The electroretinogram of albinos

Tomei, Francesca; Wirth, A

doi:10.1016/0042-6989(78)90246-8

Cited by 10 publications

(4 citation statements)

References 5 publications

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“…Our findings that some ERGs are larger from those with lighter eyes are in keeping with previous studies [2][3][4][5][6][7]. The ITs were earlier for the blue group compared with the brown group for most of ERG components, both dark-and lightadapted, which may suggest that a basic process, such as the phototransduction cascade, may be slightly accelerated in those with blue eyes.…”

Section: Discussionsupporting

confidence: 91%

“…It has been reported that human eyes with lighter fundi demonstrate larger full-field ERGs under both light-and dark-adapted conditions with normal or supranormal amplitudes in those with albinism [2][3][4][5][6][7]. Fundus pigmentation corresponds closely to iris pigmentation, iris colour and skin pigmentation [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

“…Although dark-and light-skinned humans have similar amounts of melanin pigment in their retinal pigment epithelium (RPE), humans with dark skin have, on average, twice as much melanin pigment in their choroid as those with light skin [9]. Although it seems intuitive that greater light absorption by the denser choroidal pigment should reduce the effective retinal illumination and hence the ERG amplitude, this alone does not adequately explain the larger ERGs from lighter eyes [3,7].…”

Section: Introductionmentioning

confidence: 99%

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Light- and dark-adapted electroretinograms (ERGs) and ocular pigmentation: comparison of brown- and blue-eyed cohorts

et al. 2010

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This study characterizes differences in human ERGs based on ocular pigmentation. Light- and dark-adapted luminance-response (LR) series for a-, b- and i-waves and light-adapted oscillatory potentials (OPs) were recorded in 14 healthy volunteers (7 blue-eyed Caucasians; 7 brown-eyed Asians, aged 20-22 years). Amplitude interpolations were by logistic growth (Naka-Rushton), Gaussian or the combined 'photopic hill' functions. Implicit times (IT) for dark-adapted a- and b-waves, and for light-adapted a-, b- and i-waves were earlier in the blue-eyed group than in the brown-eyed group across all flash strengths (P < 0.05). For dark-adapted ERGs, saturated a-wave amplitude was larger for blue eyes (397 vs. 318 μV, P < 0.05) as was the a-wave to strong flash (10 cd·s/m(2); 357 vs. 293 μV, P < 0.05) and the b-wave to ISCEV standard 0.01 (354 vs. 238 μV, P < 0.05). Light-adapted b-waves for midrange flash stimuli were much larger for the blue-eyed group (photopic hill, Gaussian peak: 155 vs. 82 μV, P < 0.001) with no difference in saturated amplitudes. Similarly, interpolated i-wave amplitudes were larger (48 vs. 18 μV, P < 0.01). For a light-adapted 2.6 stimulus, a- and b-waves were larger for the blue-eyed group (52 vs. 39 μV; 209 vs. 133 μV, P < 0.01) as were OP4 and OP5 (37.2 vs. 15.6 μV; 47.5 vs. 22.2 μV, P < 0.01), but OP1-OP3 did not differ. ERGs have shorter ITs in people with blue irides than in those with dark pigmentation. Amplitude differences are highly non-linear and substantially larger from eyes with light pigmentation for components thought to be associated with the OFF retinal pathways.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Light- and dark-adapted electroretinograms (ERGs) and ocular pigmentation: comparison of brown- and blue-eyed cohorts

et al. 2010

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“…This is consistent with the notion that the defects are expressed in the embryo, because the RPE becomes pigmented at early stages of eye development, long before any other pigment appears in the organism; the choroid of the eye, for instance, assumes pigment only several days after birth in mice, at a time when optic connections are for the most part well established. It is not known with which pigment, if any, the light sensitivity defect may correlate, as it has only been described in pearl mice; a similar defect does seem to be present in albino mice (unpublished observations) and it may also be reflected in visual abnormalities found in albinos of several species, including humans, which cannot be explained by light scatter or aberrant crossing (11,12).…”

mentioning

confidence: 95%

Calcium binding in pigmented and albino eyes.

Drager¹

1985

Proc. Natl. Acad. Sci. U.S.A.

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The localization of calcium binding sites in eyes was determined autoradiographically after extracting endogenous Ca from tissue sections and replacing it with 45Ca.The strongest labeling was associated with pigmented tissues due to the high concentration of melanin, which was shown to bind Ca effectively and in a pH-dependent fashion. The second strongest binding was over the tapetum lucidum of the cat eye, and moderate labeling was associated with eye muscles and epithelium and endothelium of the cornea. The neural retina was generally more lightly labeled than the surrounding tissue of the eye; here the plexiform layers stood out in comparison to the nuclear layers, as did a band located internal to the photoreceptor outer segments. The possibility that the Ca buffering capacity of melanin may represent the common denominator for the various neurological defects found in hypopigmentation mutants is discussed.Hypopigmentation mutants in mammals have two types of visual abnormalities that cannot be explained by insufficient light screening but point to another, unidentified function of pigment. The first abnormality is due to miswiring of optic connections; it includes the extensively studied defect in optic nerve crossing (1, 2) and probably also the eye movement defects (3-5). The second type is a dynamic defect that depends on direct contact of the neural retina with the retinal pigment epithelium (RPE): in optic nerve recordings from intact pearl mice, a hypopigmentation mutant not allelic with the albino, visual thresholds were elevated about 100 times at dim backgrounds, as compared to fully pigmented mice, but were about normal at bright ambient illumination (6); when recordings were done from ganglion cells in isolated retinas, however, visual thresholds of normal and pearl mice were indistinguishable (7). Defects in optic nerve crossing and eye movements are caused by mutations at any of several genes involved in pigmentation; severity of defects correlates roughly with the degree of impairment in pigmentation of the RPE and not with pigment in any other tissues (8)(9)(10). This is consistent with the notion that the defects are expressed in the embryo, because the RPE becomes pigmented at early stages of eye development, long before any other pigment appears in the organism; the choroid of the eye, for instance, assumes pigment only several days after birth in mice, at a time when optic connections are for the most part well established. It is not known with which pigment, if any, the light sensitivity defect may correlate, as it has only been described in pearl mice; a similar defect does seem to be present in albino mice (unpublished observations) and it may also be reflected in visual abnormalities found in albinos of several species, including humans, which cannot be explained by light scatter or aberrant crossing (11, 12). METHODS AND RESULTSMice were perfused with paraformaldehyde and (in some cases) glutaraldehyde, and their eyes were dissected as eye cups, cut on a cryostat at 10 ,m, e...

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Vision in albinism

Summers¹

1997

American Journal of Ophthalmology

100

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The electroretinogram of albinos

Cited by 10 publications

References 5 publications

Light- and dark-adapted electroretinograms (ERGs) and ocular pigmentation: comparison of brown- and blue-eyed cohorts

Light- and dark-adapted electroretinograms (ERGs) and ocular pigmentation: comparison of brown- and blue-eyed cohorts

Calcium binding in pigmented and albino eyes.

Vision in albinism

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