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The Journal of Neuroscience, October 26, 2005, 25(43):9913-9918; doi:10.1523/JNEUROSCI.2376-05.2005

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Cellular/Molecular
Hippocampal Neurons Express a Calcineurin-Activated Adenylyl Cyclase

Guy C.-K. Chan,¹ Susumu Tonegawa,² and Daniel R. Storm¹

¹Department of Pharmacology, University of Washington, Seattle, Washington 98195, and ²Howard Hughes Medical Institute, The Picower Center for Learning and Memory and RIKEN/Massachusetts Institute of Technology Neuroscience Research Center, Departments of Biology and Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139

Ca²⁺-stimulated adenylyl cyclases are important for several forms of neuroplasticity because they couple activity-dependent Ca²⁺ increases to cAMP in neurons. For example, the calmodulin-stimulated adenylyl cyclases, AC1 and AC8, are required for hippocampus-dependent memory and long-lasting long-term potentiation. To identify other mechanisms for Ca²⁺ stimulation of adenylyl cyclases, cultured hippocampal neurons from transgenic mice lacking both AC1 and AC8 [double knock-out (DKO) mice] were analyzed for Ca²⁺ stimulation of intracellular cAMP. Surprisingly, neurons from DKO mice showed significant Ca²⁺-stimulated cAMP accumulation that was blocked by inhibitors of calcineurin [PP2B (protein phosphatase 2B)], a Ca²⁺-activated protein phosphatase. Analysis of cultured neurons from calcineurin^-/- mice confirmed that hippocampal neurons exhibit a calcineurin-dependent cAMP increase, which may contribute to some forms of neuroplasticity.

Key words: adenylate cyclase; knock-out mice; hippocampus; phosphatase; calcium; signal transduction

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Received June 9, 2005; revised September 13, 2005; accepted September 15, 2005.

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