The term nociception refers to the sensory component of pain. It refers to the intricate, highway-like network of sensory transmission within the body, stretching from the extremities to the central nervous system and onward to the brain. But on its most fundamental level, nociception involves molecules and mechanisms. Precisely how do the individual molecules in our nerve cells generate, transmit, or sustain sensory signals? In the January 9 issue of the Proceedings of the National Academy of Sciences, National Institute of Dental and Craniofacial Research scientists and their National Institutes of Health colleagues reported that a much studied protein called cyclin-dependent kinase 5 (Cdk5) does indeed play a regulatory role in pain signaling within the dorsal root ganglia, trigeminal ganglia, and spinal cord. According to the authors, their paper offers the first direct evidence of this novel regulatory role for Cdk5. Using transgenic and knockout models the authors also report the first evidence from animal studies of the importance of Cdk5 activity in peripheral inflammation. These findings suggest that new analgesic drugs that alter Cdk5 activity may one day be beneficial in treating pain.
(Source: National Institute of Dental and Craniofacial Research, Science News in Brief, NIDCR Web site, accessed January 16, 2006)
