Abstract
An important theme in contemporary research on the nervous system is plasticity. The activity of the nervous system is in part dependent on its past activity, which implies that neural responses can be modified by prior events. The mechanisms that are thought to underlie many forms of learning and memory, such as long-term potentiation (LTP) and long-term depression (LTD), typify this type of plasticity (Riedel, et al., 1996; Thompson, et al., 1997; Daniel, et al., 1998; however, cf. Hölscher, 1997). Plasticity occurs not only in the brain, but also in the spinal cord (Windhorst, 1996; Willis, 1997), as is emphasized in this symposium volume. For example, electrophysiological response changes similar to LTP and LTD have been described in the spinal cord, both in vivo and in vitro (Randic, et al., 1993; Svendsen, et al., 1997; Liu and Sandkuhler, 1997; Sandkuhler and Liu, 1998), and rewiring of the afferent connections to the dorsal horn has been demonstrated following peripheral nerve injury (Woolf, et al., 1992). Many workers in the field of pain research refer to the form of spinal cord plasticity that will be discussed in this chapter as central sensitization and suggest that this process underlies such abnormal pain states as secondary hyperalgesia and allodynia (Woolf, 1992; Willis, 1993; cf., Kenshalo, et al., 1982; Woolf, 1983; Yaksh, 1989; Dubner and Ruda, 1992).
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Willis, W.D. (2001). Mechanisms of Central Sensitization of Nociceptive Dorsal Horn Neurons. In: Patterson, M.M., Grau, J.W. (eds) Spinal Cord Plasticity. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1437-4_6
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