Mice Lacking Gpr179 with Complete Congenital Stationary Night Blindness Are a Good Model for Myopia.
Baptiste WilmetJacques CallebertRobert DuvoisinRuben GouletChristophe TourainChristelle MichielsHelen FrederiksenFrank SchaeffelOlivier MarreJosé Alain SahelIsabelle AudoSerge PicaudChristina ZeitzPublished in: International journal of molecular sciences (2022)
Mutations in GPR179 are one of the most common causes of autosomal recessive complete congenital stationary night blindness (cCSNB). This retinal disease is characterized in patients by impaired dim and night vision, associated with other ocular symptoms, including high myopia. cCSNB is caused by a complete loss of signal transmission from photoreceptors to ON-bipolar cells. In this study, we hypothesized that the lack of Gpr179 and the subsequent impaired ON-pathway could lead to myopic features in a mouse model of cCSNB. Using ultra performance liquid chromatography, we show that adult Gpr179 -/- mice have a significant decrease in both retinal dopamine and 3,4-dihydroxyphenylacetic acid, compared to Gpr179 +/+ mice. This alteration of the dopaminergic system is thought to be correlated with an increased susceptibility to lens-induced myopia but does not affect the natural refractive development. Altogether, our data added a novel myopia model, which could be used to identify therapeutic interventions.
Keyphrases
- optic nerve
- liquid chromatography
- fatty acid
- high fat diet induced
- mouse model
- optical coherence tomography
- sleep quality
- mass spectrometry
- ejection fraction
- diabetic retinopathy
- newly diagnosed
- induced apoptosis
- intellectual disability
- high resolution
- insulin resistance
- prognostic factors
- uric acid
- bipolar disorder
- cell cycle arrest
- physical activity
- skeletal muscle
- chronic kidney disease
- young adults
- autism spectrum disorder
- adipose tissue
- patient reported outcomes
- simultaneous determination
- data analysis
- artificial intelligence
- diabetic rats
- pi k akt
- solid phase extraction
- patient reported
- duchenne muscular dystrophy