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 Schaefer, Charles C. Chavkin, Louis J. Muglia, Daniel R. Storm

Research output: Contribution to journalArticle

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 languageEnglish (US)
Pages (from-to)787-798
Number of pages12
JournalNeuron
Volume23
Issue number4
DOIs
Publication statusPublished - Aug 1999
Externally publishedYes

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ASJC Scopus subject areas

  • Neuroscience(all)

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