Constraints on Plasticity of Cerebellar Circuitry: Granule Cell-Purkinje Cell Synapses

The response of the nervous system to traumatic or attritional loss of specific cellular elements, as well as to failure of neurogenesis during development, has been addressed in a number of morphological (see reviews Cotman 1978, Lund 1978, Hillman and Chen 1984b) and physiological (Tsukahara 1981, Lynch et al. 1973) studies. Sprouting of remaining afferent axons from surrounding regions is regarded as the primary mechanism for restoring the number of connections (Liu and Chambers 1958, Westrum 1969, Raisman 1969, Raisman and Field 1973, Cotman and Nadler 1978, Lynch et al. 1975). This type of compensation has been reported in adult animals following partial destruction of afferents, developmental dysgenesis or early neuronal death. Some of these newly formed connections appear to be appropriate (Matthews et al. 1976b, Tsukahara 1981), while many others are aberrant (Westrum 1969, Llinas et al. 1973). The functional role of the latter afferents, if any, has not been determined. In general, the time course for this reorganization is prolonged (Matthews et al. 1976a) and apparently does not begin until 7–14 days after the injury.