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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Altered behavior and long-term potentiation in type I adenylyl cyclase mutant mice.
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Altered behavior and long-term potentiation in type I adenylyl cyclase mutant mice.

机译：I型腺苷酸环化酶突变小鼠的行为和长期增强作用。

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摘要

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.
机译：小鼠Ca（2+）刺激的腺苷酸环化酶（I型）（EC 4.6.1.1），主要在脑中表达，通过靶向诱变失活。 Ca（2+）刺激的腺苷酸环化酶活性降低了海马，新皮层和小脑中40-60％。相对于对照组，来自突变体的海马CA1区的长期增强受到干扰。初始斜率和最大程度的突触反应变化都减少了。尽管突变小鼠学会了正常地在莫里斯水任务中找到隐藏的平台，但是它们对平台被移除时所在的区域没有偏爱。这些结果表明，I型腺苷酸环化酶基因的破坏导致行为发生变化，并且cAMP信号转导途径可能在突触可塑性中起重要作用。

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