Loss of glutamine synthetase immunoreactivity from the retina in canine primary glaucoma.

Publications // Richard Dubielzig // May 01 2008

PubMed ID: 18435655

Author(s): Chen CT, Alyahya K, Gionfriddo JR, Dubielzig RR, Madl JE. Loss of glutamine synthetase immunoreactivity from the retina in canine primary glaucoma. Vet Ophthalmol. 2008 May-Jun;11(3):150-7. doi: 10.1111/j.1463-5224.2008.00581.x. PMID 18435655

Journal: Veterinary Ophthalmology, Volume 11, Issue 3,

PURPOSE 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.

ANIMALS 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.