Magnocellular and parvocellular visual pathways are both affected in a macaque monkey model of glaucoma.
OBJECTIVE
Neurochemical changes in nerve cells were investigated in the lateral geniculate nucleus (LGN) and primary visual cortex of macaque monkeys with experimentally induced glaucoma.


METHODS
Glaucomatous damage was induced in one eye of experimental animals by elevation of intraocular pressure following laser burns to the trabecular meshwork. Staining for the metabolic marker cytochrome oxidase, as well as immunolabelling for the neuronal markers synaptophysin and neurofilament proteins, was conducted on sections of the LGN and primary visual cortex.


RESULTS
In the LGN, staining for cytochrome oxidase and immunolabelling for synaptophysin were reduced in the parvocellular and magnocellular layers that received input from the glaucomatous eye and neurofilament protein labelling was reduced in the parvocellular layers. Cytochrome oxidase staining demonstrated the presence of denervated ocular dominance columns in layer IVC of the primary visual cortex of experimental animals.


CONCLUSIONS
Pre- and post-synaptic neurochemical alterations in the magnocellular and parvocellular visual pathways of the brain are associated with experimentally induced glaucoma in macaque monkeys.
Vickers
J C
JC
Division of Pathology, Clinical School, University of Tasmania, Hobart, Australia. James.Vickers@path.utas.edu.au
Hof
P R
PR
Schumer
R A
RA
Wang
R F
RF
Podos
S M
SM
Morrison
J H
JH
D000818:Animals; D004195:Disease Models, Animal; D003576:Electron Transport Complex IV / Q000378:metabolism; D005829:Geniculate Bodies / Q000378:metabolism / Q000473:pathology*; D005901:Glaucoma / Q000473:pathology*; D008252:Macaca fascicularis; D016900:Neurofilament Proteins / Q000378:metabolism; D016708:Synaptophysin / Q000378:metabolism; D014793:Visual Cortex / Q000378:metabolism / Q000473:pathology*; D014795:Visual Pathways / Q000378:metabolism / Q000473:pathology*
D016900:Neurofilament Proteins; D016708:Synaptophysin; D003576:Electron Transport Complex IV