title: Neuronal plasticity: increasing the gain in pain.
abstract: We describe those sensations that are unpleasant, intense, or distressing as painful. Pain is not homogeneous, however, and comprises three categories: physiological, inflammatory, and neuropathic pain. Multiple mechanisms contribute, each of which is subject to or an expression of neural plasticity-the capacity of neurons to change their function, chemical profile, or structure. Here, we develop a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain, identifying distinct forms of plasticity, which we term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.
authors.affiliation: Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, MGH-East, Charlestown, MA 02129, USA. woolf.clifford@mgh.harvard.edu
authors.forename: C J
authors.initials: CJ
authors.lastname: Woolf
authors.forename: M W
authors.initials: MW
authors.lastname: Salter
mesh_terms: D000818:Animals; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D008959:Models, Neurological; D009473:Neuronal Plasticity; D009475:Neurons, Afferent / Q000502:physiology*; D009619:Nociceptors / Q000502:physiology; D010146:Pain / Q000503:physiopathology*; D059348:Peripheral Nerve Injuries; D020671:Posterior Horn Cells / Q000502:physiology*; D015398:Signal Transduction; D009435:Synaptic Transmission