July 2018
Volume 59, Issue 9
Free
ARVO Annual Meeting Abstract  |   July 2018
Apomorphine attenuates form deprivation myopia by a dopamine D1 receptor-dependent mechanism in mice
Author Affiliations & Notes
  • Xiangtian Zhou
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, ZHEJIANG, China
  • Furong Huang
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, ZHEJIANG, China
  • Lishuai zhang
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, ZHEJIANG, China
  • Qiongsi Wang
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, ZHEJIANG, China
  • Jia Qu
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, ZHEJIANG, China
  • Footnotes
    Commercial Relationships   Xiangtian Zhou, None; Furong Huang, None; Lishuai zhang, None; Qiongsi Wang, None; Jia Qu, None
  • Footnotes
    Support  This study was sponsored by Grant LQ16H120005; Grant LZ14H120001 from the Natural Science Foundation of Zhejiang Province
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 753. doi:https://doi.org/
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Xiangtian Zhou, Furong Huang, Lishuai zhang, Qiongsi Wang, Jia Qu; Apomorphine attenuates form deprivation myopia by a dopamine D1 receptor-dependent mechanism in mice. Invest. Ophthalmol. Vis. Sci. 2018;59(9):753. doi: https://doi.org/.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose : To determine the contributions made by the dopamine receptor subtypes, D1R and D2R in mediating the inhibitory effects of the non-selective dopamine agonist apomorphine (APO) on form deprivation myopia (FDM) development in wildtype mice, we compared the described effects of this agonist in wildtype (WT) mice with those in its D2R knockout (D2R-KO) and D1R-KO counterparts.

Methods : Retinal layer thicknesses and electroretinograms (ERGs) were analyzed in both of these KOs, D1R antagonist SCH39166 and D2R antagonist sulpiride treated WT mice. The D2R-KO or D1R-KO mice and WT littermates were subjected to form deprivation during postnatal weeks 4-8. Both groups were intraperitoneally injected daily with either APO (5 µg/g body weight) dissolved in 1 µg /µL ascorbic acid or vehicle alone. Refraction, vitreous chamber depth (VCD), and axial length (AL), among other biometric parameters, were measured prior to and at the end of a treatment period by eccentric infrared photorefractor and optical coherence tomography, respectively.

Results : Both D2 KO and sulpiride treatments increased while both D1KO and SCH39166 treatments decreased ERG b-wave amplitudes. In WT mice, APO inhibited FDM development by about 80% (-0.92 ± 0.27 D vs -5.47 ± 0.96 D, P < 0.001). FDM in D2R-KO mice was inhibited by about 50% compared to FDM in WT mice (-2.97 ± 0.42 D vs -5.47 ± 0.96 D, P = 0.003), APO augmented this decline in D2R-KOs to a level that was similar to that induced by this agonist in WT mice (-0.92 ± 0.27 D vs -1.30 ± 0.39 D, P > 0.05). FDM development in D1R-KO mice was similar to that in WT mice (-5.77 ± 0.66 D vs -5.26 ± 0.75 D, P > 0.05) and APO administration had no effect on this process (-4.44 ± 0.64 D vs -5.77 ± 0.66 D, P > 0.05). The changes in VCD and AL were consistent with those in refraction.

Conclusions : APO-mediated FDM inhibition was abolished in the D1R-KO, but was unchanged in the D2R-KO. This difference indicates that APO induces this response through selectively inducing D1R activation rather than mediating any inhibition of FDM through an interaction with D2R in mice.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×