Open AccessAltered behavior and long-term potentiation in type I adenylyl cyclase mutant mice.
Author(s) -
Zhi Liang Wu,
Steven Thomas,
Enrique C. Villacres,
Zhengui Xia,
Michele L. Simmons,
Charles Chavkin,
Richard D. Palmiter,
Daniel R. Storm
Publication year - 1995
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.92.1.220
Subject(s) - adenylyl cyclase , adcy9 , long term potentiation , adcy10 , camp dependent pathway , synaptic plasticity , biology , hippocampus , signal transduction , neuroscience , chemistry , endocrinology , medicine , microbiology and biotechnology , biochemistry , receptor
The murine Ca(2+)-stimulated adenylyl cyclase (type I) (EC 4.6.1.1), which is expressed predominantly in brain, was inactivated by targeted mutagenesis. Ca(2+)-stimulated adenylyl cyclase activity was reduced 40-60% in the hippocampus, neocortex, and cerebellum. Long-term potentiation in the CA1 region of the hippocampus from mutants was perturbed relative to controls. Both the initial slope and maximum extent of changes in synaptic response were reduced. Although mutant mice learned to find a hidden platform in the Morris water task normally, they did not display a preference for the region where the platform had been when it was removed. These results indicate that disruption of the gene for the type I adenylyl cyclase produces changes in behavior and that the cAMP signal transduction pathway may play an important role in synaptic plasticity.