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Tissue Injury and Related Mediators of Pain Exacerbation

Tissue injury and inflammation result in release of various mediators that promote ongoing pain or pain hypersensitivity against mechanical, thermal and chemical stimuli. Pro-nociceptive mediators activate primary afferent neurons directly or indirectly to enhance nociceptive signal transmission to...

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Detalles Bibliográficos
Autores principales: Amaya, Fumimasa, Izumi, Yuta, Matsuda, Megumi, Sasaki, Mika
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bentham Science Publishers 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3849785/
https://www.ncbi.nlm.nih.gov/pubmed/24396335
http://dx.doi.org/10.2174/1570159X11311060003
Descripción
Sumario:Tissue injury and inflammation result in release of various mediators that promote ongoing pain or pain hypersensitivity against mechanical, thermal and chemical stimuli. Pro-nociceptive mediators activate primary afferent neurons directly or indirectly to enhance nociceptive signal transmission to the central nervous system. Excitation of primary afferents by peripherally originating mediators, so-called “peripheral sensitization”, is a hallmark of tissue injury-related pain. Many kinds of pro-nociceptive mediators, including ATP, glutamate, kinins, cytokines and tropic factors, synthesized at the damaged tissue, contribute to the development of peripheral sensitization. In the present review we will discuss the molecular mechanisms of peripheral sensitization following tissue injury.