ABSTRACT
The term neuroplasticity is generally used to refer to the capacity of the nervous system to modify its organization. However, such changes may occur as a consequence of many different events, including the normal development and maturation of the organism, the acquisition of new skills (“learning”) in immature and mature organisms, following damage to the nervous system and as a result of sensory deprivation. Studies to date of the molecular and cellular events underlying neural plasticity in such different conditions have revealed a limited set of mechanisms available to induce changes in the organization of the neural networks of the brain. Such reports raise the hypothesis and the hope that the diverse phenomena referred to as neuroplasticity will be elucidated in the not-too-distant future. However, while there is evidence to suggest that there may be considerable overlap in the mechanisms that mediate developmental and adult neuroplasticity following abnormal experience or damage, we think it is important at the present time to distinguish between them. Even if some of the mechanisms are similar or even identical, the fact that these mechanisms operate on nervous systems that are structurally and physiologically different is likely to result in quantitative and/or qualitative differences in neuroplasticity in immature and mature organisms. For example, in the immature human brain, the number of synapses is 50% greater than in the adult brain (Huttenlocher, 1994; Figure 18.1). This redundant connectivity exists at different times in different brain regions and almost certainly constrains the nature and extent of modification that can occur at different ages. Similarly, the metabolic profiles of different brain structures change dramatically over the first two decades of life. It is likely that these variables give rise to different profiles of plasticity at different times and for functions linked to different structures. Indeed, neurophysiological studies of animals indicate considerable variability and specificity in the types of plastic changes that can occur from system to system. For example, while visual experience affects the formation of ocular dominance columns only during a very limited time period in development, the remapping of the representation of the visual fields following retinal lesions extends into adulthood (Kaas et al., 1990). Similarly, while the representation of the whiskers (barrell formation) within the somatosensory cortex is modifiable only during a limited time period, remapping of the cortical representation of the digits following amputation or training can occur throughout the life of the animal (Merzenich & Jenkins, 1993).
