Peripheral cell types contributing to the hyperalgesic action of nerve growth factor in inflammation

Clifford J. Woolf, Qing Ping Ma, Andrew Allchorne, Stephen Poole

Research output: Journal PublicationArticlepeer-review

208 Citations (Scopus)

Abstract

The contribution of nerve growth factor (NGF) to inflammatory hyperalgesia potentially could be mediated by any of the three peripheral cell types that express trkA, the high-affinity NGF receptor: inflammatory cells, sympathetic neurons, and primary sensory neurons. To investigate their relative involvement, the effects of sympathectomy and mast cell degranulation were examined on the local inflammation produced by an intraplantar injection of complete Freund's adjuvant in the adult rat. Sympathectomy, produced by neonatal guanethidine treatment, elevated basal NGF levels in the skin but did not attenuate a further increase in NGF during inflammation. Although the onset of inflammatory hyperalgesia was delayed in sympathectomized animals, peak sensitivity was not affected and was still NGF-dependent. In contrast, mast cell degranulation produced by several days of treatment with the cationic secretagogue compound 48/80, while also increasing basal NGF levels, prevented a further increase in NGF levels and attenuated hypersensitivity during inflammation. Neither manipulation modified the inflammatory upregulation of interleukin-1β. We conclude that sympathetic neurons contribute transiently to inflammatory hyperalgesia, but that mast cells and sensory neurons are important sites for the sustained action of NGF in producing increased sensitivity during inflammation.

Original languageEnglish
Pages (from-to)2716-2723
Number of pages8
JournalJournal of Neuroscience
Volume16
Issue number8
DOIs
Publication statusPublished - 15 Apr 1996
Externally publishedYes

Keywords

  • cytokines
  • inflammation
  • mast cells
  • neurotrophins
  • pain
  • sensory neurons
  • sympathetic nervous system

ASJC Scopus subject areas

  • Neuroscience (all)

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