Abstract
Diffuse Noxious Inhibitory Controls (DNIC) - which involve supraspinal structures and modulate the transmission of nociceptive signals - were investigated during the development of joint inflammation in rats with acute or chronic monoarthritis and in rats with chronic polyarthritis. During both acute monoarthritis and chronic polyarthritis, DNIC triggered by nociceptive stimulations of the inflamed joint(s) were clearly exacerbated, parallel with the increased sensitivity of inflamed joints to mechanical stimulations. In contrast, in the chronic stage of monoarthritis, DNIC triggered by thermal or pressure stimuli were almost similar for both normal and inflamed ankles. The discrepancy between behavioral and electrophysiological data during chronic monoarthritis indicates that inputs activated at this stage of the disease fail to recruit DNIC. This suggests that chronic inflammatory processes can induce a re-organisation of the spinal transmission of nociceptive signals, which modifies the recruitment of DNIC.
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