Altered nociceptive C fibre input to primary somatosensory cortex in an animal model of hyperalgesia.

Evaluating potentially analgesic effects of drugs and various treatments is critically dependent on valid animal models of pain. Since primary somatosensory (SI) cortex is likely to play an important role in processing sensory aspects of pain, we here assess whether monitoring SI cortex nociceptive C fibre evoked potentials can provide useful information about central changes related to hyperalgesia in rats. Recordings of tactile and CO(2)-laser C fibre evoked potentials (LCEPs) in forelimb and hind limb SI cortex were made 20-24h after UV-B irradiation of the heel at a dose that produced behavioural signs of hyperalgesia. LCEPs from irradiated skin increased significantly in duration but showed no significant change in magnitude, measured as area under curve (AUC). By contrast, LCEPs in hind limb SI cortex from skin sites nearby the irradiated skin showed no increase in duration or onset latency but increased significantly in magnitude after UV-B irradiation. The LCEPs in forelimb or hind limb SI cortex elicited from forelimb skin did not change in magnitude, but were significantly delayed in hind limb SI cortex. Tramadol, a centrally acting analgesic known to reduce hyperalgesia, induced changes that counteracted the changes produced by UV-B irradiation on transmission to SI cortex from the hind paw, but had no significant effect on time course of LCEPs from forelimb skin. Tactile evoked potentials were not affected by UV-B irradiation or tramadol. We conclude that altered sensory processing related to hyperalgesia is reflected in altered LCEPs in SI cortex.