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

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Calcium-stimulated adenylyl cyclase activity is critical for hippocampus-dependent long-term memory and late phase LTP'. Together they form a unique fingerprint.

Cite this