Rj. Mannion et al., Neurotrophins: Peripherally and centrally acting modulators of tactile stimulus-induced inflammatory pain hypersensitivity, P NAS US, 96(16), 1999, pp. 9385-9390
Citations number
46
Categorie Soggetti
Multidisciplinary
Journal title
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Brain-derived neurotrophic factor (BDNF) is expressed in nociceptive sensor
y neurons and transported anterogradely to the dorsal horn of the spinal co
rd where it is located in dense core,vesicles in C-fiber terminals. Periphe
ral inflammation substantially up-regulates BDNF mRNA and protein in the do
rsal root ganglion (DRG) in a nerve growth factor-dependent fashion and res
ults in novel expression of BDNF by DRG neurons with myelinated axons. C-fi
ber 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 intraspina
l TrkB-Fc fusion protein administration does not, in noninflamed animals, c
hange 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 inflammat
ory 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 n
ovel expression in A fibers, has a role as a central modulator of tactile s
timulus-induced inflammatory pain hypersensitivity.