Mediation of hippocampal mossy fiber long-term potentiation by cyclic AMP

Marc G. Weisskopf; Pablo E. Castillo; Robert A. Zalutsky; Roger A. Nicoll

doi:10.1126/science.7916482

Mediation of hippocampal mossy fiber long-term potentiation by cyclic AMP

Marc G. Weisskopf, Pablo E. Castillo, Robert A. Zalutsky, Roger A. Nicoll

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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 Ca²⁺-calmodulin-sensitive adenylyl cyclase I which, through protein kinase A, causes a persistent enhancement of evoked glutamate release.

Original language	English (US)
Pages (from-to)	1878-1882
Number of pages	5
Journal	Science
Volume	265
Issue number	5180
DOIs	https://doi.org/10.1126/science.7916482
State	Published - Sep 23 1994
Externally published	Yes

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title = "Mediation of hippocampal mossy fiber long-term potentiation by cyclic AMP",

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 Ca2+-calmodulin-sensitive adenylyl cyclase I which, through protein kinase A, causes a persistent enhancement of evoked glutamate release.",

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year = "1994",

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T1 - Mediation of hippocampal mossy fiber long-term potentiation by cyclic AMP

AU - Weisskopf, Marc G.

AU - Castillo, Pablo E.

AU - Zalutsky, Robert A.

AU - Nicoll, Roger A.

PY - 1994/9/23

Y1 - 1994/9/23

N2 - 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 Ca2+-calmodulin-sensitive adenylyl cyclase I which, through protein kinase A, causes a persistent enhancement of evoked glutamate release.

AB - 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 Ca2+-calmodulin-sensitive adenylyl cyclase I which, through protein kinase A, causes a persistent enhancement of evoked glutamate release.

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Mediation of hippocampal mossy fiber long-term potentiation by cyclic AMP

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