[Myopia update 2011]. / Myopie-Update 2011.

This review summarises some recent aspects of myopia research. The following conclusions have been drawn. As long as myopia progression is visually controlled, at least three different interventions are possible: (i) spectacles/contact lenses which correct only the centre of the visual field and leave the periphery somewhat myopic, (ii) outdoor activity or equivalent temporary increase in illuminance, (iii) pharmacological intervention of retinal growth signals that are transmitted to the underlying sclera. Options (i) and (ii) can be used without risks although there is still room for improvement of the variables. Option (iii) has re-entered a new phase of orientation with new searches for candidate targets after previous testing with muskarinic antagonists (pirenzepine) in children did not enter phase 3 level. If myopia is outside the range over which it is visually controlled by emmetropisation (in the case of high and pathological myopias), in principle the possibility exists to improve the mechanical stability of the sclera pharmacologically. However, there is still a need for more research. Up to now, the mechanical weakness of the sclera in highly mopyic eyes is surgically stabilised by "scleral buckling". However, these procedures have found limited acceptance since the effects were not very reliable. In 40 - 50 % of the cases of high myopia, degenerative processes are found in the retina which can be seen as consequence of the mechanical tension in the fundus, but may also be indepedent of this factor (no significant correlation with axial length!). In part they can be slowed down by intravitreal anti-VEGF therapy. A long-term study from Denmark has shown that most patients with myopia of between 6-9 dpt during puberty reach retirement age without disabling visual loss.

[Prevention of myopia]. / Prävention der Myopie.

To avoid complications of high myopia the best solution would be to prevent myopia development from the very beginning. Many studies have suggested that the frequently quoted myopia boom is related to changes in visual experiences during more demanding education and not due to changes in genetic factors. To avoid myopia development it would therefore be best to carry out a better control of visual experience of children. In this article new approaches are described to record and improve visual habits in children, e.g. new sensors attached to the spectacle frames to document brightness, reading distance and reading duration, changes in text contrast polarity during reading, potential role of smartphones and some not yet fully explored orally applied substances to inhibit myopia.

Light- and focus-dependent expression of the transcription factor ZENK in the chick retina.

Ocular growth and refraction are regulated by visual processing in the retina. We identified candidate regulatory neurons by immunocytochemistry for immediate-early gene products, ZENK (zif268, Egr-1) and Fos, after appropriate visual stimulation. ZENK synthesis was enhanced by conditions that suppress ocular elongation (plus defocus, termination of form deprivation) and suppressed by conditions that enhance ocular elongation (minus defocus, form deprivation), particularly in glucagon-containing amacrine cells. Fos synthesis was enhanced by termination of visual deprivation, but not by defocus and not in glucagon-containing amacrine cells. We conclude that glucagon-containing amacrine cells respond differentially to the sign of defocus and may mediate lens-induced changes in ocular growth and refraction.

[Comparative analysis of light sensitivity, depth and motion perception in animals and humans]. / Vergleichende Betrachtung von Lichtempfindlichkeit, Tiefenwahrnehmung und Bewegungswahrnehmung bei Tier und Mensch.

BACKGROUND: This study examined how humans perform regarding light sensitivity, depth perception and motion vision in comparison to various animals. OBJECTIVE: The parameters that limit the performance of the visual system for these different functions were examined. METHODS: This study was based on literature studies (search in PubMed) and own results. RESULTS: Light sensitivity is limited by the brightness of the retinal image, which in turn is determined by the f­number of the eye. Furthermore, it is limited by photon noise, thermal decay of rhodopsin, noise in the phototransduction cascade and neuronal processing. In invertebrates, impressive optical tricks have been developed to increase the number of photons reaching the photoreceptors. Furthermore, the spontaneous decay of the photopigment is lower in invertebrates at the cost of higher energy consumption. For depth perception at close range, stereopsis is the most precise but is available only to a few vertebrates. In contrast, motion parallax is used by many species including vertebrates as well as invertebrates. In a few cases accommodation is used for depth measurements or chromatic aberration. In motion vision the temporal resolution of the eye is most important. The ficker fusion frequency correlates in vertebrates with metabolic turnover and body temperature but also has very high values in insects. Apart from that the flicker fusion frequency generally declines with increasing body weight. CONCLUSION: Compared to animals the performance of the visual system in humans is among the best regarding light sensitivity, is the best regarding depth resolution and in the middle range regarding motion resolution.

[Biological mechanisms of myopia]. / Biologische Mechanismen der Myopie.

Recent studies have confirmed that the prevalence of myopia has increased in most countries, that the increase must be due to environmental factors and that myopia is closely linked to the level of education. Extensive close-up work with short viewing distances, little outdoor activity and continuous exposure to low illumination are currently considered the major factors. It remains unknown how close-up work can stimulate eye growth. Animal models provide the possibility to manipulate visual experiences and to observe subsequent changes in eye growth. They have uncovered a number of unexpected aspects which have led to studies in children. When applied in low doses atropine (0.01 %) is effective against progression of myopia and shows no rebound effect after termination of the treatment, in contrast to treatment with previously used higher doses. While education cannot be limited in our society, there are now an increasing number of options to slow myopia progression so that high myopia is less frequently reached.

[Current recommendations for deceleration of myopia progression]. / Gegenwärtiger Stand der Empfehlungen zur Minderung von Myopieprogression.

BACKGROUND: Epidemiologic data demonstrate a rise in myopia prevalence. Therefore interventions to reduce the risk of myopia and its progression are needed and increasingly often asked for. METHODS: Systematic literature search via PubMed in MEDLINE. RESULTS: Myopia progression can be reduced by the following means which are listed according to their efficacy: (1) Atropine eye drops low dosed to avoid clinically relevant side effects, (2) optical means aiming at the correction of peripheral hyperopic defocus, e. g., multifocal contact lenses, and (3) increased daylight exposure. CONCLUSION: Daylight exposure reduces the risk of incident myopia. Children should be advised to spend sufficient time outdoors, especially before and in primary school. Myopia progression can be effectively attenuated by low-dose topical atropine and multifocal contact lenses.

Chick eyes under cycloplegia compensate for spectacle lenses despite six-hydroxy dopamine treatment.

PURPOSE: To test whether eye growth changes produced by spectacle lens wear are mediated by changes in ciliary muscle tonus in chicks. METHODS: Because there is evidence that deprivation myopia is based on a local-retinal mechanism in the eye that probably remains functional after cycloplegia as well as after ciliary ganglion or Edinger-Westphal lesions, none of these treatments provides insight into whether accommodation tonus is also important in the control of axial eye growth. Because 6-hydroxy dopamine (6-OHDA) suppresses deprivation myopia, to isolate growth changes mediated by accommodation the authors injected 6-OHDA and paralyzed accommodation in addition (by corneal application of vecuroniumbromide). To quantify the state of cycloplegia, the abnormal pecking responses of cyclopleged chickens were studied. RESULTS: The authors found that cycloplegia could be maintained for 3 hours daily by corneal application of vecuroniumbromide. To ensure that visual exposure was restricted to the time period of cycloplegia, chickens were transferred to a 3-hour light/21-hour dark cycle. Control experiments showed that emmetropization was still functional under the changed light cycle. Strikingly, even with suppressed local-retinal growth control mechanisms (as indicated by the lack of deprivation myopia in a 6-OHDA injected group of chickens with occluders) and paralysis of accommodation, the eyes compensated for the defocus imposed by spectacles by changing their axial growth rates to be similar to those of eyes with functional accommodation. CONCLUSIONS: The findings show that the ciliary muscle and the activity of the iris sphincter muscle are not involved in emmetropization in chicks. If accommodation mediates the growth effects with lenses, it must happen via another pathway. Based on previous results, the authors propose that either the choroidal nerves from the ciliary ganglion to the choroid are important or that another yet unknown pathway from the Edinger Westphal nucleus to the eye transmits the necessary information.

Changes in contrast sensitivity induced by defocus and their possible relations to emmetropization in the chicken.

PURPOSE: To test whether the level of contrast adaptation (CA) relates to refractive development in the chicken. (CA refers to a spatial frequency-selective increase of suprathreshold contrast sensitivity after exposure to low-contrast patterns). METHODS: CA was determined in individual chicks by comparing their optomotor gain in response to drifting low-contrast stripe patterns before and after treatment with spectacle lenses. The amount of CA was compared with the loss of contrast predicted from defocus at the tested spatial frequency. The reversion of CA and recovery from deprivation myopia were studied while the retinal image features were controlled by forcing the animals to watch spatially filtered digital video clips. RESULTS: CA was induced by wearing positive and negative lenses for 1.5 hours, both without and with cycloplegia, but was less pronounced in the case of positive lenses when accommodation was intact. The amount of CA at a tested spatial frequency was predicted from the loss of contrast calculated from the modulation transfer function for a defocused optical system. Watching low-pass-filtered video clips induced deprivation myopia and inhibited recovery from it. It also prevented the reversal of CA that was previously induced by deprivation. Both recovery from deprivation myopia and recovery from CA occurred with sharp video clips, although less so than with normal visual exposure. CONCLUSIONS: CA changes with retinal image sharpness and occurs even when accommodation is intact. Because CA correlates with myopia induced by frosted occluders, negative lenses, and low-pass-filtered video clips, and its reversal correlates with recovery from myopia, it is possible that shifts in CA may represent a signal related to refractive error development.

Changes in retinal and choroidal gene expression during development of refractive errors in chicks.

PURPOSE: During growth, the retina analyzes the projected image to achieve a close match between eye length and focal length. Because the messengers released by retina and choroid are largely unknown, genes that are differently expressed in response to changes in the retinal image were identified. In addition, because glucagon may be important in the visual control of eye growth, the transcript levels of proglucagon were studied. METHODS: Reverse transcription-polymerase chain reaction differential display was used to identify genes that were differentially expressed in chick eyes that were deprived of sharp vision or treated with positive or negative lenses. Differences were analyzed through sequencing and database searches and confirmed by Northern blot analyses. RESULTS: Combining 40 and 33 arbitrary primers with 3 oligo-dT-primers, approximately 48% and 40% of the retinal and choroidal mRNAs were screened, respectively. Twelve differences were detected in retinal tissue and five in choroidal tissue after 6 to 24 hours of exposure to defocus. Only one of 10 sequenced products could be identified as cytochrome-c oxidase, subunit I. Northern blot analysis confirmed its twofold upregulation after positive lens wear and also changes in four other unknown genes. Finally, it was shown that retinal glucagon mRNA content increased after treatment with positive lenses. CONCLUSIONS: Visual conditions that induce refractive errors produce changes in gene expression in retina and choroid within 1 day. In line with previous immunohistochemical data, it was found that the amount of glucagon mRNA was upregulated during wearing of positive lenses.

Melatonin and deprivation myopia in chickens.

Chicken eyes elongate and become myopic if they are covered with translucent diffusors which degrade the retinal image ('deprivation myopia'). Since it has been shown that dopamine D2/D4 receptors (which mediate inhibition of melatonin synthesis) are also implicated in deprivation myopia, we have studied the role of melatonin in the visual control of eye growth. We have found that (1) diurnal melatonin rhythms and melatonin content in the retina are unchanged during deprivation myopia development despite the breakdown of both diurnal growth rhythms of the eye and diurnal rhythms in retinal dopamine metabolism, (2) diurnal melatonin rhythms and melatonin content in the retina remain unchanged after application of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) and presumably also after 6-hydroxydopamine (6-OHDA) application which both have a suppressive effect on deprivation myopia and (3) deprivation myopia was slightly reduced in both eyes after unilateral intravitreal injection of melatonin, despite that deprivation myopia is based on a mechanism intrinsic to the eye. We conclude that melatonin is not involved in the retinal signaling pathway translating visual experience to deprivation myopia.

Developmental compensation of imposed astigmatism is not initiated by astigmatic accommodation in chickens.

PURPOSE: It is not clear whether emmetropization is confined to spherical refractive errors, or whether astiqmatic errors are also corrected via visual feedback. Experimental results from the animal model of the chicken are equivocal since compensation of imposed astimatic defocus was found in some but not all studies. Astigmatism could only be compensated by changes in the geometry of the cornea or lens. One has tested whether astigmatic spectacle lenses induce astigmatic accommodation as a possible first step of long-lasting compensation. METHODS: Thirty-five chickens were treated with cylinder lenses (+3/0D or -3/0D) for 5 h. Refractions were determined at 1.38 m distance without cycloplegia in hand-held chicks before attaching the lenses, with the lenses on (0 h), and after 3 and 5 h, and after removal of the lenses. Spheres (S), cylinders (C) and axes (A) were determined using infrared photoretinocopy in three axes (the 'PowerRefractor', equipped with a 135 mm lens). RESULTS: (1) The performance of the 'PowerRefractor' was tested in the chickens with trial lenses and gave correct refractions. (2) Astigmatic trial lenses induced refractive errors as expected from their powers in the case of +3/0D lenses: (S) +3.26 +/- 0.93D, (C) -3.45 +/- 0.87D). In the case of -3/0D lenses, slightly more hyperopic spheres were induced (refractions (S) +4.5 +/- 0.48D) but the cylinders were still as expected (-3.25 +/- 0.49D). The axes of astigmatism were correctly reproduced, since rotating the lenses changed the axes of the induced cylinders as expected. (3) Neither after 3 nor after 5 h of lens wear were there significant changes in the axes or the magnitude of astigmatism. Directly after removal of the lens, the refractions did not differ from their start-up values (with +3/0D lenses: (S) +3.31 +/- 1.05D vs. +3.22 +/- 0.76D, (C) -1.19 +/- 1.77D vs. -0.65 +/- 0.94D, (A) 96 +/- 49 vs. 113 +/- 45 deg; with -3/0D lenses: (S) 2.63 +/- 1.12D vs. 2.97 +/- 0.94D, (C) -1.11 +/- 1.15D vs. -0.53 +/- 0.56D, (A) 78 +/- 24 vs. 131 +/- 35 deg). CONCLUSIONS: The most intuitive mechanism for compensation of astigmatic refractive errors, astigmatic accommodation, could not be demonstrated in chickens. In light of this finding, it seems unlikely that a visually controlled mechanism is operating during development to reduced astigmatism by changing corneal or lenticular growth.

Barn owls have symmetrical accommodation in both eyes, but independent pupillary responses to light.

We have studied accommodation behaviour in the barn owl (Tyto alba). By defocussing one eye with various spectacle lenses and recording the refractive state in both eyes continuously during pecking, we found that the owls' accommodation was symmetrical in both eyes, with no regard to the power of the lens used. Even with no visual input to one eye, the amount of accommodation was always identical in both eyes. On the other hand, pupillary responses to light were independent. This finding differs from an earlier observation in the chicken, where both accommodation and pupillary responses were found to be independent. The result is discussed with regard to current knowledge on the central pathways for control of accommodation and pupillary responses in birds.

Local changes in eye growth induced by imposed local refractive error despite active accommodation.

We have tested whether defocus imposed on local retinal areas can produce local changes in eye growth, even if accommodation is available to clear part of the imposed defocus. Hemi-field lenses were attached to little leather hoods that were worn by young chickens from day 11-15 post-hatching. The lens segments defocused either the nasal or the temporal visual field, or covered the full field. We found that negative lenses (-7.5 D) were incompletely compensated in all three cases but caused significant myopia in the defocused parts of the visual field (differences to fellow eyes with normal vision: nasal visual field -3.13 +/- 1.56 D, P < 0.001; temporal visual field -4.02 +/- 1.38 D, P < 0.001; full field -3.82 +/- 2.48 D, P = 0.01). Myopia was not enhanced if the lenses covered the entire visual field. Positive lenses (+6.9 D) caused larger changes in refraction than negative lenses and, again, there was no significant difference in the amount of induced hyperopia in the nasal or temporal retina, or in the amount of hyperopia with full-field lenses (difference to fellow eyes with normal vision: nasal visual field +6.2 +/- 2.69 D, P < 0.001; temporal visual field +5.95 +/- 2.22 D, full field +7.22 +/- 2.44 D, P < 0.001). To compare the shapes of the excised eyes after lens treatment, we wrote a fully automated image processing program that traced their outlines in digitized video images. We found that the shapes of the eyes treated with positive lenses did scarcely differ from their fellow eyes with normal vision, indicating that hyperopia over this 4 day period was caused mostly by choroidal thickening. Full field negative lenses produced significant axial eye elongation; the effects of locally imposed defocus on eye shape were less conspicuous and were significant only in some areas. That local compensation of defocus was possible for both negative and positive lenses, suggests that the retina can recognize the sign of defocus without accommodation cues. Even more striking is that the presence of accommodation is apparently ignored since the drift in the plane of focus during accommodation does not disturb the compensation process. We re-analyze previous experimental results that argue for different mechanisms for deprivation myopia and lens-induced refractive errors. We propose that lens-induced refractive errors are compensated by similar retinal mechanisms as the ones proposed by Bartmann and Schaeffel [(1994). Vision Research, 34, pp. 873-876] to explain deprivation myopia. The proposed mechanisms can integrate with long time constants over the spatial frequency content in the retinal image while the viewing distances change, and control both choroidal thickening and scleral growth. However, it turns out that the compensation of imposed myopia cannot be explained if only one constant viewing is available. Apparently, there is more than a retinal blur detector to guide refractive development.

The growing eye: an autofocus system that works on very poor images.

It is unknown which retinal image features are analyzed to control axial eye growth and refractive development. On the other hand, identification of these features is fundamental for the understanding of visually acquired refractive errors. Cyclopleged chicks were individually kept in the center of a drum with only one viewing distance possible. Defocusing spectacle lenses were used to stimulate the retina with defined defocus of similar magnitude but different sign. If spatial frequency content and contrast were the only cues analyzed by the retina, all chicks should have become myopic. However, compensatory eye growth was still always in the right direction. The most likely cues for emmetropization, spatial frequency content and image contrast, do therefore not correlate with the elongation of the eye. Rather, the sign of defocus was extracted even from very poor images.

Long-term changes in retinal contrast sensitivity in chicks from frosted occluders and drugs: relations to myopia?

Experiments in animal models have shown that the retinal analyzes the image to identify the position of the plane of focus and fine-tunes the growth of the underlying sclera. It is fundamental to the understanding of the development of refractive errors to know which image features are processed. Since the position of the image plane fluctuates continuously with accommodative status and viewing distance, a meaningful control of refractive development can only occur by an averaging procedure with a long time constant. As a candidate for a retinal signal for enhanced eye growth and myopia we propose the level of contrast adaptation which varies with the average amount of defocus. Using a behavioural paradigm, we have found in chickens (1) that contrast adaptation (CA, here referred to as an increase in contrast sensitivity) occurs at low spatial frequencies (0.2 cyc/deg) already after 1.5 h of wearing frosted goggles which cause deprivation myopia, (2) that CA also occurs with negative lenses (-7.4D) and positive lenses (+6.9D) after 1.5 h, at least if accommodation is paralyzed and, (3) that CA occurs at a retinal level or has, at least, a retinal component. Furthermore, we have studied the effects of atropine and reserpine, which both suppress myopia development, on CA. Quisqualate, which causes retinal degeneration but leaves emmetropization functional, was also tested. We found that both atropine and reserpine increase contrast sensitivity to a level where no further CA could be induced by frosted goggles. Quisqualate increased only the variability of refractive development and of contrast sensitivity. Taken together, CA occurring during extended periods of defocus is a possible candidate for a retinal error signal for myopia development. However, the situation is complicated by the fact that there must be a second image processing mode generating a powerful inhibitory growth signal if the image is in front of the retina, even with poor images (Diether, S., & Schaeffel, F. (1999).

A simple mechanism for emmetropization without cues from accommodation or colour.

We propose and test the simple hypothesis that a chicken eye can emmetropize without cues derived from accommodation or colour just by maximizing retinal image contrast. Using different translucent occluders with known modulation transfer functions we found that deprivation myopia is correlated with the amount of image degradation. Equipped with a long-term integrator, a mechanism minimizing image degradation by changing the axial eye growth rate would therefore be sufficient to place the plane of focus of the eye at the average viewing distance.

Flicker parameters are different for suppression of myopia and hyperopia.

Axial eye growth rates in the chicken are controlled by local retinal image-processing circuits. These circuits quantify the loss of contrast for different spatial frequencies and promote axial eye growth rates in correlation with the amount of retinal image degradation ("deprivation myopia"). They also distinguish whether the plane of focus lies in front of or behind the retina. How the sign of defocus is detected still remains unclear. Cues from chromatic aberration are not important. In an attempt to isolate retinal circuits controlling the development of myopia or hyperopia, young chickens were raised in flickering light of different frequencies (12 and 6 Hz) and duty cycles (4-75%) produced by rotating chopper disks. The effects of flickering light on refractive errors and change in axial growth rates induced by translucent occluders or defocusing lenses were measured by infrared retinoscopy and A-scan ultrasound, respectively. Retinal electrical activity was evaluated by flicker ERG after matching flicker parameters and stimulation brightness at retinal surface. Changes in retinal and vitreal dopamine content caused by flicker in occluded and normal eyes were determined by HPLC-ECD. Strikingly, suppression of myopia occurred for similar flicker parameters, whether induced by translucent occluders ("deprivation") or negative lenses ("defocus"). The degree to which myopia was suppressed was correlated with the duration of flicker dark phase and with the ERG amplitude. In contrast, suppression of hyperopia did not correlate with these parameters. We conclude that two different retinal circuits with different temporal characteristics are involved in the processing of hyperopic defocus/deprivation and of myopic defocus, the first one dependent on flicker ERG amplitude. However, we did not find any correlation between the rate of dopamine release and the degree of inhibition of deprivation myopia in flickering light.

Properties of the feedback loops controlling eye growth and refractive state in the chicken.

Recent experiments in chickens provide evidence that axial eye growth and refractive state are guided by mechanisms sensitive to refractive error. To determine whether or not the sign of refractive error is derived from longitudinal chromatic aberration we raised chicks with spectacle lenses in monochromatic light. The eyes showed an appropriate growth response to correct for the defocus imposed by the lenses no different than in previous experiments in white light. Thus, in normally accommodating chicks chromatic cues are not necessary for emmetropization to occur. We examined the linearity of feedback loops controlling axial eye growth: positive spectacle lenses were found to inhibit axial growth very efficiently making the eyes shorter than normal whereas negative lenses had little effect on axial elongation: feedback loops for regulation of axial growth are highly nonlinear and act most efficiently on the myopic side. We found that, subsequent to a period of binocular deprivation of form vision, the refractive errors acquired are highly correlated in both eyes. Since both eyes grew without visual feedback we conclude that the gains in the feedback loops that control axial growth must be similar in both eyes. We suggest that the gains are genetically determined and are typical for each individual. Chicks made near-sighted in both eyes by "deprivation of form vision" were corrected by appropriate negative lenses. Three out of five chicks recovered from myopia despite the correction. Also two chicks that were made near-sighted in one eye recovered with no regard to the correcting lens. Three chicks remained more myopic than the correcting lens required and finally started to recover while the lens was still in place. Two out of three chicks that were made far-sighted showed recovery despite appropriate correction by positive lenses. We conclude that there must be a nonvisual mechanism highly sensitive to abnormal eye shape. During expt (4) we found unexpectedly that the development of form deprivation myopia is inhibited if no part of the retina in an animal is exposed to normal visual experience. The result indicates that some communication between both eyes exists, although form deprivation myopia itself has been shown to develop independently in both eyes.

Natural accommodation in the growing chicken.

A new technique, Infrared Photoretinoscopy, has been employed for recording natural accommodation in the chicken. The illumination of the pupil by the fundus reflection of infrared light provided by high output light emitting diodes (I.R. LED's) was monitored on a video screen. The defocus of the eye could be calculated by evaluating the fraction of the pupil which was illuminated. It was found that: in the chick the full range of accommodation (about 17D) is present in the first day after hatching, accommodation acts completely independently in both eyes, the "near pupillary response" is weaker in younger chicks, the pupil constriction in response to light starts at higher luminance in the younger chicks the developmental decrease of the f/number is not sufficient to explain the change of the pupil reaction to light. Problems resulting from the use of drugs in order to measure the refractive state using normal retinoscopy are discussed.

Studies on the role of the retinal dopamine/melatonin system in experimental refractive errors in chickens.

We have found that development of both deprivation-induced and lens-induced refractive errors in chickens implicates changes of the diurnal growth rhythms in the eye (Fig. 1). Because the major diurnal oscillator in the eye is expressed by the retinal dopamine/melatonin system, effects of drugs were studied that change retinal dopamine and/or serotonin levels. Vehicle-injected and drug-injected eyes treated with either translucent occluders or lenses were compared to focus on visual growth mechanisms. Retinal biogenic amine levels were measured at the end of each experiment by HPLC with electrochemical detection. For reserpine (which was most extensively studied) electroretinograms were recorded to test retinal function [Fig. 3 (C)] and catecholaminergic and serotonergic retinal neurons were observed by immunohistochemical labelling [Fig. 3(D)]. Deprivation myopia was readily altered by a single intravitreal injection of drugs that affected retinal dopamine or serotonin levels; reserpine which depleted both serotonin and dopamine stores blocked deprivation myopia very efficiently [Fig. 3(A)], whereas 5,7-dihydroxy-tryptamine (5,7-DHT), sulpiride, melatonin and Sch23390 could enhance deprivation myopia (Table 1, Fig. 5). In contrast to other procedures that were previously employed to block deprivation myopia (6-OHDA injections or continuous light) and which had no significant effect on lens-induced refractive errors, reserpine also affected lens-induced changes in eye growth. At lower doses, the effect was selective for negative lenses (Fig. 4). We found that the individual retinal dopamine levels were very variable among individuals but were correlated in both eyes of an animal; a similar variability was previously found with regard to deprivation myopia. To test a hypothesis raised by Li, Schaeffel, Kohler and Zrenner [(1992) Visual Neuroscience, 9, 483-492] that individual dopamine levels might determine the susceptibility to deprivation myopia, refractive errors were correlated with dopamine levels in occluded and untreated eyes of monocularly deprived chickens (Fig. 6). The hypothesis was rejected. Although it has been previously found that the static retinal tissue levels of dopamine are not altered by lens treatment, subtle changes in the ratio of DOPAC to dopamine were detected in the present study. The result indicates that retinal dopamine might be implicated also in lens-induced growth changes. Surprisingly, the changes were in the opposite direction for deprivation and negative lenses although both produce myopia. Currently, there is evidence that deprivation-induced and lens-induced refractive errors in chicks are produced by different mechanisms. However, findings (1), (3) and (5) suggest that there may also be common features. Although it has not yet been resolved how both mechanisms merge to produce the appropriate axial eye growth rates, we propose a scheme (Fig. 7).