55-101 Lecture Notes - Synaptic Plasticity, Excitatory Postsynaptic Potential, Classical Conditioning

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Outline of Lecture 28 (02-26 D; Baraban)
Synaptic Plasticity
I. Long term potentiation
- LTP is the phenomena that the peak excitatory post-synaptic potential (epsp) to low-frequency
input is greater after a high-frequency input (tetanus), and that this effect persists for a long time
- Of presyn, postsyn, or both, most people believe postsyn changes mediate LTP
- LTP is a bistable switch toggled by NMDA
- AMPA receptors require Glu for to open and do not allow Ca flux
- NMDA receptors require Glu and depolarization to open and allow Ca flux
- Mechanism of toggling: tetanus prolonged depol. AMPA nad NMDA opens Ca flux
due to NMDA signals for insertion of more AMPA receptors greater postsyn depol
in future
- “Silent” synapses with no AMPA can still undergo LTP if NMDA receptors are still present at
synapse and if surrounding synapses provide depol. for NMDA activation
- Two major properties of LTP
- Input specificity: only synapse receiving tetanus gets LTP
- Associativity: (however) a weak input at another synapse at the same time as a strong input at
another provides depol. to the former and causes LTP at both
- The broader picture
- LTP provides a mechanism to begin explaining learning and memory
- Associativity provides a simplistic mechanism to explain Pavlovian conditioning
II. Long term depression
- LTD can result in un-learning, and decrease in synaptic efficiency but is not well understood
III. Other forms of synaptic plasticity
- Dendritic spines: addition or deletion, shape changes
- Genetic defects in NMDA receptor function/regulation are linked to schizophrenia
Summary of major points
- See Objectives on p. 1
- There really isn’t much in this lecture beyond LTP
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