ABSTRACT
Dorsal neurons are the origin of ascending pathways subserving ‘‘normal’’ pain and pathophysiological pain. Impulses in primary nociceptive afferents evoke brief high-intensity excitation followed by a lower-intensity, prolonged impulse discharge in dorsal horn nociceptive neurons (1). Furthermore, continuous input over C polymodal nociceptive afferents, but not other types of nociceptive afferents, additionally evokes temporal summation by activation of NMDAreceptors (2,3). These mechanisms are considered to provide part of the basis for centrally mediated hyperalgesia that occurs in persistent pain states, such as inflammatory pain that follows tissue injury. This hyperalgesia is a normal consequence of injury and subsides with healing of the injured tissue. Generally, similar central mechanisms of hyperalgesia also occur with nerve injury (4,5). Temporal summation of C-afferent-evoked responses of dorsal horn nocicep-
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tive neurons is likely to be mediated by the release of glutamate-aspartate and their activation of NMDA-receptors, leading to prolonged depolarizations (3,6).
