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Missing optomotor head-turning reflex in the DBA/2J mouse.

Peter Barabas1, Wei Huang, Hui Chen

  • 1Department of Ophthalmology and Visual Sciences, John Moran Eye Center, University of Utah School of Medicine, Salt Lake City, UT 84132, USA. sirmook12@gmail.com

Investigative Ophthalmology & Visual Science
|July 16, 2011
PubMed
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DBA/2J mice lack an optomotor reflex before glaucoma develops, independent of retinal function. This visual deficit is specific to the D2 strain and warrants caution when using this reflex to monitor glaucoma progression.

Area of Science:

  • Neuroscience
  • Ophthalmology
  • Genetics

Background:

  • The DBA/2J (D2) mouse strain is a common model for studying glaucoma, characterized by elevated intraocular pressure (IOP) and retinal ganglion cell (RGC) degeneration.
  • However, the precise timing and nature of visual deficits in D2 mice, particularly concerning the optomotor reflex, remain incompletely understood.

Purpose of the Study:

  • To compare the optomotor reflex, RGC firing patterns, direction selectivity, vestibulomotor function, and central vision between DBA/2J (D2) and C57BL/6J (B6) mouse strains.
  • To investigate the relationship between early visual deficits and the onset of glaucoma in D2 mice.

Main Methods:

  • Assessed optomotor reflex using head-turning assays.
  • Measured intraocular pressure (IOP), performed real-time PCR, and immunohistochemistry to track glaucomatous changes.

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  • Utilized the Morris water maze and Rotarod tests for behavioral analysis of vision and vestibulomotor function.
  • Employed multielectrode array (MEA) electrophysiology to characterize RGC spiking and direction selectivity.

    • Main Results:

    • D2 mice exhibited a progressive increase in IOP and loss of Brn3a signals, indicative of glaucoma after 6 months of age.
    • A significant lack of optomotor response to visual stimuli was observed in D2 mice compared to robust responses in B6 mice, even before overt IOP elevation.
    • While RGCs (including direction-selective types) and outer retinal function (assessed by ERG) were normal in young D2 mice, central vision and vestibulomotor function were also unaffected initially.

    Conclusions:

    • The D2 mouse strain displays a strain-specific deficit in the optomotor reflex that precedes detectable IOP elevation and RGC degeneration.
    • This behavioral abnormality is independent of retinal function and the glaucomatous process itself.
    • The optomotor reflex may not be a reliable indicator for monitoring glaucoma progression in the D2 mouse model due to its early and independent nature.