Petersen M, Eckert A S, Segond von Banchet G, Heppelmann B, Klusch A, Kniffki K D
Physiologisches Institut, Universität Würzburg, Germany.
Neuroscience. 1998 Apr;83(3):949-59. doi: 10.1016/s0306-4522(97)00465-x.
The pro-inflammatory mediator bradykinin plays an important role in hyperalgesia during inflammatory conditions. Here, we used unilateral ligation of the sciatic nerve to investigate whether the expression of bradykinin binding sites in isolated rat dorsal root ganglion neurons is changed following nerve injury. Under control conditions, the percentage 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 isolation of the somata, the percentage of neurons from ipsilateral ganglia that expressed bradykinin binding sites was already 87% and 86%, respectively, at day 0.8 in culture; this level was maintained at day 1.8 and decreased slightly at day 3.8. In control neurons, high densities of bradykinin binding sites on individual neurons were observed no sooner than at day 1.8, but already at day 0.8 following nerve ligation, due 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 either 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 in sensory neurons could contribute to chronic pain conditions.
