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) |
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Pages (from-to) | 787-798 |
Number of pages | 12 |
Journal | Neuron |
Volume | 23 |
Issue number | 4 |
DOIs | |
State | Published - Aug 1999 |
Externally published | Yes |
ASJC Scopus subject areas
- Neuroscience(all)