PLASTICITY IN THE EXPRESSION OF BRADYKININ BINDING-SITES IN SENSORY NEURONS AFTER MECHANICAL NERVE INJURY

Citation
M. Petersen et al., PLASTICITY IN THE EXPRESSION OF BRADYKININ BINDING-SITES IN SENSORY NEURONS AFTER MECHANICAL NERVE INJURY, Neuroscience, 83(3), 1998, pp. 949-959
Citations number
56
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03064522
Volume
83
Issue
3
Year of publication
1998
Pages
949 - 959
Database
ISI
SICI code
0306-4522(1998)83:3<949:PITEOB>2.0.ZU;2-I
Abstract
The pro-inflammatory mediator bradykinin plays an important role in hy peralgesia during inflammatory conditions. Here, we used unilateral li gation of the sciatic nerve to investigate whether the expression of b radykinin binding sites in isolated rat dorsal root ganglion neurons i s changed following nerve injury. Under control conditions, the percen tage of neurons expressing bradykinin binding sites increased from 52% at day 0.8 in culture to 93% at day 1.8 and decreased to 67% at day 3 .8. Following nerve ligation either two or 10 days prior to the isolat ion of the somata, the percentage of neurons from ipsilateral ganglia that expressed bradykinin binding sites was already 87% and 86%, respe ctively, at day 0.8 in culture; this level was maintained at day 1.8 a nd decreased slightly at day 3.8. In control neurons, high densities o f bradykinin binding sites on individual neurons were observed no soon er than al day 1.8, but already at day 0.8 following nerve ligation, d ue to a ''de novo'' expression of B1 receptors and augmentation of B2 receptors. Neurons from the contralateral side responded similarly to ipsilateral neurons after a two day nerve ligation, however, after eit her a 10 day ligation or a sham operation neurons responded similarly to control neurons. These data are the first evidence that expression of B1 receptors is induced and expression of B2 receptors is enhanced in sensory neurons following nerve ligation. Under pathophysiological conditions, increased expression of subtypes of bradykinin receptors i n sensory neurons could contribute to chronic pain conditions. (C) 199 8 IBRO. Published by Elsevier Science Ltd.