Abstract
Repetitive activation of hippocampal mossy fibers evokes a long-term potentiation (LTP) of synaptic responses in pyramidal cells in the CA3 region that is independent of N-methyl-D-aspartate receptor activation. Previous results suggest that the site for both the induction and expression of this form of LTP is presynaptic. Experimental elevation of cyclic adenosine 3',5'-monophosphate (cAMP) both mimics and interferes with tetanus-induced mossy fiber LTP, and blockers of the cAMP cascade block mossy fiber LTP. It is proposed that calcium entry into the presynaptic terminal may activate Ca(2+)-calmodulin-sensitive adenylyl cyclase I which, through protein kinase A, causes a persistent enhancement of evoked glutamate release.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Calcium / metabolism
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Carbazoles*
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Colforsin / pharmacology
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Cyclic AMP / metabolism*
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Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
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Cyclic AMP-Dependent Protein Kinases / metabolism
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Glutamates / metabolism
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Glutamates / pharmacology
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Glutamic Acid
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Guinea Pigs
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Hippocampus / physiology*
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In Vitro Techniques
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Indoles / pharmacology
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Isoquinolines / pharmacology
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Long-Term Potentiation* / drug effects
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Models, Biological
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Nerve Fibers / physiology*
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Presynaptic Terminals / metabolism
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Pyramidal Cells / physiology
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Pyrroles / pharmacology
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Sulfonamides*
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Synaptic Transmission / drug effects
Substances
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Carbazoles
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Glutamates
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Indoles
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Isoquinolines
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Pyrroles
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Sulfonamides
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Colforsin
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Glutamic Acid
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KT 5720
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Cyclic AMP
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Cyclic AMP-Dependent Protein Kinases
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N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide
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Calcium