Inflammatory pain plasticity

Woolf CJ, Costigan M (1999) Transcriptional and posttranslational plasticity and the generation of inflammatory pain. Proc Natl Acad Sci USA 96 7723-7730 Wu D, Doods H, Arndt K, Schindler M (2002) Development and potential of non-peptide antagonists for calcitonin-gene-related peptide (CGRP) receptors evidence for CGRP receptor... 

Woolf CJ, Costigan M (1999) Transcriptional and posttranslational plasticity and the generation of inflammatory pain. Proc Natl Acad Sci USA 96 7723-7730. 

The mechanisms of pain and the ability to control pain may vary in different pain states. This is of particular importance in consideration of a rational basis for the treatment of both inflammatory and neuropathic pain where the damage to tissue and nerve leads to alterations in both the peripheral and central mechanisms of pain signalling. In respect of existing drug therapies, this plasticity, the ability of the system to change in the face of a particular pain syndrome, explains the effectiveness of NSAIDs in inflammatory conditions and yet is also responsible for some of the limitations in the effectiveness of opioids in neuropathic pain. 

Glial cells play an important role in the control of pain in fact, it is known that neuronal plasticity is triggered by many inflammatory mediators and these are mainly produced by glial cells in the central nervous system. Indeed, in the past... 

It is well known that peripheral nerve injury or inflammatory states induce neuronal plastic changes in the spinal cord. These plasticity changes are responsible for the production and maintainance of persistent pain states, allodynia, and hyperalgesia occurring in both affected areas (primary sensitization) and non-affected areas (secondary sensitization). In inflammatory states, the NC OF FQ system is up-regulated [4]. This is reflected by increased NC levels and binding in the spinal cord, specifically at the level of the dorsal 51Q horns - mainly limited to the superficial laminae I and II. Inflammatory states also induce the expression of... 

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