Perry, Gary W.

Astrogliosis may contribute to the pathogenesis of CNS dysfunction as in Alzheimer's Disease or Sudden Infant Death Syndrome (SIDS). Investigating astrocytic expression in the brain may provide valuable insights into and/or models of CNS disease or injury. This study was designed to test astrocyte expression and distribution in the mature rat and immature rat and cat brain utilizing different fixatives (aldehyde or ethanol), immunocytochemistry (glial fibrillary acidic protein, GFAP, or vimentin), and lesion conditions in the cortex, cerebellum, and brainstem. Findings include a paucity of GFAP positive astrocytes in most regions of the normal rat brainstem, evidence of astrogliosis in lesions, and the most intense, reactive astrocytes in the 7 day post-lesion condition. The results imply that the rat (brainstem) may make a suitable animal model for investigating the role of hypoxia and astrogliosis in neural trauma such as postulated in SIDS.

Mammals, unlike lower vertebrates, cannot normally regenerate injured central nervous system neurons. Although rat retinal ganglion cells (RGCs), following optic nerve crush, will undergo an initial period of sprouting, axon outgrowth is limited and subsequently aborted. This study examined how extensive the changes in fast transported proteins (FTPs) were during the early response to RGC damage and whether these changes were comparable to those known to occur in lower vertebrate RGCs. Changes in mRNA for several known proteins were also analyzed. It was found that, within 2 days, axotomized rat RGCs initiated a program of cell growth, involving the differential synthesis and transport of a broad range of FTPs. This response is very similar to that of lower vertebrates and indicates that rat RGCs are capable of initiating the metabolic responses necessary for regeneration to begin. This response, however, was not sustained beyond 5 days axotomy.