Natcher Conference Center
National Institutes of Health
June 9–10, 2005
James L. Henry, Michael G. DeGroote Institute for Pain Research and Care, McMaster University, Hamilton, Ontario, Canada
The objective of this presentation is to present data that describe the effects of sensory inputs on spinal sensory mechanisms under normal conditions. Importantly, these effects are altered in animal models of chronic pain. Data will be presented that indicate that sensory inputs, particularly nociceptive inputs, are exaggerated in these models. Further investigation indicates that the explosive nature of nociceptive inputs in these models is partially due to increased excitability to excitatory chemical mediators of synaptic transmission. In addition, however, there is also a change in effects of inhibitory transmitters, whereby these now express not only inhibitory effects, but also excitatory effects. It is concluded that under pathological conditions, the neural substrate of pain transmission and integration in the spinal cord undergoes a loss of the normal buffering capacity that governs the flow of sensory information. This loss of buffering capacity could account for at least some types of chronic pain, but would also suggest that extrasegmental sensory inputs could have greater inhibitory effects under conditions of pathology, and this warrants further investigation.
(Supported by the Canadian Institutes for Health Research, the University of Western Ontario and McMaster University)