Neurochemical correlates of cortical plasticity after unilateral elevated intraocular pressure in a primate model of glaucoma.
OBJECTIVE
To examine the time course of changes in the expression patterns of several synaptic plasticity markers in the primary visual cortex after unilateral elevated intraocular pressure (IOP) in a primate model of glaucoma.


METHODS
A monkey model of experimental glaucoma was combined with immunohistochemical and histochemical methods to assess changes in expression patterns and metabolic activity of cortical neurons in V1.


RESULTS
Experimental unilateral glaucoma altered the spatial and temporal distribution of several neurochemicals associated with cortical plasticity in V1 of the primate. Within-animal comparisons of immunohistochemical studies revealed that GABAa receptor protein and GAP-43 were significantly lower in glaucomatous versus normal eye bands after 2, 4, and 7 months of elevated IOP. SYN immunoreactivity was also lower in the glaucomatous versus the normal eye bands but only at 4 months of elevated IOP. CAMKIIalpha immunoreactivity levels were higher in the glaucomatous versus the normal eye bands. Between-animal comparisons revealed that the levels of GAP-43 and SYN were upregulated, whereas levels of GABAa receptor protein were downregulated, in glaucomatous eyes when compared with levels in the visual cortex of normal animals.


CONCLUSIONS
Unilateral elevation of IOP affects both the metabolic activity of cortical neurons and the expressed levels of GAP-43, SYN, GABAa receptor protein, and CAMKIIalpha, as measured immunohistochemically in the primary visual cortex of adult monkeys. Because these neurochemicals are thought to be necessary for synaptic plasticity, their redistribution may support functional recovery of cortical neurons after damage to retinal ganglion cells induced by elevated IOP.
Lam
Dawn Y
DY
Department of Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
Kaufman
Paul L
PL
Gabelt
B'Ann T
BT
To
Eleanor C
EC
Matsubara
Joanne A
JA
D000818:Animals; D015415:Biomarkers / Q000032:analysis*; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism; D004195:Disease Models, Animal; D003576:Electron Transport Complex IV / Q000378:metabolism; D005260:Female; D005625:Frontal Lobe / Q000502:physiology; D019922:GAP-43 Protein / Q000378:metabolism; D005901:Glaucoma / Q000378:metabolism*; D007124:Immunoenzyme Techniques; D007429:Intraocular Pressure; D008252:Macaca fascicularis; D008253:Macaca mulatta; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000502:physiology*; D009798:Ocular Hypertension / Q000378:metabolism; D011963:Receptors, GABA-A / Q000378:metabolism; D016708:Synaptophysin / Q000378:metabolism; D013997:Time Factors; D015854:Up-Regulation; D014793:Visual Cortex / Q000502:physiology*
D015415:Biomarkers; D019922:GAP-43 Protein; D009419:Nerve Tissue Proteins; D011963:Receptors, GABA-A; D016708:Synaptophysin; D003576:Electron Transport Complex IV; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases