Purchase this article with an account.
Xiangtian Zhou, Furong Huang, Jiangfan Chen, Jia Qu; Apomorphine attenuates form-deprivation myopia (FDM) by a dopamine D2R-independent mechanism. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2154.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
The dopamine agonist apomorphine (APO) can profoundly attenuate form-deprivation myopia (FDM) development in animals. Here, we determine whether APO acts at dopamine D2 receptors (D2R) to exert its effect on myopia development using D2R knockout (KO) mice.
Wild-type (WT) littermates and D2R KO were subjected to FDM at postnatal days 28-56. Both groups were intraperitoneally injected daily with either APO (5 mg/kg/day) or vehicle for 4 weeks (starting from postnatal day 28). Their body weight, refraction, corneal radius of curvature and ocular axial components were measured at the end of 4-week treatment.
Consistent with our recent report, D2R KO attenuated FDM development compared to WT littermates. As expected, APO treatment attenuated myopia development compared with vehicle treatment in WT mice. Importantly, APO treatment in D2R KO mice further attenuated myopia development compared with the vehicle treatment in D2R KO mice. In parallel with refractory changes, D2R KO alone or APO alone also attenuated FDM-induced elongation of vitreous chamber depth and axial length compared to their corresponding controls. Moreover, combined treatment of D2R KO an APO treatment attenuated FDM-induced elongation of vitreous chamber depth and axial length compared to the D2R KO treated with vehicle.
The inhibition of APO on FDM development was still effective in absence of D2Rs, suggesting that APO attenuates myopia development by a D2R-independent mechanism.
This PDF is available to Subscribers Only