Does sensitization of responses to excitatory amino acids underlie the psychophysical reports of two modalities of increased sensitivity in zones of secondary hyperalgesia?

Abstract

S ensitization, or enhancement of the responses of dorsal horn neurons to afferent stimuli, is emerging as one mechanism for the production of secondary hyperalgesia. The focus article by Dr. Wilcox does a wonderful job of highlighting the complexity of the chemical bases for sensitization of dorsal horn neurons. In general, sensitization of the responses of sensory neurons in the spinal cord appears to fall into two broad classes: that produced by loss of normal inhibitory processes, disinhibition,~5,2s; and that produced by an increase in the efficacy of excitatory pathways, facil i tation? ,3, 6-11,14.21,24 Both of these processes, which presumably result in an increase in the activity of projection neurons, potentially involve multiple mechanisms. We would like to raise a few additional points concerning enhancement of excitatory pathways in the dorsal horn after peripheral injury or inflammation. Dr. Wilcox reviews many studies in his focus article that show that sensitization of neurons in the dorsal horn appears to require the actions of excitatory amino acids, primarily glutamate, but also aspartate, and the neurokinin peptide, substance P (SP). The excitatory amino acids and the neuropeptides seem