Neuronal Plasticity: Increasing the Gain in Pain

• Published in: Science (American Association for the Advancement of Science) Vol. 288; no. 5472; pp. 1765 - 1768
• Main Authors: Woolf, Clifford J., Salter, Michael W.
• Format: Journal Article
• Language: English
• Published: Washington, DC American Society for the Advancement of Science 09.06.2000; American Association for the Advancement of Science; The American Association for the Advancement of Science
• Subjects: Anatomy; Animals; Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Humans; Inflammation - physiopathology; Models, Neurological; N methyl D aspartate receptors; Neurology; Neuronal Plasticity; Neurons; Neurons, Afferent - physiology; Neuroplasticity; Neuroscience; Nociceptors; Nociceptors - physiology; Pain; Pain - physiopathology; Peripheral Nerve Injuries; Physiological aspects; Posterior horn; Posterior Horn Cells - physiology; Receptors; Reviews; Sensitization; Sensory neurons; Signal Transduction; Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors; Stimuli; Synaptic Transmission; Vertebrates: nervous system and sense organs; Nociception; Nociceptor; Pain; Somesthetic pathway; Plasticity; Sensory neuron; Sensitization; Review
• ISSN: 0036-8075; 1095-9203
• DOI: 10.1126/science.288.5472.1765

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.