Abstract
Conversion of "silent" synapses into active ones is a likely mechanism for long-term potentiation (LTP), an experimental paradigm for studying information storage. A widely accepted mechanism that has been suggested for synaptic silence is that functional AMPA glutamate receptors (AMPARs) are absent on the subsynaptic membrane. Evidence is presented here that in many cases the cause of apparent "silence" is presynaptic and due to a low level of glutamate release. Increased transmitter release is crucial for early LTP maintenance. Delayed modifications in postsynaptic receptors matched with transmitter release changes underlie structural alterations associated with late LTP phases.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Action Potentials / drug effects
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Action Potentials / physiology*
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Animals
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Humans
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Long-Term Potentiation / drug effects
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Long-Term Potentiation / physiology
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Presynaptic Terminals / physiology*
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Receptors, AMPA / agonists
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Receptors, AMPA / antagonists & inhibitors
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Receptors, AMPA / physiology
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Receptors, N-Methyl-D-Aspartate / agonists
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Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
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Receptors, N-Methyl-D-Aspartate / physiology
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Receptors, Presynaptic / agonists
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Receptors, Presynaptic / antagonists & inhibitors
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Receptors, Presynaptic / physiology
Substances
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Receptors, AMPA
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Receptors, N-Methyl-D-Aspartate
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Receptors, Presynaptic