Genetic elimination of behavioral sensitization in mice lacking calmodulin-stimulated adenylyl cyclases

Feng Wei, Chang Shen Qiu, Susan J. Kim, Lisa Muglia, James W. Maas, Victor V. Pineda, Hai Ming Xu, Zhou Feng Chen, Daniel R. Storm, Louis J. Muglia, Min Zhuo

Research output: Contribution to journalArticlepeer-review

204 Scopus citations

Abstract

Adenylyl cyclase types 1 (AC1) and 8 (AC8), the two major calmodulin-stimulated adenylyl cyclases in the brain, couple NMDA receptor activation to cAMP signaling pathways. Cyclic AMP signaling pathways are important for many brain functions, such as learning and memory, drug addiction, and development. Here we show that wild-type, AC1, AC8, or AC1&8 double knockout (DKO) mice were indistinguishable in tests of acute pain, whereas behavioral responses to peripheral injection of two inflammatory stimuli, formalin and complete Freund's adjuvant, were reduced or abolished in AC1&8 DKO mice. AC1 and AC8 are highly expressed in the anterior cingulate cortex (ACC), and contribute to inflammation-induced activation of CREB. Intra-ACC administration of forskolin rescued behavioral allodynia defective in the AC1&8 DKO mice. Our studies suggest that AC1 and AC8 in the ACC selectively contribute to behavioral allodynia.

Original languageEnglish
Pages (from-to)713-726
Number of pages14
JournalNeuron
Volume36
Issue number4
DOIs
StatePublished - Nov 14 2002

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