-
- Hai-Ying M Cheng, Graham M Pitcher, Steven R Laviolette, Ian Q Whishaw, Kit I Tong, Lisa K Kockeritz, Teiji Wada, Nicholas A Joza, Michael Crackower, Jason Goncalves, Ildiko Sarosi, James R Woodgett, Antonio J Oliveira-dos-Santos, Mitsuhiko Ikura, Derek van der Kooy, Michael W Salter, and Josef M Penninger.
- Amgen Institute, 620 University Avenue, Toronto, Ontario M5G 2C1, Canada.
- Cell. 2002 Jan 11; 108 (1): 31-43.
AbstractControl and treatment of chronic pain remain major clinical challenges. Progress may be facilitated by a greater understanding of the mechanisms underlying pain processing. Here we show that the calcium-sensing protein DREAM is a transcriptional repressor involved in modulating pain. dream(-/-) mice displayed markedly reduced responses in models of acute thermal, mechanical, and visceral pain. dream(-/-) mice also exhibited reduced pain behaviors in models of chronic neuropathic and inflammatory pain. However, dream(-/-) mice showed no major defects in motor function or learning and memory. Mice lacking DREAM had elevated levels of prodynorphin mRNA and dynorphin A peptides in the spinal cord, and the reduction of pain behaviors in dream(-/-) mice was mediated through dynorphin-selective kappa (kappa)-opiate receptors. Thus, DREAM appears to be a critical transcriptional repressor in pain processing.
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