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Chapter Thirteen The Biology of Learning and Memory

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Hippocampus and Amnesia. Anterograde Amnesia-loss of memories for events that happen after brain damage ... Brain Damage and Amnesia ... – PowerPoint PPT presentation

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Title: Chapter Thirteen The Biology of Learning and Memory


1
Chapter Thirteen The Biology of Learning and
Memory
2
Lashleys 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

3
Figure 13.3  Cuts that Lashley made in the brains
of various rats He found that no cut or
combination of cuts interfered with a rats
memory of a maze.
4
Figure 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.
5
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6
Modern 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

7
Short-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

8
Hippocampus 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

9
H.M.
10
Brain 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

11
A 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

12
Aplysia
13
Invertebrates 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

14
Habituation in Aplysia
15
Long Term Potentiation
16
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17
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18
Biochemical 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

19
Figure 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.
20
Calcium 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).

21
NO and LTP
22
Evidence 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
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