title: Loss of glutamine synthetase immunoreactivity from the retina in canine primary glaucoma.
abstract: OBJECTIVE
  Changes in retinal glutamate distribution occur in primary glaucoma (PG) in dogs. Although the redistribution resembles that induced by ischemia, decreases in glutamine synthetase (GS) activity may also induce a similar glutamate redistribution. We examined the distribution of GS, glutamate, and glial fibrillary acidic protein (GFAP), a marker for reactive glia, in PG retinas by immunohistochemistry to determine whether decreases in GS and formation of reactive glia are associated with glutamate redistribution and neuronal damage.
  
  
  METHODS
  Sections from 14 control dog eyes and 22 eyes from dogs with PG.
  
  
  METHODS
  Sections from 14 control and 22 glaucomatous globes were immunohistochemically stained for GS, glial fibrillary acidic protein or glutamate.
  
  
  RESULTS
  In semiquantitative immunogold studies, decreases in GS staining density were strongly correlated with glutamate redistribution and neuronal damage. In less quantitative immunoperoxidase staining of acute (< or = 5 days after clinical signs) and chronic PG retinas, GS immunoreactivity was decreased in focal regions of some acute PG retinas, and there were widespread decreases in chronic PG retinas. GFAP immunoreactivity was increased in Müller cells primarily in severely damaged regions of chronic PG retinas.
  
  
  CONCLUSIONS
  Decreases in GS immunoreactivity were associated with glutamate redistribution. These decreases in GS occurred even in mildly damaged regions of retina before retinal thinning. Reactive Müller cells were seen primarily in chronic PG in severely damaged regions. Decreases in GS may potentiate ischemia-induced early glutamate redistribution and neuronal damage in canine PG.
authors.affiliation: Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado 80523, USA.
authors.forename: Chu-Te
authors.initials: CT
authors.lastname: Chen
authors.forename: Khaleel
authors.initials: K
authors.lastname: Alyahya
authors.forename: Juliet R
authors.initials: JR
authors.lastname: Gionfriddo
authors.forename: Richard R
authors.initials: RR
authors.lastname: Dubielzig
authors.forename: James E
authors.initials: JE
authors.lastname: Madl
mesh_terms: D000818:Animals; D016022:Case-Control Studies; D004283:Dog Diseases / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology; D004285:Dogs; D005901:Glaucoma / Q000201:enzymology / Q000378:metabolism / Q000473:pathology / Q000662:veterinary*; D005904:Glial Fibrillary Acidic Protein / Q000276:immunology / Q000378:metabolism; D005974:Glutamate-Ammonia Ligase / Q000276:immunology / Q000378:metabolism*; D018698:Glutamic Acid / Q000276:immunology / Q000378:metabolism; D007150:Immunohistochemistry / Q000662:veterinary; D012160:Retina / Q000201:enzymology* / Q000473:pathology
chemical_list: D005904:Glial Fibrillary Acidic Protein; D018698:Glutamic Acid; D005974:Glutamate-Ammonia Ligase