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The Journal of Neuroscience, January 18, 2006, 26(3):851-861; doi:10.1523/JNEUROSCI.3292-05.2006

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Neurobiology of Disease
Calcium Calmodulin-Stimulated Adenylyl Cyclases Contribute to Activation of Extracellular Signal-Regulated Kinase in Spinal Dorsal Horn Neurons in Adult Rats and Mice

Feng Wei,¹ Kunjumon I. Vadakkan,² Hiroki Toyoda,² Long-Jun Wu,² Ming-Gao Zhao,² Hui Xu,² Fanny W.F. Shum,² Yong Heng Jia,² and Min Zhuo²

¹Department of Biomedical Sciences, University of Maryland Dental School, Baltimore, Maryland 21201 and ²Department of Physiology, Faculty of Medicine, University of Toronto, University of Toronto Centre for the Study of Pain, Toronto, Ontario, Canada M5S 1A8

The extracellular signal-regulated kinase (Erk) cascades are suggested to contribute to excitatory synaptic plasticity in the CNS, including the spinal cord dorsal horn. However, many of their upstream signaling pathways remain to be investigated. Here, we demonstrate that glutamate and substance P (SP), two principal mediators of sensory information between primary afferent fibers and the spinal cord, activate Erk in dorsal horn neurons of both adult rat and mouse spinal cord. In genetic knock-out mice of calcium calmodulin-stimulated adenylyl cyclase subtypes 1 (AC1) and 8 (AC8), activation of Erk in dorsal horn neurons were significantly reduced or blocked, either after peripheral tissue inflammation or by glutamate or SP in spinal cord slices. Our studies suggest that AC1 and AC8 act upstream from Erk activation in spinal dorsal horn neurons and the calcium-AC1/AC8-dependent Erk signaling pathways may contribute to spinal sensitization, an underlying mechanism for the development of persistent pain after injury.

Key words: adenylyl cyclases; Erk; spinal dorsal horn; mice; spinal cord; glutamate; substance P; cyclic Amp; Camp; C-Amp

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Received March 18, 2005; revised November 8, 2005; accepted November 14, 2005.

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