Alteration of descending modulation of nociception during the course of monoarthritis in the Rat

Citation
N. Danziger et al., Alteration of descending modulation of nociception during the course of monoarthritis in the Rat, J NEUROSC, 19(6), 1999, pp. 2394-2400
Citations number
41
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROSCIENCE
ISSN journal
02706474 → ACNP
Volume
19
Issue
6
Year of publication
1999
Pages
2394 - 2400
Database
ISI
SICI code
0270-6474(19990315)19:6<2394:AODMON>2.0.ZU;2-B
Abstract
Diffuse noxious inhibitory controls (DNIC), which involve supraspinal struc tures and modulate the transmission of nociceptive signals, were investigat ed at different stages during the development of adjuvant-induced monoarthr itis in the rat. After behavioral evaluation, recordings of trigeminal conv ergent neurons were performed in anesthetized animals with acute (24-48 hr) or chronic (3-4 weeks) monoarthritis of the ankle. Inhibitions of C-fiber- evoked neuronal responses during and after the application of noxious condi tioning stimuli to the ankle were measured to evaluate DNIC, The conditioni ng stimuli consisted of mechanical (maximal flexion and graded pressures) a nd graded thermal stimuli and were applied alternately to normal and arthri tic ankles. Behaviorally, the two groups of animals exhibited a similar inc reased sensitivity to mechanical stimuli applied to the arthritic joint (i. e., an increased ankle-bend score and a decreased vocalization threshold to pressure stimuli). However, they showed different electrophysiological pro files. In the animals with acute monoarthritis, the DNIC-induced inhibition s produced by mechanical or thermal stimulation of the arthritic joint were significantly increased at all intensities compared with the normal joint. In contrast, in the chronic stage of monoarthritis, the DNIG-induced inhib itions triggered by thermal or pressure stimuli were similar for both ankle s, except with the most intense mechanical stimuli. This discrepancy betwee n the behavioral and electrophysiological findings suggests that inputs act ivated during chronic monoarthritis may fail to recruit DNIC and may thus b e functionally different from those activated in the acute stage of inflamm ation.