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Marcin L. Kordasz, Caroline Manicam, Andreas Steege, Evgeny Goloborodko, Claudia Amato, Panagiotis Laspas, Christoph Brochhausen, Norbert Pfeiffer, Adrian Gericke; Role of α1-Adrenoceptor Subtypes in Pupil Dilation Studied With Gene-Targeted Mice. Invest. Ophthalmol. Vis. Sci. 2014;55(12):8295-8301. doi: 10.1167/iovs.14-15706.
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The α1A-adrenoceptor (α1A-AR) subtype was suggested to mediate contraction and trophic effects in the iris dilator muscle, and thus its pharmacological blockade may be involved in intraoperative floppy iris syndrome. We tested the hypothesis that the α1A-AR mediates pupil dilation and trophic effects in the mouse iris.
The α1-AR subtype mRNA expression was quantified in iris tissue by real-time PCR. To assess the role of individual α1-ARs for mediating pupil dilation, the α1-AR agonist phenylephrine was topically applied to the ocular surface of mice deficient in one of the three α1-AR subtypes (α1A-AR−/−, α1B-AR−/−, α1D-AR−/−, respectively) and wild-type controls. Changes in pupil diameter were measured under a microscope in restrained mice. Moreover, iris and iris muscle thickness were determined in cryosections.
Messenger RNA for all three α1-AR subtypes was detected the iris of wild-type mice with a rank order of abundance of α1A ≥ α1B > > α1D. The lack of a single α1-AR gene did not affect mRNA expression of the remaining two receptor subtypes. Phenylephrine induced pupil dilation in wild-type mice that was reduced in extent and duration in α1A-AR−/− and, less so, in α1B-AR−/− but not in α1D-AR−/− mice. The lack of a single α1-AR subtype had no effect on iris or iris muscle thickness.
The α1-AR–induced mydriasis in mice is mediated mainly by the α1A-AR, with a smaller contribution of the α1B-AR, matching the relative abundance of these subtypes at the mRNA level. The lack of a single α1-AR subtype does not appear to cause atrophy in the mouse iris.
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