The mechanisms underlying hyperalgesia have been intensively studied over the last decade using a variety of molecular, electrophysiological, and behavioral approaches. These experiments have led to the generalized scheme that persistent nociceptor input, as a result of tissue or nerve injury, removes a magnesium block on spinal NMDA receptors, allowing for calcium influx, translocation of protein kinase C, and activation of nitric oxide synthase and soluble guanylate cyclase as important central components of hyperalgesia. However, the hypothesis proposed here suggests a need for a critical reevaluation of the generalized applicability of these events to our understanding of the mechanisms of hyperalgesia. It is proposed that thermal and mechanical hyperalgesia rely on activation of two different intracellular cascades in the spinal cord. Thermal hyperalgesia relies principally on activation of spinal NMDA receptors, translocation of protein kinase C, and production of nitric oxide and cGMP. In contrast, mechanical hyperalgesia relies principally on coactivation of spinal AMPA and metabotropic glutamate receptors, activation of phospholipase A2 (PLA2), and production of cyclooxygenase products.
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