aplysia
- Marine Invertebrate/Sea slug
- Fewer and Larger neurons
- Neurons are consistent across all aplysia
- We understand the pathway of the withdrawal
response-touch results in the withdrawal of the
siphon, mantle or gill
12Aplysia
13Invertebrates and Learning
- Habituation-if you persistently touch the
aplysias gills, it will stop withdrawing - Dependent on change in the synapse between the
sensory and motor neuron
14Habituation in Aplysia
15Long Term Potentiation
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18Biochemical Mechanisms of LTP
- Glutamate receptors involved in LTP
- AMPA-ionotropic receptor opening sodium channels
- NMDA-when partly depolarized, magnesium leaves
and glutamate opens channel (sodium and calcium
enter) - Calcium enhances the later responsiveness of the
synapse by altering genes and activating proteins
19Figure 13.23 The AMPA and NMDA receptors during
LTP If one or (better) more AMPA receptors have
been repeatedly stimulated, enough sodium enters
to largely depolarize the dendrites membrane.
Doing so displaces the magnesium ions and
therefore enables glutamate to stimulate the NMDA
receptor. Both sodium and calcium enter through
the NMDA receptors channel.
20Calcium Effects on Future Synapses
- AMPA receptor becomes more responsive to
glutamate. - Dendrite builds more AMPA receptors or moves them
to a better place. - Dendrites make more branches to the axon (spines).
21NO and LTP
22Evidence for an LTP/Learning Link
Mice with abnormal NMDA receptors have difficulty
learning Mice with more than normal NMDA
receptors have super memory Drugs that block
LTP block learning Drugs that facilitate LTP
facilitate learning