Sensitization of Nociceptor-Specific Neurons by Capsaicin or Mustard Oil: Effect of GABA_A-Receptor Blockade

摘要

The sensory alterations that characterize postinjury hypersensitivity include a change in the modality of sensation evoked by low-threshold mecha-noreceptors (allodynia or "touch-evoked pain") and an increase in magnitude of the pain sensations evoked by mechanically sensitive nociceptors (hyperalgesia) (LaMotte et al. 1991). In areas of hyperalgesia remote from the injury site (secondary hyperalgesia), both of these changes are due to alterations in the central processing of sensory input and are induced and maintained by the arrival in the central nervous system of the afferent barrage evoked by the originating injury in peripheral nociceptors (LaMotte et al. 1991; Torebjork et al. 1992). Most models of secondary hyperalgesia revolve around the notion of "central sensitization," whereby injury discharges in nociceptive afferents cause spinal cord neurons to enhance their excitability and/or to increase their responsiveness to other peripheral drives (Woolf and Thompson 1991; Dubner and Ruda 1992). Increases in neuronal excitability after an injury have also been suggested to change the afferent properties of nociceptor-specific neurons (Simone et al. 1989; Woolf et al. 1994). In this case the process would include the expression of previously inhibited low-threshold inputs as part of a general mechanism of central sensitization.