Expression of glial fibrillary acidic protein and glutamine synthetase by Müller cells after optic nerve damage and intravitreal application of brain-derived neurotrophic factor.
Müller glia play an important role in maintaining retinal homeostasis, and brain-derived neurotrophic factor (BDNF) has proven to be an effective retinal ganglion cell (RGC) neuroprotectant following optic nerve injury. The goal of these studies was to investigate the relation between optic nerve injury and Müller cell activation, and to determine the extent to which BDNF affects the injury response of Müller cells. Using immunocytochemistry and Western blot analysis, temporal changes in the expression of glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS) were examined in rats after optic nerve crush alone, or in conjunction with an intravitreal injection of BDNF (5 microg). GFAP protein levels were normal at 1 day post-crush, but increased approximately 9-fold by day 3 and remained elevated over the 2-week period studied. Müller cell GS expression remained stable after optic nerve crush, but the protein showed a transient shift in its cellular distribution; during the initial 24-h period post-crush the GS protein appeared to translocate from the cell body to the inner and outer glial processes, and particularly to the basal endfeet located in the ganglion cell layer. BDNF alone, or in combination with optic nerve crush, did not have a significant effect on the expression of either GFAP or GS compared with the normal retina, or after optic nerve crush alone, respectively. The data indicate that although BDNF is a potent neuroprotectant in the vertebrate retina, it does not appear to have a significant influence on Müller cell expression of either GS or GFAP in response to optic nerve injury.
Chen
Hao
H
Department of Pharmacology, University of Tennessee at Memphis, USA.
Weber
Arthur J
AJ
D000818:Animals; D015153:Blotting, Western; D019208:Brain-Derived Neurotrophic Factor / Q000494:pharmacology*; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis / Q000096:biosynthesis*; D005974:Glutamate-Ammonia Ligase / Q000032:analysis / Q000096:biosynthesis*; D007150:Immunohistochemistry; D009409:Nerve Crush; D009457:Neuroglia / Q000737:chemistry / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000494:pharmacology; D020221:Optic Nerve Injuries / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012162:Retinal Degeneration / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D012165:Retinal Ganglion Cells / Q000473:pathology
D019208:Brain-Derived Neurotrophic Factor; D005904:Glial Fibrillary Acidic Protein; D018696:Neuroprotective Agents; D005974:Glutamate-Ammonia Ligase