The role of MAP kinase cascades in cell signaling,neural plasticity and pain facilitation
- VernacularTitle:MAP激酶在细胞内信号传递,神经可塑性及痛觉易化中的作用
- Author:
Ji RU-RONG
1
;
ZHANG YU-QIU
Author Information
1. Pain Research Center
- Keywords:
pathological pain;
pain hypersensitivity;
ERK/MAPK;
neural plasticity
- From:
Neuroscience Bulletin
2005;21(1):3-9
- CountryChina
- Language:Chinese
-
Abstract:
Pathological pain, normally referring to tissue injury-induced inflammatory pain and nerve injury-induced neuropathic pain, is an expression of neural plasticity. Injuries and intense noxious stimuli result in pain hypersensitivity,which is contributed by peripheral sensitization (increased sensitivity of primary sensory nociceptors) and central sensitization (increased sensitivity of spinal dorsal horn and other CNS neurons). Activation of several protein kinases causes both forms of sensitization via posttranslational regulation, such as phosphorylation of key membrane receptors and channels. In particular, activation of multiple signal cascades converge on the activation of MAPK (mitogen-activated protein kinase).Activation of MAPK family members of ERK and p38 by nociceptive activity, growth factors, and inflammatory mediators in primary sensory and secondary order neurons, not only results in posttranslational modification, but also increases the expression of numerous genes via transcriptional and non-transcriptional regulation. Eventually this activation contributes to the development and maintenance of heightened pain sensitivity following injury.
