Parasympathetic and sympathetic control of emmetropization in chick.

Emmetropization can be altered by temporal visual stimulation and the spectral properties of the visual environment. The goal of the current experiment is to test the hypothesis that there is an interaction between these properties and autonomic innervation. For that purpose, selective lesions of the autonomic nervous system were performed in chickens followed by temporal stimulation. Parasympathetic lesioning involved transection of both the ciliary ganglion and the pterygopalatine ganglion (PPG_CGX; n = 38), while sympathetic lesioning involved transection of the superior cervical ganglion (SCGX; n = 49). After one week of recovery, chicks were then exposed to temporally modulated light (3 days, 2 Hz, Mean: 680 lux) that was either achromatic (with blue [RGB], or without blue [RG]), or chromatic (with blue [B/Y] or without blue [R/G]). Control birds with lesions, or unlesioned, were exposed to white [RGB] or yellow [RG] light. Ocular biometry and refraction (Lenstar and a Hartinger refractometer) was measured before and after exposure to light stimulation. Measurements were statistically analyzed for the effects of a lack of autonomic input and the type of temporal stimulation. In PPG_CGX lesioned eyes, there was no effect of the lesions one-week post-surgery. However, after exposure to achromatic modulation, the lens thickened (with blue) and the choroid thickened (without blue) but there was no effect on axial growth. Chromatic modulation thinned the choroid with R/G. In the SGX lesioned eye, there was no effect of the lesion 1-week post-surgery. However, after exposure to achromatic modulation (without blue), the lens thickened and there was a reduction in vitreous chamber depth and axial length. Chromatic modulation caused a small increase in vitreous chamber depth with R/G. Both autonomic lesion and visual stimulation were necessary to affect the growth of ocular components. The bidirectional responses observed in axial growth and in choroidal changes suggest that autonomic innervation combined with spectral cues from longitudinal chromatic aberration may provide a mechanism for homeostatic control of emmetropization.

Effects of Morning or Evening Narrow-band Blue Light on the Compensation to Lens-induced Hyperopic Defocus in Chicks.

SIGNIFICANCE: Exposure to blue light before bedtime is purported to be deleterious to various aspects of human health. In chicks, blue evening light stimulated ocular growth, suggesting a role in myopia development. To further investigate this hypothesis, we asked if brief blue light altered the compensatory responses to hyperopic defocus. PURPOSE: Previous work showed that several hours' evening exposure to blue light stimulated ocular growth in chicks, but morning exposure was only effective at a lower illuminance. By contrast, rearing in blue light has inhibited ocular growth in untreated eyes and eyes exposed to form deprivation or defocus. We studied the effects of brief exposures to blue light on the compensation to hyperopic defocus. METHODS: Chicks wore monocular negative lenses (-10 D) starting at age 10 days. They were subsequently exposed to blue light (460 nm) for 4 hours in the morning or evening for 8 to 9 days ("dim," 200 lux[morning, n = 9; evening, n = 11]; "bright," 600 lux[morning, n = 8; evening, n = 20]); controls wore lenses in white light (n = 14). Ultrasonography was done on days 1, 5, 8, and 9 for "evening" groups and days 1, 6, and 8 for "morning." All data are reported as interocular differences (experimental minus fellow eyes). Refractions were measured on the last day. RESULTS: For evening exposure, dim blue light enhanced the axial compensation at all times (change in axial length: day 6: 465 vs. 329 µm/9 days, analysis of variance P < .001, P = .03; day 9: 603 vs. 416 µm/9 days, analysis of variance P < .001; P < .05). Bright blue light had a transient inhibitory effect (day 5: 160 vs. 329 µm; P < .005). Refractive errors were consistent with axial growth, with dim causing more myopia than bright (-9.4 vs. -4.7 D; P < .05). Morning blue light had no significant effect. CONCLUSIONS: We speculate that these findings reflect a complex interaction between illuminance, defocus, and time of day.

Parasympathetic innervation of emmetropization.

Emmetropization is affected by the temporal parameters of visual stimulation and the spectral composition of light, as well as by autonomic innervation. The goal of the current experiments is to test the hypothesis that different types of visual stimulation interact with ocular innervation in the process of emmetropization. For that, selective lesions of the autonomic nervous system were performed in chickens: involving transection of parasympathetic input to the eye from either the ciliary ganglion, innervating accommodation and pupil responses (CGX; n = 32), or pterygopalatine ganglion, innervating choroidal blood vessels and cornea (PPGX; n = 26). After 1 week of recovery, chicks were exposed to sinusoidally modulated light (3 days, 2 Hz, 680 lux) that was either achromatic (black to white [RGB], or black to yellow [RG]), or chromatic (blue to yellow [B/Y] or red to green [R/G]). Exposure to light stimulation was followed by ocular biometry (Lenstar and a Hartinger refractometer). Surgical conditions revealed a small reduction in anterior chamber depth with CGX but no other significant changes in ocular biometry/refraction under standard light conditions. With RGB achromatic stimulation, CGX eyes produced an effect on ocular components, with a further reduction in anterior chamber depth and an increase in vitreous chamber depth, while RG stimulation showed no effect. No effect was detected in PPGX under both achromatic protocols. With chromatic stimulation, CGX with R/G modulation increased eye length, while PPGX with B/Y modulation decreased eye length. We conclude that the two different types of parasympathetic innervations have antagonistic effects on eye growth and the anterior eye when challenged with the appropriate stimulus, with possible implications for the role of choroidal blood flow in emmetropization.

Effects of morning and evening exposures to blue light of varying illuminance on ocular growth rates and ocular rhythms in chicks.

Recent evidence indicates that moderate levels of blue light are sufficient to suppress the nighttime rise in serum melatonin in humans, suggesting that luminous screens may be deleterious to sleep cycles and to other functions. Little is known however, about the effects of exposures to blue light on ocular physiology. We tested the effects of transient blue light exposures of various illuminances on ocular growth rates and ocular rhythms in chicks. 10-day old chicks were exposed to narrow band blue light (460 nm) of specific illuminance for 4 h in the evening (ZT8-ZT12) or the morning (ZT0-ZT4) for 9 days; for the remainder of the day they were in white light (588 lux). For the evening, four illuminances were tested: 0.15 lux (n = 15), 200 lux (radiometrically matched to white controls; n = 16), 600 lux (photometrically matched to white controls; n = 15) or 1000 lux (n = 8). The 600 lux condition was also tested using a 2-h duration (n = 8). The 200 and 600 lux conditions were extended to 14 and 21 days (n = 8 each). For morning exposures, 200 lux (n = 9), 600 lux (n = 9) and 1000 lux (n = 8) were tested. Controls remained in white light (n = 23). Ocular dimensions were measured by A-scan ultrasonography on days 1 and 9 to assess growth rates. On day 8 or 9, measurements were made at 6-h intervals over 24 h starting at noon to assess rhythm parameters. Evening exposure to blue light stimulated ocular growth rates relative to controls for all except the bright condition (0.15 lux, 200 lux, 600 lux vs bright and white respectively: 845 µm, 838 µm, 898 µm vs 733 µm and 766 µm; p < 0.05 for all comparisons). 2 h exposures to 600 lux were similarly effective (915 µm vs 766 µm; p < 0.05). Morning exposures only resulted in growth stimulation for the 200 lux condition (200 lux vs white: 884 µm vs 766 µm; p < 0.05). Furthermore, for this group only, growth of the anterior chamber had a significant contribution to the overall effect (vs white: p < 0.05), and choroids showed significant thickening. For evening exposures to 200 and 600 lux, the growth stimulatory effect lasted for 14 days (p = 0.01); by 21 days only the 600 lux group still differed (p < 0.0001). Evening exposures caused circadian disruptions in the choroidal thickness rhythms, and morning exposures disrupted both axial and choroidal rhythms. Exposure to 4 h of blue light at lower illuminances (less than 1000 lux) at transition times of lights-on and lights-off stimulates ocular growth rates and affects ocular rhythms in chicks, suggesting that such exposures may be deleterious to emmetropization in children.

Spectral composition of artificial illuminants and their effect on eye growth in chicks.

In broadband light, longitudinal chromatic aberration (LCA) provides emmetropization signals from both wavelength defocus and the resulting chromatic cues. Indoor illuminants vary in their spectral output, potentially limiting the signals from LCA. Our aim is to investigate the effect that artificial illuminants with different spectral outputs have on chick emmetropization with and without low temporal frequency modulation. In Experiment 1, two-week-old chicks were exposed to 0.2 Hz, square-wave luminance modulation for 3 days. There were 4 spectral conditions: LED strips that simulated General Electric (GE) LED "Soft" (n = 13), GE LED "Daylight" (n = 12), a novel "Equal" condition (n = 12), and a novel "High S" condition (n = 10). These conditions were all tested at a mean level of 985 lux. In Experiment 2, the effect of intensity on the "Equal" condition was tested at two other light levels (70 lux: n = 10; 680 lux: n = 7). In Experiment 3, the effect of temporal modulation on the "Equal" condition was tested by comparing the 0.2 Hz condition with 0 Hz (steady). Significant differences were found in axial growth across lighting conditions. At 985 lux, birds exposed to the "Equal" condition showed a greater reduction in axial growth (both p < 0.01) and a greater hyperopic shift compared to "Soft" and "Daylight" (both p < 0.01). The "High S" birds experienced more axial growth compared to "Equal" (p < 0.01) but less than in "Soft" and "Daylight" (p < 0.01). Axial changes in "Equal" were only observed at 985 lux with 0.2 Hz temporal modulation, and not with lower light levels or steady light. We conclude that axial growth and refraction were dependent on the lighting condition in a manner predicted by wavelength defocus signals arising from LCA.

Temporal color contrast guides emmetropization in chick.

As a result of longitudinal chromatic aberration (LCA), longer wavelengths are blurred when shorter wavelengths are in focus, and vice versa. As a result, LCA affects the color and temporal aspects of the retinal image with hyperopic defocus. In this experiment, we investigated how the sensitivity to temporal color contrast affects emmetropization. Ten-day-old chicks were exposed for three days to sinusoidal color modulation. The modulation was either blue/yellow flicker (BY) (n = 57) or red/green flicker (RG) (n = 60) simulating hyperopic defocus with and without a blue light component. The color contrasts tested were 0.1, 0.2, 0.3, 0.4, 0.6, and 0.8 Michelson contrast. The mean illuminance of all stimuli was 680 lux. Temporal modulation was either of a high (10 Hz) or low (0.2 Hz) temporal frequency. To test the role of short- and double-cone stimulation, an additional condition silenced these cones in RG_0.4 (D-) and was compared with RG_0.4 (D+) (n = 14). Changes in ocular components and refractive error were measured using Lenstar and a photorefractometer. With high temporal frequency BY representing an in-focus condition for shorter-wavelengths, we found that high temporal frequency BY contrast was positively correlated with vitreous expansion (R2 = 0.87, p < 0.01), expanding the vitreous to compensate for hyperopic defocus. This expansion was offset by low temporal frequency RG, which represented blurred longer wavelengths. The reduction in vitreous expansion in RG_0.4, was enhanced in D+ compared to D- (p < 0.001), indicating a role for short- and/or double-cones. With high temporal frequency RG representing an in-focus condition for longer-wavelengths, we found that high temporal frequency RG contrast was also positively correlated with a linear increase in vitreous chamber depth (R2 = 0.84, p < 0.01) and eye length (R2 = 0.30, p ≤ 0.05), required to compensate for hyperopic defocus, but also with RG sensitive choroidal thickening (R2 = 0.18: p < 0.0001). These increases in the vitreous and eye length were enhanced with D+ compared to D- (p = 0.003) showing the role of short- and double-cones in finessing the vitreous response to hyperopic defocus. Overall, the increase in vitreous chamber depth in RG was offset by reduced expansion in BY, indicating sensitivity to the shorter focal length of blue light and wavelength defocus. Predictable changes in cone contrast and temporal frequency of the retinal image that occur with LCA and defocus result in homeostatic control of emmetropization.

Signals for defocus arise from longitudinal chromatic aberration in chick.

Chicks respond to two signals from longitudinal chromatic aberration (LCA): a wavelength defocus signal and a chromatic signal. Wavelength defocus predicts reduced axial eye growth in monochromatic short-wavelength light, compared to monochromatic long-wavelength light. Wavelength defocus may also influence growth in broadband light. In contrast, a chromatic signal predicts increased growth when short-wavelength contrast > long-wavelength contrast, but only when light is broadband. We aimed to investigate the influence of blue light, temporal frequency and contrast on these signals under broadband conditions. Starting at 12 to 13 days-old, 587 chicks were exposed to the experimental illumination conditions for three days for 8h/day and spent the remainder of their day in the dark. The stimuli were flickering lights, with a temporal frequency of 0.2 or 10 Hz, low (30%) or high contrast (80%), and a variety of ratios of cone contrast simulating the effects of defocus with LCA. There were two color conditions, with blue contrast (bPlus) and without (bMinus). Stimuli in the "bPlus" condition varied the amounts of long- (L), middle- (M_) and double (D-) cone contrast, relative to short- (S-) and (UV-) cone contrast, to simulate defocus. Stimuli in the "bMinus" condition only varied the relative modulations of the L + D vs. M cones. In all cases, the average of the stimuli was white, with an illuminance of 777 lux, with cone contrast created through temporal modulation. A Lenstar LS 900 and a Hartinger refractometer were used to measure ocular components and refraction. Wavelength defocus signals with relatively high S-cone contrast resulted in reduced axial growth, and more hyperopic refractions, under low-frequency conditions (p = 0.002), in response to the myopic defocus of blue light. Chromatic signals with relatively high S-cone contrast resulted in increased axial growth and more myopic refractions, under high frequency, low contrast, conditions (p < 0.001). We conclude that the chromatic signals from LCA are dependent on the temporal frequency, phase, and relative contrast of S-cone temporal modulation, and recommend broadband spectral and temporal environments, such as the outdoor environment, to optimize the signals-for-defocus in chick.

Effect of duration, and temporal modulation, of monochromatic light on emmetropization in chicks.

Previous experiments disagree on the effect of monochromatic light on emmetropization. Some species respond to wavelength defocus created by longitudinal chromatic aberration and become more myopic in monochromatic red light and more hyperopic in monochromatic blue light, while other species do not. Using the chicken model, we studied the effect of the duration of light exposure, modes of lighting, and circadian interruption on emmetropization in monochromatic light. To achieve this goal, we exposed one-week-old chicks to flickering or steady monochromatic red or blue light for a short (10 days) or long (17 days) duration; other chicks were exposed to white light for 10 days. Refraction and ocular biometry were measured. Activity was measured via a motion detection algorithm and an IR camera. The results showed that in both steady and flickering light, there was a greater increase in axial length and vitreous chamber depth in chicks exposed to red or white light compared to chicks exposed to blue light. With a longer duration of exposure, axial length and vitreous chamber depth differences were no longer observed, except at an intermediate time point. Chicks exposed to red light were more active during the day compared to chicks exposed to blue light. We conclude that our results indicate that with short duration monochromatic light exposure, chicks rely on wavelength defocus to guide emmetropization. With longer exposure from hatching, our results support the notion that responses to wavelength defocus can be transient and that the difference between species may be due to differences in experimental duration and/or interference with circadian activity rhythms.

The role of dopamine in eye growth responses to color and luminance flicker in chicks.

Stroboscopic luminance flicker has been found to prevent the increase in eye growth normally associated with form deprivation through the release of retinal dopamine. In this study, we sought to investigate whether dopamine plays a role in the decreased growth observed with 2 Hz sine-wave luminance flicker and increased growth with color flicker. Starting 5-7 days after hatching, chicks were exposed to 2 Hz sinusoidally modulated illumination (Mean: 680 lux) for 4 days and were otherwise in the dark. Chicks were exposed to color-modulated red and green (RG) light, to luminance modulated RGB components (LUM), or to a no-flicker (NF) control. Chicks received daily 10 µL intravitreal injections of apomorphine, spiperone, or saline. Fellow eyes received no injection. Spiperone injections prevented the decrease in eye growth typically seen with LUM flicker, with a relative increase in eye length, but no other significant effects compared with saline controls. Apomorphine injections prevented the increase in eye growth typically seen with RG flicker, with a relative decrease in eye length compared to saline controls. These results indicate a role for the activation of D2-receptor types in the inhibition of eye growth in response to luminance flicker, and a lack of dopamine receptor activation associated with the increase in eye growth with color flicker.

Monochromatic and white light and the regulation of eye growth.

Experiments employing monochromatic light have been used to investigate the role of longitudinal chromatic aberration (LCA) as possible signals for emmetropization for many years. LCA arising from the dispersion of light, causes differences in the focal length at different wavelengths and can impose defocus (wavelength defocus). Short-wavelength light focuses with a shorter focal length than long-wavelength light and, as such, would be expected to produce a smaller, more hyperopic eye. Emmetropization can respond to wavelength defocus since animals reared in monochromatic light adjust their refractive state relative to that measured in white light. In many species, animals reared in monochromatic light respond as predicted by wavelength defocus, becoming more hyperopic in blue light and more myopic in red light. However, tree shrews and rhesus monkey become more hyperopic in red light, and while tree shrews initially become more hyperopic in blue light, they later become more myopic. This review examines the experiments performed in monochromatic light and highlights the potential differences in protocols affecting the results, including experiment duration, circadian rhythm stimulation, light intensity, bandwidth, humoral factors and temporal sensitivity.

Color and Temporal Frequency Sensitive Eye Growth in Chick.

Purpose: Longitudinal chromatic aberration can provide luminance and chromatic signals for emmetropization. A previous experiment examined the role of temporal sensitivity to luminance flicker in the emmetropization response. In the current experiment, we investigate the role of temporal sensitivity to color flicker. Methods: Five-day-old chicks were exposed to sinusoidal color modulation of blue/yellow (N = 73) or red/green LEDs (N = 84) at 80% contrast for 3 days. The modulation frequencies used were as follows: 0, 0.2, 1, 2, 5, and 10 Hz. There were 5 to 16 chicks per condition. Mean illumination was 680 lux. Changes in ocular components were measured using Lenstar, and refraction was measured with a Hartinger refractometer. Results: Eyes grew less when exposed to high temporal frequencies and more at low temporal frequencies. With blue/yellow modulation, the temporal variation was small; eyes grew 268 ± 15 µm at 0 Hz and 224 ± 12 µm at 10 Hz, representing a 16.4% growth reduction. With red/green modulation, eyes grew 336 ± 31 µm at 0 Hz and 218 ± 20 µm at 10 Hz, representing a 35% growth reduction. Choroidal and anterior chamber changes compensated for eye growth, reducing refractive effects; blue/yellow refraction changes ranged from -0.63 to 1.04 diopters. Conclusions: At high temporal frequencies, color is not a factor, but at low temporal frequencies, red/green modulation produced maximal growth. The pattern of changes observed in each ocular component with changes in the temporal frequency and/or the color of the stimulus was consistent with the idea that the natural sunlight spectrum may be optimal for emmetropization.

Sensitivity to S-Cone Stimuli and the Development of Myopia.

Purpose: Longitudinal chromatic aberration (LCA) is a color signal available to the emmetropization process that causes greater myopic defocus of short wavelengths than long wavelengths. We measured individual differences in chromatic sensitivity to explore the role LCA may play in the development of refractive error. Methods: Forty-four observers were tested psychophysically after passing color screening tests and a questionnaire for visual defects. Refraction was measured and only subjects with myopia or hyperopia without severe astigmatism participated. Psychophysical detection thresholds for 3 cyc/deg achromatic, L-, M-, and S-cone-isolating Gabor patches and low-frequency S-cone increment (S+) and decrement (S-) blobs were measured. Parametric Pearson correlations for refractive error versus threshold were calculated and nonparametric bootstrap 95% percentage confidence intervals (BCIs) for r were computed. Results: S-cone Gabor detection thresholds were higher than achromatic, L-, and M-cone Gabors. S-cone Gabor thresholds were higher than either S+ or S- blobs. These results are consistent with studies using smaller samples of practiced observers. None of the thresholds for the Gabor stimuli were correlated with refractive error (RE). A negative correlation with RE was observed for both S+ (r = -0.28; P = 0.06; BCI: r = -0.5, -0.04) and S- (r = -0.23; P = 0.13; BCI = -0.46, 0.01) blobs, although this relationship did not reach conventional statistical significance. Conclusions: Thresholds for S+ and S- stimuli were negatively related to RE, indicating that myopes may have reduced sensitivity to low spatial frequency S-cone stimuli. This reduced S-cone sensitivity might have played a role in their failure to emmetropize normally.

The role of temporal contrast and blue light in emmetropization.

A previous experiment showed that blue light (as a component of white light) protected against low temporal frequency dependent eye growth. This experiment investigated the role of temporal contrast. White leghorn chicks were exposed to white (with blue) or yellow (without blue) LED lighting modulated at either low (0.2Hz) or high (10Hz) temporal frequencies. Four cone contrast conditions were used: low (16%), medium (32%), medium-high (60%) and very-high (80%). Chicks were exposed to the lighting condition for 3days (mean 680lux). Exposure to high temporal frequencies, with very high temporal contrast, reduced eye growth, regardless of spectral content. However, at low temporal frequencies, eye growth was dependent on the illuminant. At lower temporal contrast levels, growth increased regardless of temporal or spectral characteristics. To conclude, very high temporal contrast, white light, provides a "stop" signal for eye growth that overrides temporal cues for growth that manifest in yellow light.

Opposing effects of atropine and timolol on the color and luminance emmetropization mechanisms in chicks.

This study analyzed the luminance and color emmetropization response in chicks treated with the nonselective parasympathetic antagonist atropine and the sympathetic ß-receptor blocker timolol. Chicks were binocularly exposed (8h/day) for 4days to one of three illumination conditions: 2Hz sinusoidal luminance flicker, 2Hz sinusoidal blue/yellow color flicker, or steady light (mean 680lux). Atropine experiments involved monocular daily injections of either 20µl of atropine (18nmol) or 20µl of phosphate-buffered saline. Timolol experiments involved monocular daily applications of 2 drops of 0.5% timolol or 2 drops of distilled H2O. Changes in the experimental eye were compared with those in the fellow eye after correction for the effects of saline/water treatments. Atropine caused a reduction in axial length with both luminance flicker (-0.078±0.021mm) and color flicker (-0.054±0.017mm), and a reduction in vitreous chamber depth with luminance flicker (-0.095±0.023mm), evoking a hyperopic shift in refraction (3.40±1.77D). Timolol produced an increase in axial length with luminance flicker (0.045±0.030mm) and a myopic shift in refraction (-4.07±0.92D), while color flicker caused a significant decrease in axial length (-0.046±0.017mm) that was associated with choroidal thinning (-0.046±0.015mm). The opposing effects on growth and refraction seen with atropine and timolol suggest a balancing mechanism between the parasympathetic and ß-receptor mediated sympathetic system through stimulation of the retina with luminance and color contrast.

Blue Light Protects Against Temporal Frequency Sensitive Refractive Changes.

PURPOSE: Time spent outdoors is protective against myopia. The outdoors allows exposure to short-wavelength (blue light) rich sunlight, while indoor illuminants can be deficient at short-wavelengths. In the current experiment, we investigate the role of blue light, and temporal sensitivity, in the emmetropization response. METHODS: Five-day-old chicks were exposed to sinusoidal luminance modulation of white light (with blue; N = 82) or yellow light (without blue; N = 83) at 80% contrast, at one of six temporal frequencies: 0, 0.2, 1, 2, 5, 10 Hz daily for 3 days. Mean illumination was 680 lux. Changes in ocular components and corneal curvature were measured. RESULTS: Refraction, eye length, and choroidal changes were dependent on the presence of blue light (P < 0.03, all) and on temporal frequency (P < 0.03, all). In the presence of blue light, refraction did not change across frequencies (mean change -0.24 [diopters] D), while in the absence of blue light, we observed a hyperopic shift (>1 D) at high frequencies, and a myopic shift (>-0.6 D) at low frequencies. With blue light there was little difference in eye growth across frequencies (77 µm), while in the absence of blue light, eyes grew more at low temporal frequencies and less at high temporal frequencies (10 vs. 0.2 Hz: 145 µm; P < 0.003). Overall, neonatal astigmatism was reduced with blue light. CONCLUSIONS: Illuminants rich in blue light can protect against myopic eye growth when the eye is exposed to slow changes in luminance contrast as might occur with near work.

The role of luminance and chromatic cues in emmetropisation.

PURPOSE: At birth most, but not all eyes, are hyperopic. Over the course of the first few years of life the refraction gradually becomes close to zero through a process called emmetropisation. This process is not thought to require accommodation, though a lag of accommodation has been implicated in myopia development, suggesting that the accuracy of accommodation is an important factor. This review will cover research on accommodation and emmetropisation that relates to the ability of the eye to use colour and luminance cues to guide the responses. RECENT FINDINGS: There are three ways in which changes in luminance and colour contrast could provide cues: (1) The eye could maximize luminance contrast. Monochromatic light experiments have shown that the human eye can accommodate and animal eyes can emmetropise using changes in luminance contrast alone. However, by reducing the effectiveness of luminance cues in monochromatic and white light by introducing astigmatism, or by reducing light intensity, investigators have revealed that the eye also uses colour cues in emmetropisation. (2) The eye could compare relative cone contrast to derive the sign of defocus information from colour cues. Experiments involving simulations of the retinal image with defocus have shown that relative cone contrast can provide colour cues for defocus in accommodation and emmetropisation. In the myopic simulation the contrast of the red component of a sinusoidal grating was higher than that of the green and blue component and this caused relaxation of accommodation and reduced eye growth. In the hyperopic simulation the contrast of the blue component was higher than that of the green and red components and this caused increased accommodation and increased eye growth. (3) The eye could compare the change in luminance and colour contrast as the eye changes focus. An experiment has shown that changes in colour or luminance contrast can provide cues for defocus in emmetropisation. When the eye is exposed to colour flicker the eye grows almost twice as much, and becomes more myopic, compared to when the eye is exposed to luminance flicker. SUMMARY: Neural responses of the luminance and colour mechanisms direct accommodation and emmetropisation mechanisms to different focal planes. Therefore, it is likely that the set point of refraction and accommodation is dependent on the sensitivity of the eye to changes in spatial and temporal, colour and luminance contrast.

Chicks use changes in luminance and chromatic contrast as indicators of the sign of defocus.

As the eye changes focus, the resulting changes in cone contrast are associated with changes in color and luminance. Color fluctuations should simulate the eye being hyperopic and make the eye grow in the myopic direction, while luminance fluctuations should simulate myopia and make the eye grow in the hyperopic direction. Chicks without lenses were exposed daily (9 a.m. to 5 p.m.) for three days on two consecutive weeks to 2 Hz sinusoidally modulated illumination (mean illuminance of 680 lux) to one of the following: in-phase modulated luminance flicker (LUM), counterphase-modulated red/green (R/G Color) or blue/yellow flicker (B/Y Color), combined color and luminance flicker (Color + LUM), reduced amplitude luminance flicker (Low LUM), or no flicker. After the three-day exposure to flicker, chicks were kept in a brooder under normal diurnal lighting for four days. Changes in the ocular components were measured with ultrasound and with a Hartinger Coincidence Refractometer (aus Jena, Jena, East Germany. After the first three-day exposure, luminance flicker produced more hyperopic refractions (LUM: 2.27 D) than did color flicker (R/G Color: 0.09 D; B/Y Color: -0.25 D). Changes in refraction were mainly due to changes in eye length, with color flicker producing much greater changes in eye length than luminance flicker (R/G Color: 102 µm; B/Y Color: 98 µm; LUM: 66 µm). Our results support the hypothesis that the eye can differentiate between hyperopic and myopic defocus on the basis of the effects of change in luminance or color contrast.

Chick eyes compensate for chromatic simulations of hyperopic and myopic defocus: evidence that the eye uses longitudinal chromatic aberration to guide eye-growth.

Longitudinal chromatic aberration (LCA) causes short wavelengths to be focused in front of long wavelengths. This chromatic signal is evidently used to guide ocular accommodation. We asked whether chick eyes exposed to static gratings simulating the chromatic effects of myopic or hyperopic defocus would "compensate" for the simulated defocus. We alternately exposed one eye of each chick to a sine-wave grating (5 or 2 cycle/deg) simulating myopic defocus ("MY defocus": image focused in front of retina; hence, red contrast higher than blue) and the other eye to a grating of the same spatial frequency simulating hyperopic defocus ("HY defocus": blue contrast higher than red). The chicks were placed in a drum with one eye covered with one grating, and then switched to another drum with the other grating with the other eye covered. To minimize the effects of altered eye-growth on image contrast, we studied only the earliest responses: first, we measured changes in choroidal thickness 45 min to 1 h after one 15-min episode in the drum, then we measured glycosaminoglycans (GAG) synthesis in sclera and choroid (by the incorporation of labeled sulfate in tissue culture) after a day of four 30-min episodes in the drum. The eyes compensated in the appropriate directions: The choroids of the eyes exposed to the HY simulation showed significantly more thinning (less thickening) over the course of the experiment than the choroids of the eyes exposed to the MY simulation (all groups mean:-17 microm; 5 c/d groups: -24 microm; paired t-test (one-tailed): p=0.0006). The rate of scleral GAG synthesis in the eye exposed to the HY simulation was significantly greater than in the eye exposed to the MY simulation (HY/MY ratio=1.20; one sample t-test (one-tailed): p=0.015). There was no significant interaction between the sign of the simulated defocus and either the spatial frequency or the presence of a +3 D lens used to compensate for the 33 cm distance of the drum. Although previous work has shown that chromatic cues to defocus are not essential for lens-compensation, in that chicks can compensate in monochromatic light, our evidence implies that the eye may be able to infer whether the eye is myopic or hyperopic from the different chromatic contrasts that result from different signs of defocus.

Potential signal to accommodation from the Stiles-Crawford effect and ocular monochromatic aberrations.

The purpose of this study is to determine if cues within the blurred retinal image due to the Stiles-Crawford (SC) effect and the eye's monochromatic aberrations can drive accommodation with a small pupil (3 mm) that is typical of bright photopic conditions.The foveal, psychophysical SC function (17 min arc) and ocular monochromatic aberrations were measured in 21 visually normal adults. The retinal image of a 10.2 min arc disc was simulated for spherical defocus levels of -1 D, 0 D and +1 D in each of four conditions consisting of combinations of the presence or absence of the individual SC function and monochromatic aberrations with a 3 mm pupil. Accommodation was recorded in eleven participants as each viewed the simulations through a 0.75-mm pinhole.The SC effect alone did not provide a significant cue to accommodation. Monochromatic aberrations provided a statistically significant but rather small cue to monocular accommodation.

Cone signals for spectacle-lens compensation: differential responses to short and long wavelengths.

Chick eyes compensate for defocus imposed by spectacle lenses by making compensatory changes in eye length and choroidal thickness, a laboratory model of emmetropization. To investigate the roles of longitudinal chromatic aberration and of chromatic mechanisms in emmetropization, we examined the participation of different cone classes, and we compared the efficacy of lens compensation under monochromatic illumination with that under white light of the same illuminance to the chick eye. Chicks wore positive or negative 6D or 8D lenses on one eye for 3 days, under either blue (460 nm) or red (620 nm) light at 0.67 lux or under white light at 0.67 or 0.2 lux (all measures are corrected for chick photopic sensitivity). The illumination conditions were chosen to differentially stimulate either the short-wavelength and ultraviolet cones or the long-wavelength and double cones. Measurements are expressed as the relative change: the inter-ocular difference in the amount of change over the 3 days of lens wear. We find that under this low illumination the two components of lens compensation were differentially affected by the monochromatic illumination: in blue light lens compensation was mainly due to changes in eye length, whereas in red light lens compensation was mainly due to changes in choroidal thickness. In general, white light produced better lens compensation than monochromatic illumination. NEGATIVE LENSES: Under white light negative lenses caused an increase in eye length (60 microm) together with a decrease in choroidal thickness (-51 microm) relative to the fellow eye. Under blue light, although there was an increase in eye length (32 microm), there was no change in choroidal thickness (5 microm). In contrast, under red light there was a decrease in choroidal thickness (-62 microm) but no increase in eye length (8 microm). Relative ocular elongation was the same in white and monochromatic light. POSITIVE LENSES: Under white light positive lenses caused a decrease in eye length (-142 microm) together with an increase in choroidal thickness (68 microm) relative to the fellow eye. Under blue light, there was a decrease in eye length (-64 microm), but no change in choroidal thickness (2 microm). In contrast, under red light there was an increase (90 microm) in choroidal thickness but less of a decrease (-36 microm) in eye length. Lens compensation by inhibition of ocular elongation was less effective under monochromatic illumination than under white light (white v red: p=0.003; white v blue p=.014). The differential effects of red and blue light on the choroidal and ocular length compensatory responses suggest that they are driven by different proportions of the cone-types, implying that, although chromatic contrast is not essential for lens compensation and presumably for emmetropization as well, the retinal substrates exist for utilizing chromatic contrast in these compensatory responses. The generally better lens compensation in white than monochromatic illumination suggests that longitudinal chromatic aberration may be used in lens compensation.