It is well known that the efficacy of nociceptive transmission to dorsal horn neurons is enhanced following a strong painful stimulus (Simone et al. 1991; Brennan et al. 1996; Dougherty et al. 1998). This central sensitization leads to an increase in pain sensitivity in a large area around the conditioned skin site (neurogenic secondary hyperalgesia; LaMotte et al. 1991). Neuro-genic hyperalgesia also forms an integral part of some neuropathic pain states caused by dysfunction and/or lesion of the peripheral or central nervous system (Treede et al. 1992; Fields et al. 1998; Baumgartner et al. 2002). Brief incidents such as tissue or nerve injury may enhance pain perception for many hours or even months and years. It is thus tempting to propose that long-term potentiation (LTP) of synaptic strength in nociceptive pathways, at least in part, may underlie neurogenic hyperalgesia and chronic pain (Randic et al. 1993; Willis 1997; Miletic and Miletic 2000; Sandkuhler 2000; Woolf and Salter 2000). LTP represents an ubiquitous phenomenon of synaptic plasticity that has been extensively studied in the hippocampus and neocortex (Bliss and Collingridge 1993). An N-methyl D-aspartate (NMDA)-receptor dependent form of homosynaptic LTP of C-fiber input was recently found in nociceptive pathways of the spinal cord (Randic et al. 1993; Liu and Sandkuhler 1997; Svendsen et al. 1998).
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