TY - JOUR
T1 - Neuropathic pain and spinal microglia
T2 - A big problem from molecules in 'small' glia
AU - Tsuda, Makoto
AU - Inoue, Kazuhide
AU - Salter, Michael W.
N1 - Funding Information:
We thank J. Hicks for corrections of the manuscript. This work was supported partly by a grant from the Organization for Pharmaceutical Safety and Research, by a grant-in-aid for the scientific research from the Ministry of Education, Science, Sports, and Culture of Japan, by a grant from the Japan Health Sciences Foundation and by a grant from the Japan Society for the Promotion of Science (JSPS) and Canadian Institutes of Health Research (CIHR) Joint Health Research Program Project. M.T. is a Research Scientist of National Institute of Health Sciences and was a CIHR Strategic Training Fellow. M.W.S. is a Canada Research Chair (Tier I) in Neuroplasticity and Pain.
PY - 2005/2
Y1 - 2005/2
N2 - Neuropathic pain is a common and severely disabling state that affects millions of people worldwide. Such pain can be experienced after nerve injury or as part of diseases that affect peripheral nerve function, such as diabetes and AIDS; it can also be a component of pain in other conditions, such as cancer. Following peripheral nerve injury, microglia in the spinal cord become activated. Recent evidence indicates that activated microglia are key cellular intermediaries in the pathogenesis of nerve injury-induced pain hypersensitivity because P2X4 purinoceptors and p38 mitogen-activated protein kinase, which are present in activated microglia, are required molecular mediators. It is important to establish how these molecules are activated in spinal microglia following nerve injury and how they cause signaling to neurons in the dorsal horn pain transmission network. Answers to these questions could lead to new strategies that assist in the diagnosis and management of neuropathic pain - strategies not previously anticipated by a neuron-centric view of pain plasticity in the dorsal horn.
AB - Neuropathic pain is a common and severely disabling state that affects millions of people worldwide. Such pain can be experienced after nerve injury or as part of diseases that affect peripheral nerve function, such as diabetes and AIDS; it can also be a component of pain in other conditions, such as cancer. Following peripheral nerve injury, microglia in the spinal cord become activated. Recent evidence indicates that activated microglia are key cellular intermediaries in the pathogenesis of nerve injury-induced pain hypersensitivity because P2X4 purinoceptors and p38 mitogen-activated protein kinase, which are present in activated microglia, are required molecular mediators. It is important to establish how these molecules are activated in spinal microglia following nerve injury and how they cause signaling to neurons in the dorsal horn pain transmission network. Answers to these questions could lead to new strategies that assist in the diagnosis and management of neuropathic pain - strategies not previously anticipated by a neuron-centric view of pain plasticity in the dorsal horn.
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U2 - 10.1016/j.tins.2004.12.002
DO - 10.1016/j.tins.2004.12.002
M3 - Review article
C2 - 15667933
AN - SCOPUS:13144276331
SN - 0378-5912
VL - 28
SP - 101
EP - 107
JO - Trends in Neurosciences
JF - Trends in Neurosciences
IS - 2
ER -
