Abstract
Long-term potentiation (LTP) of synaptic transmission in the hippocampus is a widely studied model of memory processes. In the CA1 region, LTP is triggered by the entry of Ca2+ through N-methyl-D-aspartate (NMDA) receptor channels and maintained by the activation of Ca2(+)-sensitive intracellular messengers. We now report that in CA1, a transient block by tetraethylammonium of IC, IM and the delayed rectifier (IK) produces a Ca2(+)-dependent NMDA-independent form of LTP. Our results suggest that this new form of LTP (referred as to LTPK) is induced by a transient enhanced release of glutamate which generates a depolarization by way of the non-NMDA receptors and the consequent activation of voltage-dependent Ca2+ channels.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Calcium Channels / drug effects*
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Calcium Channels / physiology
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Ibotenic Acid / analogs & derivatives*
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Ibotenic Acid / antagonists & inhibitors
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Ibotenic Acid / pharmacology
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Male
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N-Methylaspartate / antagonists & inhibitors
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N-Methylaspartate / pharmacology*
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Potassium Channels / drug effects*
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Potassium Channels / physiology
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Rats
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Rats, Inbred Strains
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Synapses / physiology*
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Synaptic Transmission / drug effects*
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Tetraethylammonium
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Tetraethylammonium Compounds / pharmacology*
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Time Factors
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alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
Substances
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Calcium Channels
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Potassium Channels
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Tetraethylammonium Compounds
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Ibotenic Acid
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N-Methylaspartate
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Tetraethylammonium
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alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid