Pain: Molecular mechanisms

Our understanding of chronic inflammatory and neuropathic pain at the molec ular and cellular level has developed at an extraordinary rate in recent ye ars. Inflammatory, or neuropathic, neuronal plasticity describes the proces s by which the neurons involved in pain transmission are converted from a s tate of normosensitivity to one in which they are hypersensitive. Here we s ummarize current theories on somatosensory neuroplasticity in a molecular c ontext, highlighting key receptors, ion channels, and signal molecules invo lved. We also suggest new possibilities for drug design, based on the ratio nal targeting of these molecular players.