Synopses & Reviews
This volume is intended to bring together recent advances in the often separate fields of pain and neurogenic inflammation. To this end, eminent researchers from both domains have contributed in-depth discussion of the mechanisms underlying these processes. Individual chapters focus on important recent discoveries such as the cloning of the capsaicin receptor and the discovery of RAMP proteins for CGRP receptors. This book provides an integrated account of recent advances in the fields of pain and neurogenic inflammation. The volume is intended to bring together studies from eminent researchers in the often separate research fields of pain and inflammation. "Pain and Neurogenic Inflammation" is aimed primarily at postgraduate researchers as well as academic and industrial researchers in pain and inflammation but is also likely to be of interest to undergraduate students seeking a firm grounding in the mechanisms underlying these important clinical conditions.
Synopsis
Pain and inflammation are inextricably linked phenomena. The observation that chemical mediators with combined pro-inflammatory, algesic and/or hyperalgesic activity occur at the site of inflammation is fundamental not only to our present understanding of the inflammatory process but also to our attempts to devise clini- cally useful anti-inflammatory therapies. Over a hundred years ago it was recognised that primary sensory neurones play a crucially important "dual" role in inflammation. By affecting the transfer of infor- mation from peripheral nociceptors to the spinal cord, a subpopulation of sensory nerves {"pain fibres"} initiate algesia and hyperalgesia, whose sensations are then modified and fine-tuned in the central nervous system. Equally important is the release from the peripheral terminals of sensory neurones of neuropeptides, the acute effects of which are observed as changes in microvascular tone and perme- ability leading to neurogenic inflammation. Over the last decade it has become increasingly clear that this view of the func- tion of sensory nerves is somewhat over-simplified. For example, the mechanisms underlying hyperalgesia may, in certain circumstances, be mimicked in other condi- tions such as the hypersensivity associated with asthma. Furthermore, it has become increasingly evident that over a longer time period the release of neuropeptides from peripheral sensory nerve endings may also have modulating effects on inmune cells and that this may be relevant to chronic inflammatory disease and possibly also to inflammatory hyperalgesia.