Abstract
The mechanism of ATP-induced long-term potentiation was studied pharmacologically using guinea-pig hippocampal slices. Application of 1-10 microM ATP for 10 min transiently depressed and then slowly augmented the synaptic transmission in CA1 neurons leading to long-term potentiation (LTP). This ATP-induced LTP was blocked by the addition of K-252b, an ecto-protein kinase inhibitor, but was enhanced by the addition of RK682, an ecto-phosphatase inhibitor, both of which do not permeate the cell membrane. These results suggest that ATP applied to the perfusate provides enough substrate for ecto-protein kinase to induce LTP through phosphorylation of extracellular domains of membrane proteins in CA1 neurons.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphate / pharmacology*
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Animals
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Carbazoles / pharmacology
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Extracellular Space / metabolism*
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Guinea Pigs
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Hippocampus / cytology
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Hippocampus / drug effects*
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Hippocampus / physiology*
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In Vitro Techniques
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Indole Alkaloids
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Long-Term Potentiation*
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Membrane Proteins / metabolism*
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Neurons / physiology*
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Phosphoprotein Phosphatases / antagonists & inhibitors
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Phosphoprotein Phosphatases / pharmacology
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Phosphorylation
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Protein Kinase Inhibitors
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Protein Kinases*
Substances
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Carbazoles
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Indole Alkaloids
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Membrane Proteins
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Protein Kinase Inhibitors
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RK 682
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Adenosine Triphosphate
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staurosporine aglycone
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Protein Kinases
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ectoprotein kinase
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Phosphoprotein Phosphatases