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Makoto Aihara, James D. Lindsey, Robert N. Weinreb; Effect on Diurnal Intraocular Pressure Variation of Eliminating the α-2 Adrenergic Receptor Subtypes in the Mouse. Invest. Ophthalmol. Vis. Sci. 2008;49(3):929-933. doi: https://doi.org/10.1167/iovs.07-0386.
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purpose. To investigate the effect on circadian variation of intraocular pressure (IOP) of eliminating the α2A-, α2B-, or the α2C-adrenergic receptor subtypes in the mouse.
methods. A microneedle method was used to measure IOP in knockout mice lacking the α2A-, α2B-, or the α2C-receptor (α2A-R−/−, α2B-R−/−, α2C-R−/−), in wild-type mice of the α2B knockout strain (α2B-R+/+), and in the background strain mice, C57BL/6. All mice were maintained in a 12-hour light–dark cycle commencing at 0600 hours. IOP was measured at 0900 and 2100 hours in the five groups: C57BL/6 (n = 8), α2A-R−/− (n = 10), α2B-R−/− (n = 8), α2B-R+/+ (n = 8), and α2C-R−/− (n = 10). In parallel experiments, eyes from the α2A-R−/−, α2B-R−/−, α2C-R−/−, and C57BL/6 mice were embedded in epoxy resin, and semithin sections were stained with toluidine blue.
results. IOP at 0900 hours in B6, α2A-R−/−, α2B-R−/−, α2B-R+/+, and α2C-R−/− mice was 17.1 ± 1.8, 17.7 ± 1.4, 17.1 ± 2.1, 17.6 ± 1.3, and 17.3 ± 0.9 mm Hg, respectively (mean ± SD). IOP at 2100 hours in the same eyes was 19.6 ± 1.9, 19.2 ± 2.2, 20.5 ± 1.5, 19.7 ± 0.8, and 21.3 ± 2.7 mm Hg, respectively. There was no significant difference among these genotypes in IOP measured at either time point (P > 0.05, ANOVA). Within each genotype, IOP at 2100 hours was significantly higher than IOP at 0900 hours (C57BL/6, α2B-R−/−, α2B-R+/+, and α2C-R−/−: P < 0.01; α2A-R−/−: P < 0.05, paired t-test). Differences in the diurnal IOP change among the different genotypes were insignificant (P > 0.05, ANOVA). Histopathologic assessment found minimal differences in the structural organization of the anterior segment among the α2A-R−/−, α2B-R−/−,α2C-R−/−, or C57BL/6 mice.
conclusions. These results indicate that IOP magnitude and circadian variation are minimally altered by the absence of the α2A-, α2B-, or α2C-receptor subtypes in transgenic mice.
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