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Vol. 302, Issue 3, 839-845, September 2002
Department of Pharmacology and Toxicology (J.D.R., M.R.V.) and
Department of Anesthesia (M.R.V.), Indiana University School of
Medicine, Indianapolis, Indiana
Since the initial observations that stimulation of sensory neurons
produces vasodilation, plasma extravasation, and hypersensitivity, much
progress has been made in understanding the etiology of neurogenic inflammation. Studies have focused largely on the role of the neuropeptides, substance P and calcitonin gene-related peptide, which
are released in the periphery by activation of small diameter sensory
neurons. Recent work, however, has begun to emphasize the cellular
mechanisms involved in regulating the release of proinflammatory
substances from sensory neurons. In this perspective, discussion
centers on a number of inflammatory mediators that activate various
signal transduction pathways to augment excitability of and transmitter
release from sensory neurons. Emphasis is placed on those pathways
where multiple lines of evidence support their importance in initiating
neurogenic inflammation. Recent studies, however, support the notion
that there are novel compounds released during injury that can
stimulate or sensitize sensory neurons. Furthermore, only now are
intracellular signaling pathways that have been identified in other
cell systems being studied in sensory neurons to establish their role
in neurogenic inflammation. The challenge remains to ascertain the
critical transduction pathways that regulate transmitter release from
sensory neurons since this phenomenon triggers neurogenic inflammation.
In addition, the cellular mechanisms involved in alterations in
neuronal excitability during injury and the cellular pathways that
maintain the inflammatory response over time need to be determined.
With these advances, we will be able to develop therapeutic
interventions to minimize deleterious consequences of neurogenic inflammation.
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