Abstract
Quantal analysis has provided evidence for a presynaptic contribution to long-term potentiation in hippocampal CA1 cells. This however leaves unexplained the observation that long-term potentiation has little or no effect on the NMDA receptor-mediated component of the synaptic signal. Here, I report that, in baseline conditions, the coefficient of variation of the AMPA/kainate receptor-mediated signal (CVA/K) is consistently larger than that of the NMDA component (CVNMDA), a result which can be explained if AMPA/kainate receptors are absent or nonfunctional at a proportion of synapses. Long-term potentiation is associated with a reduction in CVA/K, but no change in either the average amplitude of the NMDA component or CVNMDA. This is consistent with the proposal that long-term potentiation induction uncovers clusters of latent AMPA/kainate receptors, with no change in transmitter release.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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2-Amino-5-phosphonovalerate / pharmacology
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Anesthetics, Local / pharmacology
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Animals
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Evoked Potentials / drug effects
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Evoked Potentials / physiology*
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Guinea Pigs
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Hippocampus / physiology*
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In Vitro Techniques
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Lidocaine / analogs & derivatives
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Lidocaine / pharmacology
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Long-Term Potentiation / drug effects
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Long-Term Potentiation / physiology*
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Nerve Fibers / drug effects
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Nerve Fibers / physiology
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Pyramidal Cells / drug effects
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Pyramidal Cells / physiology*
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Quinoxalines / pharmacology
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Receptors, AMPA / physiology
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Receptors, Kainic Acid / physiology
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Receptors, N-Methyl-D-Aspartate / drug effects
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Receptors, N-Methyl-D-Aspartate / physiology
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Synapses / drug effects
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Synapses / physiology
Substances
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Anesthetics, Local
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Quinoxalines
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Receptors, AMPA
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Receptors, Kainic Acid
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Receptors, N-Methyl-D-Aspartate
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QX-314
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FG 9041
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2-Amino-5-phosphonovalerate
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Lidocaine