Altered nociceptive C fibre input to primary somatosensory cortex in an animal model of hyperalgesia
Article first published online: 13 JAN 2012
2011 European Federation of Chapters of the International Association for the Study of Pain
European Journal of Pain
Volume 15, Issue 4, pages 368–375, April 2011
How to Cite
Jensenl, T., Granmo, M. and Schouenborg, J. (2011), Altered nociceptive C fibre input to primary somatosensory cortex in an animal model of hyperalgesia. European Journal of Pain, 15: 368–375. doi: 10.1016/j.ejpain.2010.09.009
- Issue published online: 13 JAN 2012
- Article first published online: 13 JAN 2012
- Received 14 June 2010; received in revised from 15 September 2010; accepted 20 September 2010
- Animal pain model
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 CO2-laser C fibre evoked potentials (LCEPs) in forelimb and hind limb SI cortex were made 20–24 h 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.