Speed, Spatial, and Temporal Tuning of Rod and Cone Vision in Mouse

Umino, Yumiko; Solessio, Eduardo; Barlow, Robert B.

doi:10.1523/jneurosci.3551-07.2008

Cited by 204 publications

(295 citation statements)

References 32 publications

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“…Hence, it is probable that these light effects are input through the eyes of the mice as in birds , rather than the pineal gland as in newts (Phillips et al 2001). However, to properly support this suggestion, blind or transgenic mice with rod and/or cone and other receptor deficits (Umino et al 2008) should be tested. It is clear from the experiments (summarized in figure 9) that blue light abolishes the induced analgesia for intensities ranging from 251, 106, 51, 25 and probably 12.5% of the amount of ambient blue light in the animal housing facility.…”

Section: Discussionmentioning

confidence: 99%

“…It is important to note that our suggestion of similar light intensity thresholds between mice and birds is based on irradiance values (photons s K1 m K2 ) rather than actual intensity at the retina (Jacobs et al (2004) suggest using photons/s/sr, which allows for correction of differences in animal pupil area). However, it is still possible that the actual biophysical transduction mechanisms may be in another receptor besides the cones, and experiments using transgenic/knockout mice with deficient rods or cones (Umino et al 2008) or deficient in other light-sensitive compounds (Sancar 2004) are needed to resolve this issue.…”

Section: Discussionmentioning

confidence: 99%

“…Thalau et al (2006) have presented data suggesting that 'magnetic compass mechanisms of birds and rodents are based on different physical principles', but in fact, the experiments were all performed on mole rats for which there is evidence that their visual system may be quite different from most rodents Peichl et al 2004). Hence, their work cannot be extrapolated directly to mice with full rod and cone vision (Jacobs et al 2004;Umino et al 2008). Interestingly, Muheim et al (2006) have shown that mice can use a geomagnetic field as the sole method of finding their nest; however, it is still unclear whether the response is light dependent.…”

Section: Introductionmentioning

confidence: 99%

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Light alters nociceptive effects of magnetic field shielding in mice: intensity and wavelength considerations

Prato

Desjardins-Holmes

Keenliside

et al. 2008

J. R. Soc. Interface.

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Previous experiments with mice have shown that repeated 1 hour daily exposure to an ambient magnetic field-shielded environment induces analgesia (antinociception). The exposures were carried out in the dark (less than 2.0!10 16 photons s K1 m K2 ) during the midlight phase of the diurnal cycle. However, if the mice were exposed in the presence of visible light (2.0!10 18 photons s K1 m K2 , 400-750 nm), then the analgesic effects of shielding were eliminated. Here, we show that this effect of light is intensity and wavelength dependent. Introduction of red light (peak at 635 nm) had little or no effect, presumably because mice do not have photoreceptors sensitive to red light above 600 nm in their eyes. By contrast, introduction of ultraviolet light (peak at 405 nm) abolished the effect, presumably because mice do have ultraviolet A receptors. Blue light exposures (peak at 465 nm) of different intensities demonstrate that the effect has an intensity threshold of approximately 12% of the blue light in the housing facility, corresponding to 5!10 16 photons s K1 m K2 (integral). This intensity is similar to that associated with photoreceptor-based magnetoreception in birds and in mice stimulates photopic/cone vision. Could the detection mechanism that senses ambient magnetic fields in mice be similar to that in bird navigation?

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Light alters nociceptive effects of magnetic field shielding in mice: intensity and wavelength considerations

Prato

Desjardins-Holmes

Keenliside

et al. 2008

J. R. Soc. Interface.

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“…After acclimatization, contrast sensitivity was determined under scotopic conditions ( < 0.003 cds/m 2 ). Contrast sensitivity was measured at a spatial frequency of 0.064 cycles/degree and at a rotation speed of 0.75 Hz, settings previously determined as optimal for maximal stimulation in wildtype mice under scotopic conditions [22]. A staircase paradigm program was used to measure independent contrast sensitivity thresholds in both eyes, defined as the % contrast yielding ‡ 70% correct observer responses.…”

Section: Gnat1mentioning

confidence: 99%

Migration, Integration and Maturation of Photoreceptor Precursors Following Transplantation in the Mouse Retina

Warre-Cornish

Barber

Sowden

et al. 2014

Stem Cells and Development

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Retinal degeneration leading to loss of photoreceptors is a major cause of untreatable blindness. Recent research has yielded definitive evidence for restoration of vision following the transplantation of rod photoreceptors in murine models of blindness, while advances in stem cell biology have enabled the generation of transplantable photoreceptors from embryonic stem cells. Importantly, the amount of visual function restored is dependent upon the number of photoreceptors that migrate correctly into the recipient retina. The developmental stage of the donor cells is important for their ability to migrate; they must be immature photoreceptor precursors. Little is known about how and when donor cell migration, integration, and maturation occurs. Here, we have performed a comprehensive histological analysis of the 6-week period following rod transplantation in mice. Donor cells migrate predominately as single entities during the first week undergoing a stereotyped sequence of morphological changes in their translocation from the site of transplantation, through the interphotoreceptor matrix and into the recipient retina. This includes initial polarization toward the outer nuclear layer (ONL), followed by formation of an apical attachment and rudimentary segment during migration into the ONL. Strikingly, acquisition of a nuclear architecture typical of mature rods was accelerated compared with normal development and a feature of migrating cells. Once within the ONL, precursors formed synaptic-like structures and outer segments in accordance with normal maturation. The restoration of visual function mediated by transplanted photoreceptors correlated with the later expression of rod a-transducin, achieving maximal function by 5 weeks.

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“…Using the two-alternative forced choice paradigm as previously described (Umino et al, 2008;Boye et al, 2010), light-adapted spatial frequency and contrast sensitivity measurements were made in 1-year-old C57BL/6J mice (M1-M5), and AAV-GC1-treated (M6-M9) and untreated (M10-M14) GCdko mice with a virtual optokinetic instrument (Optomotry, Cerebral Mechanics). The single eyetreated GCdko mice analyzed were chosen from cohort 1 (P18-treated, ''M6'') and cohort 3 (P37-P49-treated,''M7,'' ''M8,'' and ''M9'').…”

Section: Optomotor Testingmentioning

confidence: 99%

AAV-Mediated Gene Therapy in the Guanylate Cyclase (RetGC1/RetGC2) Double Knockout Mouse Model of Leber Congenital Amaurosis

et al. 2013

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Mutations in GUCY2D are associated with recessive Leber congenital amaurosis-1 (LCA1). GUCY2D encodes photoreceptor-specific, retinal guanylate cyclase-1 (RetGC1). Reports of retinal degeneration in LCA1 are conflicting; some describe no obvious degeneration and others report loss of both rods and cones. Proof of concept studies in models representing the spectrum of phenotypes is warranted. We have previously demonstrated adeno-associated virus (AAV)-mediated RetGC1 is therapeutic in GC1ko mice, a model exhibiting loss of cones only. The purpose of this study was to characterize AAV-mediated gene therapy in the RetGC1/RetGC2 double knockout (GCdko) mouse, a model lacking rod and cone function and exhibiting progressive loss of both photoreceptor subclasses. Use of this model also allowed for the evaluation of the functional efficiency of transgenic RetGC1 isozyme. Subretinal delivery of AAV8(Y733F) vector containing the human rhodopsin kinase (hGRK1) promoter driving murine Gucy2e was performed in GCdko mice at various postnatal time points. Treatment resulted in restoration of rod and cone function at all treatment ages and preservation of retinal structure in GCdko mice treated as late as 7 weeks of age. Functional gains and structural preservation were stable for at least 1 year. Treatment also conferred cortical-and subcortical-based visually-guided behavior. Functional efficiency of transgenic RetGC1 was indistinguishable from that of endogenous isozyme in congenic wild-type (WT) mice. This study clearly demonstrates AAV-mediated RetGC1 expression restores function to and preserves structure of rod and cone photoreceptors in a degenerative model of retinal guanylate cyclase deficiency, further supporting development of an AAV-based vector for treatment of LCA1.

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Speed, Spatial, and Temporal Tuning of Rod and Cone Vision in Mouse

Cited by 204 publications

References 32 publications

Light alters nociceptive effects of magnetic field shielding in mice: intensity and wavelength considerations

Light alters nociceptive effects of magnetic field shielding in mice: intensity and wavelength considerations

Migration, Integration and Maturation of Photoreceptor Precursors Following Transplantation in the Mouse Retina

AAV-Mediated Gene Therapy in the Guanylate Cyclase (RetGC1/RetGC2) Double Knockout Mouse Model of Leber Congenital Amaurosis

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