樋浦, 明夫 Department of Oral Histology, School of Dentistry, Tokushima University Hospital, University of Tokushima KAKEN研究者をさがす
Studies into the interactions between glia/immune cells and neurons have focused on the induction of patho-logical (neuropathic or inflammatory) pain. Growing evidence of close relationships between peripheral and central glia and pathological pain has emerged during the last 2 decades. Numerous experimental studies have showed the release of cytokines and inflammatory neuropeptides from peripheral and central terminals of primary sensory neurons and from ac-tivated peripheral and central glia after nerve injury (crush, ligation or transection), which in turn act in a paracrine or autocrine manner. Cytokines induce the synthesis of algogens (pain-inducing substances such as prostaglandin) which leads to the primary (peripheral) or secondary (central) sensitization responsible for hyperalgesia or allodynia under in-flammatory conditions. The review has also highlighted the role of thermo transient receptor potential (TRP) channels TRPV1, TRPA1 and TRPM8 in the induction of pathological pain. The noxious heat sensor TRPV1 has an overt role in noxious heat hyperalgesia or allodynia, whereas TRPA1 and TRPM8 seem to have roles in noxious cold or mechanical al-lodynia, although results are inconsistent. Close mutual interrelationships between immune and glial cells and thermoTRP channels via cytokines or pro-inflammatory neuropeptides cannot be ignored when attempting to explain the induction and continuation of pathological pain. Investigations on the initial signals sent to the central area (superficial dorsal horn) remote from injured (or infectious) sites are a key point to clarify the mechanisms of pathological pain.
The Open Neuroscience Journal
Copyright(c)2012 Hiura et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The Open Neuroscience Journal （2012） Vol.6 p.10-26
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