January 11, 2006
When researchers use the term “nociception,” they mean the sensory component of pain. The term refers to the intricate, highway-like network of sensory transmission within our bodies, stretching from our 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, NIDCR scientists and their NIH colleagues report 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 one day may be beneficial in treating pain.