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Plasticity of pain signaling: Role of neurotrophic factors exemplified by acid-induced pain by Stephen B. McMahon; Nicholas G. Jones is a Neuroscience article available to read on EtoBox.

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## Abstract Acute noxious stimuli activate a specialized neuronal detection system that generates sensations of pain and, generally, adaptive behavioral responses. More persistent noxious stimuli notably those associated with some chronic injuries and disease states not only activate the pain‐signaling system but also dramatically alter its properties so that weak stimuli produce pain. These hyperalgesic states arise from at least two distinct broad classes of mechanisms. These are peripheral and central sensitization associated with increased responsiveness of peripheral nociceptor terminals and dorsal horn neurons, respectively. Here we review the key features of these sensitized states and discuss the role of one neurotrophic factor, nerve growth factor, as a peripheral mediator of sensitization and of another factor, brain‐derived neurotrophic factor, as a mediator of central sensitization. We use as a specific example the pain induced by acid stimuli. We review the neurobiology of such pain states, and discuss how acid stimuli both initiate sensitization and how the neuronal processing of acid stimuli is subject to sensitization. © 2004 Wiley Periodicals, Inc. J Neurobiol 61:

Who reads Plasticity of pain signaling: Role of neurotrophic factors exemplified by acid-induced pain?

Author

Stephen B. McMahon; Nicholas G. Jones

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0022-3034)

Published

2004

Language

EN

Field

Neuroscience (Life Sciences)