Extensive cortical reorganization following sciatic nerve injury in adult rats versus restricted reorganization after neonatal injury: implications for spatial and temporal limits on somatosensory plasticity.

Expansion of the saphenous representation in rat S-I cortex following sciatic nerve injury, examined at different times after injury and following injury at different developmental stages, has contributed to the beginnings of a comprehensive view of spatial and temporal patterns of cortical reorganization. In the first few days or weeks after deafferentation in adult animals, cortical reorganization may be spatially constrained to convergence zones between central representations of peripheral nerves (Wall and Cusick, 1984; Garraghty et al., 1994a; Schroeder et al., 1995). The apparent steady state of the rat hindpaw system up to 5-6 months after sciatic nerve injury contrasts with the additional, nearly complete reorganization shown at times longer than 7-8 months. The late reorganization supports the concept that reorganized cortical maps can continue to be altered throughout life. The prolonged time course of change in the rat hindpaw system suggests that studies of "chronic" nerve injuries need to carefully define the reorganizational state of the system at the time intervals studied. For humans with peripheral nerve or amputation injuries, the results imply that the short term postinjury status can be further altered at longer times, perhaps decades later. To characterize the neurochemical consequences or mechanisms of cortical reorganization, it is necessary to consider possible differences between early versus late changes. Time dependent changes in neurotransmitters and their receptors have been described following peripheral injury (e.g., Avendaño et al., 1995). In addition, both early and late mechanisms or consequences of reorganization may differ spatially. In the example of changes in rat hindpaw cortex after sciatic nerve transection, neurochemical changes in "expansion" cortex may differ quantitatively or qualitatively from changes in the deafferented "sciatic dominant" zone. To accurately define neurochemical changes, it may thus be necessary to characterize sample zones as having intact or reorganized inputs, or as deprived of inputs. The studies of cortical reorganization following neonatal sciatic nerve injury underscore the importance of developmental age at time of injury. Most studies of critical periods in the central nervous system have emphasized greater plasticity in developing as opposed to adult animals. Early lesions or deprivation, however, not only result in connectional alterations, but can produce dramatically more atrophy or cell loss (e.g., see Cunningham, 1982; Waite, 1984; Himes and Tessler, 1989). A number of authors have commented on the seeming paradox of greater transneuronal and retrograde cell death, yet greater neuronal plasticity, in infant animals. How developmental stage influences plastic responses to peripheral injury in the somatosensory system is not completely understood. Early peripheral lesions may deprive central neurons of necessary trophic factors, accentuate naturally occurring central cell death, and thereby result in smaller central representations. Or, smaller central representations may be produced by competitive interactions of deprived with adjacent intact pathways. In addition, throughout all stages of development, the capacity for reorganization may be spatially limited and depend on the size or pattern of the peripheral injury.