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Genetic enhancement of neuropathic and inflammatory pain by forebrain upregulation of CREB-mediated transcription

Giannina Descalzi1, Hotaka Fukushima3, Akinobu Suzuki3, Satoshi Kida3 and Min Zhuo12*

Author Affiliations

1 Department of Physiology, Faculty of Medicine, University of Toronto, 1 King's College Circle; University of Toronto Center for the study of Pain, Toronto, Ontario, M5S 1A8, Canada

2 Center for Neuron and Disease, Frontier Institute of Science and Technology, Xi’an Jiaotong University, 28 Xianning West Road, Xian, Shaanxi, 710049, China

3 Department of Bioscience, Faculty of Applied Bioscience, Tokyo University of Agriculture, Tokyo, Japan

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Molecular Pain 2012, 8:90  doi:10.1186/1744-8069-8-90

Published: 31 December 2012


CREB has been reported to be activated by injury and is commonly used as marker for pain-related plasticity changes in somatosensory pathways, including spinal dorsal horn neurons and the anterior cingulate cortex (ACC). However no evidence has been reported to support the direct role of activated CREB in injury-related behavioral sensitization (or allodynia). Here we report that genetic enhancement of CREB-mediated transcription selectively in forebrain areas enhanced behavioral responses to non-noxious stimuli after chronic inflammation (CFA model) or nerve injury. In contrast, behavioral acute responses to peripheral subcutaneous injection of formalin did not show any significant difference. Furthermore, acute pain responses to noxious thermal stimuli were also not affected. Our results thus provide direct evidence that cortical CREB-mediated transcription contributes to behavioral allodynia in animal models of chronic inflammatory or neuropathic pain.