| Abstract: | These experiments were designed to examine the relationship of glial hypertrophy to the time course of reactive synaptogenesis in the ventral posterolateral nucleus of the rat thalamus after lesions in the dorsal column nuclei. Because synaptogenesis is delayed for 30 days following lesions of the dorsal column nuclei, the initial hypertrophy of the glial processes in response to degeneration can be separated temporally from synaptogenesis. Glial hypertrophy was determined by measuring the relative area of neuropil occupied by profiles of glial processes on electron micrographs. The initial glial hypertrophy reached its peak 2 days after the lesion. However, at the time when synaptogenesis began, the area of neuropil occupied by glial processes was less than normal. When synaptogenesis was complete, the area of glial profiles also returned to normal. The role of glia in synaptogenesis was clearly different from its role in response to degeneration. In those systems such as the hippocampus, in which reactive synaptogenesis starts early in the recovery sequence, the relationship of glia to synaptogenesis may be masked by the glial response to degeneration. Hypertrophy of glial processes after lesions of other afferent pathways to the ventral posterolateral nucleus was compared to the hypertrophy following lesions of the dorsal column nuclei in order to see if there was a special relationship between glia and the lemniscal afferents to the ventral posterolateral nucleus. Lesions were placed in the medial lemniscus, somatosensory cortex, and the mesencephalon in addition to the dorsal column nuclei. The area of neuropil occupied by the glial processes expanded markedly after each of the lesions.(ABSTRACT TRUNCATED AT 250 WORDS) |
