The optomotor response: A robust first-line visual screening method for mice

Jellali, Abdeljalil; Méziane, Hamid; Abdel-mouttalib, Ouagazzal; Rousseau, Stéphane; Romand, R.; Auwerx, Johan; José, Sahel; Chambon, Pierre; Picaud, Serge

doi:10.1016/j.visres.2004.12.015

Cited by 115 publications

(110 citation statements)

References 42 publications

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“…For this, we used the optomotor test that provides a measure of visual acuity (Prusky et al, 2004;Abdeljalil et al, 2005). In preliminary studies we noted that the finest square wave contrast grating that would reliably induce head movements in a majority of wild-type C56BL/6 mice was an optotype of 0.375 cpd (data not shown).…”

Section: Resultsmentioning

confidence: 99%

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Otx2 Promotes the Survival of Damaged Adult Retinal Ganglion Cells and Protects against Excitotoxic Loss of Visual AcuityIn Vivo

Ibad¹,

Rheey²,

Mrejen³

et al. 2011

J. Neurosci.

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Retinal ganglion cells (RGCs) are the projection neurons from the eye to the brain and their loss results in visual impairment in a number of diseases. Transcription factors with a homeodomain can translocate between cells and, in at least one reported case, can stimulate neuronal survival. Otx2 is a homeoprotein transcription factor expressed in the retina that is taken up by RGCs. We thus hypothesized that Otx2 capture could regulate the survival of adult RGCs. We report that Otx2 stimulates the survival of adult mouse and rat RGCs in vitro and protects RGCs against NMDA-induced toxicity in vivo in mice. In the latter model, Otx2 also preserves visual acuity.

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Section: Resultsmentioning

confidence: 99%

“…Changes in visual acuity were assessed by optomotor response as described (Abdeljalil et al, 2005) with modifications. Briefly, mice adapted to ambient light were placed on a raised grid platform centered in a well lit motorized drum with 100% contrast black and white vertical stripes.…”

Section: Recombinant Proteinmentioning

confidence: 99%

Otx2 Promotes the Survival of Damaged Adult Retinal Ganglion Cells and Protects against Excitotoxic Loss of Visual AcuityIn Vivo

Ibad¹,

Rheey²,

Mrejen³

et al. 2011

J. Neurosci.

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“…The a-wave amplitude was measured from the base line to the first negative peak, whereas the b-wave amplitude was measured from the a-wave to the next positive peak. After Optomotor Testing-Optomotor responses were obtained and analyzed as described previously (20).…”

Section: Generation Of Lama1mentioning

confidence: 99%

Mutations in Lama1 Disrupt Retinal Vascular Development and Inner Limiting Membrane Formation

Edwards

Mammadova‐Bach

Alpy

et al. 2010

Journal of Biological Chemistry

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The Neuromutagenesis Facility at the Jackson Laboratory generated a mouse model of retinal vasculopathy, nmf223, which is characterized clinically by vitreal fibroplasia and vessel tortuosity. nmf223 homozygotes also have reduced electroretinogram responses, which are coupled histologically with a thinning of the inner nuclear layer. The nmf223 locus was mapped to chromosome 17, and a missense mutation was identified in Lama1 that leads to the substitution of cysteine for a tyrosine at amino acid 265 of laminin ␣1, a basement membrane protein.Despite normal localization of laminin ␣1 and other components of the inner limiting membrane, a reduced integrity of this structure was suggested by ectopic cells and blood vessels within the vitreous. Immunohistochemical characterization of nmf223 homozygous retinas demonstrated the abnormal migration of retinal astrocytes into the vitreous along with the persistence of hyaloid vasculature. The Y265C mutation significantly reduced laminin N-terminal domain (LN) interactions in a bacterial twohybrid system. Therefore, this mutation could affect interactions between laminin ␣1 and other laminin chains. To expand upon these findings, a Lama1 null mutant, Lama1 tm1.1Olf , was generated that exhibits a similar but more severe retinal phenotype than that seen in nmf223 homozygotes. The increased severity of the Lama1 null mutant phenotype is probably due to the complete loss of the inner limiting membrane in these mice. This first report of viable Lama1 mouse mutants emphasizes the importance of this gene in retinal development. The data presented herein suggest that hypomorphic mutations in human LAMA1 could lead to retinal disease.

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“…In recent years, coincident with the growing popularity of mouse models for retinal disease, a number of techniques for rapidly assaying mouse vision have been proposed [30][31][32][33]. These assays involve a variety of different response measures and in pursuing them it has often proven convenient to use computer monitors to generate visual stimuli.…”

Section: Co-expression Of Mouse Cone Photopigmentsmentioning

confidence: 99%

Contributions of the mouse UV photopigment to the ERG and to vision

Jacobs

Williams

2007

Doc Ophthalmol

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The mouse retina contains two classes of cone photopigment with respective peak sensitivities in the middle (M) wavelengths and in the ultraviolet (UV) portion of the spectrum. To examine the functional roles subserved by the UV pigment, the absorption of light by the mouse lens was measured and voltage versus intensity (V-log I) functions were derived from recordings of the flicker ERG made under test conditions designed to maximize the relative sensitivities of the two pigment types. These V-log I data accurately predict ERG-based spectral sensitivity functions, but they fail to provide a similarly accurate account of behaviorally based measurements of spectral sensitivity in that the ERG spectral sensitivity function has much higher sensitivity in the UV wavelengths than does the behavioral spectral sensitivity function. The disparity between these two is argued to be a consequence of the widespread receptor co-expression of the two types of cone pigment in the mouse and of the pattern of retinal wiring that is thought to be characteristic of all mammalian retinas.

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The optomotor response: A robust first-line visual screening method for mice

Cited by 115 publications

References 42 publications

Otx2 Promotes the Survival of Damaged Adult Retinal Ganglion Cells and Protects against Excitotoxic Loss of Visual AcuityIn Vivo

Otx2 Promotes the Survival of Damaged Adult Retinal Ganglion Cells and Protects against Excitotoxic Loss of Visual AcuityIn Vivo

Mutations in Lama1 Disrupt Retinal Vascular Development and Inner Limiting Membrane Formation

Contributions of the mouse UV photopigment to the ERG and to vision

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