Calcium-stimulated adenylyl cyclase activity is critical for hippocampus-dependent long-term memory and late phase LTP

Scott T. Wong; Jaime Athos; Xavier A. Figueroa; Victor V. Pineda; Michele L. Schaefer; Charles C. Chavkin; Louis J. Muglia; Daniel R. Storm

doi:10.1016/S0896-6273(01)80036-2

Calcium-stimulated adenylyl cyclase activity is critical for hippocampus-dependent long-term memory and late phase LTP

Scott T. Wong, Jaime Athos, Xavier A. Figueroa, Victor V. Pineda, Michele L. Schaefer, Charles C. Chavkin, Louis J. Muglia, Daniel R. Storm

Research output: Contribution to journal › Article › peer-review

Abstract

It is hypothesized that Ca²⁺ stimulation of calmodulin (CaM)-activated adenylyl cyclases (AC1 or AC8) generates cAMP signals critical for late phase LTP (L-LTP) and long-term memory (LTM). However, mice lacking either AC1 orAC8 exhibit normal L-LTP and LTM. Here, we report that mice lacking both enzymes (DKO) do not exhibit L-LTP or LTM. To determine if these defects are due to a loss of cAMP increases in the hippocampus, DKO mice were unilaterally cannulated to deliver forskolin. Administration of forskolin to area CA1 before training restored normal LTM. We conclude that Ca²⁺- stimulated adenylyl cyclase activity is essential for L-LTP and LTM and that AC1 or AC8 can produce the necessary cAMP signal.

Original language	English (US)
Pages (from-to)	787-798
Number of pages	12
Journal	Neuron
Volume	23
Issue number	4
DOIs	https://doi.org/10.1016/S0896-6273(01)80036-2
State	Published - Aug 1999
Externally published	Yes

ASJC Scopus subject areas

Neuroscience(all)

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Calcium-stimulated adenylyl cyclase activity is critical for hippocampus-dependent long-term memory and late phase LTP. / Wong, Scott T.; Athos, Jaime; Figueroa, Xavier A.; Pineda, Victor V.; Schaefer, Michele L.; Chavkin, Charles C.; Muglia, Louis J.; Storm, Daniel R.

In: Neuron, Vol. 23, No. 4, 08.1999, p. 787-798.

Research output: Contribution to journal › Article › peer-review

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title = "Calcium-stimulated adenylyl cyclase activity is critical for hippocampus-dependent long-term memory and late phase LTP",

abstract = "It is hypothesized that Ca2+ stimulation of calmodulin (CaM)-activated adenylyl cyclases (AC1 or AC8) generates cAMP signals critical for late phase LTP (L-LTP) and long-term memory (LTM). However, mice lacking either AC1 orAC8 exhibit normal L-LTP and LTM. Here, we report that mice lacking both enzymes (DKO) do not exhibit L-LTP or LTM. To determine if these defects are due to a loss of cAMP increases in the hippocampus, DKO mice were unilaterally cannulated to deliver forskolin. Administration of forskolin to area CA1 before training restored normal LTM. We conclude that Ca2+- stimulated adenylyl cyclase activity is essential for L-LTP and LTM and that AC1 or AC8 can produce the necessary cAMP signal.",

author = "Wong, {Scott T.} and Jaime Athos and Figueroa, {Xavier A.} and Pineda, {Victor V.} and Schaefer, {Michele L.} and Chavkin, {Charles C.} and Muglia, {Louis J.} and Storm, {Daniel R.}",

note = "Funding Information: This study was supported by National Institutes of Health grants NS 37056 and NS 20498 to D. R. S. as well as the Howard Hughes Medical Institutes and a Burroughs Wellcome Fund Career Development Award to L. J. M. Support to J. A. was given by PHS NRSA T32 GM07270 from NIGMS. Copyright: Copyright 2017 Elsevier B.V., All rights reserved.",

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doi = "10.1016/S0896-6273(01)80036-2",

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AU - Wong, Scott T.

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AU - Pineda, Victor V.

AU - Schaefer, Michele L.

AU - Chavkin, Charles C.

AU - Muglia, Louis J.

AU - Storm, Daniel R.

N1 - Funding Information: This study was supported by National Institutes of Health grants NS 37056 and NS 20498 to D. R. S. as well as the Howard Hughes Medical Institutes and a Burroughs Wellcome Fund Career Development Award to L. J. M. Support to J. A. was given by PHS NRSA T32 GM07270 from NIGMS. Copyright: Copyright 2017 Elsevier B.V., All rights reserved.

PY - 1999/8

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N2 - It is hypothesized that Ca2+ stimulation of calmodulin (CaM)-activated adenylyl cyclases (AC1 or AC8) generates cAMP signals critical for late phase LTP (L-LTP) and long-term memory (LTM). However, mice lacking either AC1 orAC8 exhibit normal L-LTP and LTM. Here, we report that mice lacking both enzymes (DKO) do not exhibit L-LTP or LTM. To determine if these defects are due to a loss of cAMP increases in the hippocampus, DKO mice were unilaterally cannulated to deliver forskolin. Administration of forskolin to area CA1 before training restored normal LTM. We conclude that Ca2+- stimulated adenylyl cyclase activity is essential for L-LTP and LTM and that AC1 or AC8 can produce the necessary cAMP signal.

AB - It is hypothesized that Ca2+ stimulation of calmodulin (CaM)-activated adenylyl cyclases (AC1 or AC8) generates cAMP signals critical for late phase LTP (L-LTP) and long-term memory (LTM). However, mice lacking either AC1 orAC8 exhibit normal L-LTP and LTM. Here, we report that mice lacking both enzymes (DKO) do not exhibit L-LTP or LTM. To determine if these defects are due to a loss of cAMP increases in the hippocampus, DKO mice were unilaterally cannulated to deliver forskolin. Administration of forskolin to area CA1 before training restored normal LTM. We conclude that Ca2+- stimulated adenylyl cyclase activity is essential for L-LTP and LTM and that AC1 or AC8 can produce the necessary cAMP signal.

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Calcium-stimulated adenylyl cyclase activity is critical for hippocampus-dependent long-term memory and late phase LTP

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