The specific neuronal environment in which astrocytes are located determines not only their morphology but also many of their metabolic properties. The influence of the neuronal environment on reactive astrocytosis is explored in a number of animal models, including trauma, demyelination, and toxic-metabolic injury. Several general findings emerged from these studies: astrocytic hypertrophy precedes, and is more pronounced than astrocyte hyperplasia; increases in glial fibrillary acidic protein (GFAP) immunoreactivity are not necessarily associated with increases in protein content; and astrocyte hypertrophy can occur in seemingly non-damaged brain at sites remote from the injury. Cerebral ischemia provides a unique opportunity to study neuronal-astrocytic interaction in brain injury since global ischemia produces neuronal necrosis in selectively vulnerable brain areas. Regional differences in the astrocytic response, therefore, are likely to be due to differences in their neuronal environment since astrocytes throughout the cerebral hemispheres experience a uniform ischemic insult. The chapter presents the studies designed to determine if the early proliferative response of astrocytes indicates increased metabolic activity and offers possible protection from ischemic-induced neuronal injury.
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