Elevated pressure induced astrocyte damage in the optic nerve.

Astrocytes maintain an intimate relationship with central nervous system (CNS) neurons and play a crucial role in regulating their biochemical environment. A rise in neural tissue pressure in the CNS is known to lead to axonal degeneration however the response of astrocytes during the early stages of neural injury has not been studied in great detail. The optic nerve is a readily accessible model in which to study CNS axonal injury. Previous work from our laboratory has shown that an acute increase in intraocular pressure (IOP) results in axonal cytoskeleton changes and axonal transport retardation within the optic nerve head. Axonal changes occurred in a time-dependent manner with the magnitude of change being proportional to the duration of the IOP rise. Using glial fibrillary acidic protein (GFAP) as a marker of astrocytes we have now studied pressure induced changes in astrocyte structure in the optic nerve head. Using confocal microscopy we found that an increase in IOP resulted in morphological changes in the astrocytes that were consistent with previous reports of swelling. In addition there was also a decrease in GFAP intensity within these astrocytes. These changes occurred in a time-dependent manner with the chronology of change coinciding with that of axonal change. There was no evidence of apoptosis in regions where astrocyte changes were found. The present results provide evidence that in the early stages of neural tissue pressure rise there are both astrocyte and axonal injury.