Neurotrophins: peripherally and centrally acting modulators of tactile stimulus-induced inflammatory pain hypersensitivity

Détails

ID Serval
serval:BIB_427E4414A679
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Neurotrophins: peripherally and centrally acting modulators of tactile stimulus-induced inflammatory pain hypersensitivity
Périodique
Proceedings of the National Academy of Sciences of the United States of America
Auteur(s)
Mannion  R. J., Costigan  M., Decosterd  I., Amaya  F., Ma  Q. P., Holstege  J. C., Ji  R. R., Acheson  A., Lindsay  R. M., Wilkinson  G. A., Woolf  C. J.
ISSN
0027-8424 (Print)
Statut éditorial
Publié
Date de publication
08/1999
Volume
96
Numéro
16
Pages
9385-90
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Aug 3
Résumé
Brain-derived neurotrophic factor (BDNF) is expressed in nociceptive sensory neurons and transported anterogradely to the dorsal horn of the spinal cord where it is located in dense core vesicles in C-fiber terminals. Peripheral inflammation substantially up-regulates BDNF mRNA and protein in the dorsal root ganglion (DRG) in a nerve growth factor-dependent fashion and results in novel expression of BDNF by DRG neurons with myelinated axons. C-fiber electrical activity also increases BDNF expression in the DRG, and both inflammation and activity increase full-length TrkB receptor levels in the dorsal horn. Sequestration of endogenous BDNF/neurotrophin 4 by intraspinal TrkB-Fc fusion protein administration does not, in noninflamed animals, change basal pain sensitivity nor the mechanical hypersensitivity induced by peripheral capsaicin administration, a measure of C fiber-mediated central sensitization. TrkB-Fc administration also does not modify basal inflammatory pain hypersensitivity, but does block the progressive hypersensitivity elicited by low-intensity tactile stimulation of inflamed tissue. BDNF, by virtue of its nerve growth factor regulation in sensory neurons including novel expression in A fibers, has a role as a central modulator of tactile stimulus-induced inflammatory pain hypersensitivity.
Mots-clé
Animals Axonal Transport Brain-Derived Neurotrophic Factor/*genetics Decerebrate State Electric Stimulation Ganglia, Spinal/physiology/physiopathology *Gene Expression Regulation In Situ Hybridization Inflammation/*physiopathology Male Motor Neurons/physiology Nerve Fibers/physiology Neurons, Afferent/*physiology Pain/*physiopathology Physical Stimulation Protein Biosynthesis RNA, Messenger/genetics Rats Rats, Sprague-Dawley Receptor Protein-Tyrosine Kinases/genetics/physiology Receptor, Ciliary Neurotrophic Factor Receptors, Nerve Growth Factor/genetics/physiology Recombinant Fusion Proteins/pharmacology Spinal Cord/*physiology/physiopathology Time Factors Touch Transcription, Genetic
Pubmed
Web of science
Open Access
Oui
Création de la notice
28/01/2008 11:45
Dernière modification de la notice
08/05/2019 17:44
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