In pain research, it has been assumed that most nociceptive neurons are polymodal, responding to different damaging stimuli by means of a repertoire of cell surface receptors specialized for the detection of particular types of insult. Attempts to ascribe pain modalities and behavior to individual sensory neuron receptors have been problematic, probably because of the existence of multiple damage-sensing molecules. Now, however, by genetically ablating subsets of nociceptors, followed by behavioral and electrophysiological assays, Abrahamsen et al. have found that sensory neurons expressing a specific type of sodium channel (Nav1.8) have a modality-specific function in pain transmission. Nav1.8-expressing sensory neurons are essential for cold, mechanical, and inflammatory pain behavior. Strikingly, neuropathic and heat pain behavior do not require Nav1.8-expressing neurons.
B. Abrahamsen, J. Zhao, C. O. Asante, C. M. Cendan, S. Marsh, J. P. Martinez-Barbera, M. A. Nassar, A. H. Dickenson, J. N. Wood, The cell and molecular basis of mechanical, cold, and inflammatory pain. Science 321, 702-705 (2008). [Abstract] [Full Text]