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Research ArticlePERSPECTIVES IN PHARMACOLOGY

Cellular Mechanisms of Neurogenic Inflammation

Jennelle Durnett Richardson and Michael R. Vasko
Journal of Pharmacology and Experimental Therapeutics September 2002, 302 (3) 839-845; DOI: https://doi.org/10.1124/jpet.102.032797
Jennelle Durnett Richardson
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Michael R. Vasko
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Abstract

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.

Footnotes

  • This work supported by National Institutes of Health Grant RO1-NS34159 to M.R.V.

  • DOI: 10.1124/jpet.102.032797

  • Abbreviations:
    SP
    substance P
    CGRP
    calcitonin gene-related peptide
    DRG
    dorsal root ganglion
    PKC
    protein kinase C
    PLC
    phospholipase C
    IP3
    inositol 1,4,5-trisphosphate
    DAG
    1,2-diacylglycerol
    PAR
    proteinase-activated receptor
    CaM kinase
    calcium/calmodulin-dependent protein kinase
    PGE2
    prostaglandin E2
    PGI2
    prostaglandin I2
    TNFα
    tumor necrosis factor-α
    COX2
    cyclooxygenase 2
    5-HT
    5-hydroxytryptamine
    NO
    nitric oxide
    MAP kinase
    mitogen-activated protein kinase
    • Received February 25, 2002.
    • Accepted May 9, 2002.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 302 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 302, Issue 3
1 Sep 2002
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Research ArticlePERSPECTIVES IN PHARMACOLOGY

Cellular Mechanisms of Neurogenic Inflammation

Jennelle Durnett Richardson and Michael R. Vasko
Journal of Pharmacology and Experimental Therapeutics September 1, 2002, 302 (3) 839-845; DOI: https://doi.org/10.1124/jpet.102.032797

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Research ArticlePERSPECTIVES IN PHARMACOLOGY

Cellular Mechanisms of Neurogenic Inflammation

Jennelle Durnett Richardson and Michael R. Vasko
Journal of Pharmacology and Experimental Therapeutics September 1, 2002, 302 (3) 839-845; DOI: https://doi.org/10.1124/jpet.102.032797
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  • Article
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    • Neurogenic Inflammation
    • Agents and Mechanisms That Increase Transmitter Release Directly
    • Agents That Alter Sensitivity of Sensory Neurons
    • Cellular Mechanisms Mediating Sensitization of Sensory Neurons
    • Unresolved Issues and Future Directions
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