Anterior segment growth and peripheral neural pathways in chick.

PURPOSE: To learn if peripheral nerve pathways are necessary for corneal expansion and anterior segment growth under a 12-hr light:dark cycle or for the inhibition of corneal expansion under constant light rearing. METHODS: Recently hatched White Leghorn chicks under anesthesia received unilateral ciliary ganglionectomy (CGx), cranial cervical ganglionectomy (Sx), or section of the ophthalmic nerve (TGx), along with sham-operated and/or never-operated control cohorts. Chicks were reared postoperatively under either a 12-hr light:dark cycle or under constant light. After 2 weeks and with the chicks under anesthesia, corneal radii of curvature and diameters were obtained with a photokeratoscope, refractometry and A-scan ultrasonography were performed, and the axial and equatorial dimensions of enucleated eyes were measured with digital calipers. Corneal areas were calculated from corneal curvatures and diameters. RESULTS: Despite the rich peripheral innervation to the eye, the selective denervations performed here exerted remarkably limited effects on corneal expansion and anterior segment development in chicks reared under either lighting condition. Ophthalmic nerve section did reverse in large part the inhibition of equatorial expansion of the vitreous chamber occurring under constant light rearing. CONCLUSIONS: The ciliary, sympathetic, or ophthalmic peripheral nerve pathways to the eye are not required either for corneal expansion and anterior segment development under a 12-hr light:dark cycle or for the inhibition of corneal expansion under constant light rearing. The ocular sensory innervation may be a means for regulating vitreous cavity shape.

Local patterns of image degradation differentially affect refraction and eye shape in chick.

PURPOSE: To evaluate visual blur as a mechanism for modulating eye shape. METHODS: Chicks wore a unilateral full goggle or one of several goggles modified with apertures. After 2 weeks, eyes were measured with refractometry, ultrasound, and calipers, and three retinal regions were assayed for dopamine and DOPAC (3,4-dihydroxyphenylacetic acid). RESULTS: Goggled eyes were diffusely enlarged or enlarged predominantly along the axial dimension, depending on the goggle. Myopia developed under goggle types inducing primarily axial growth and under some of the goggles inducing diffuse eye expansion. Enlarged eyes remained emmetropic beneath other goggles that caused diffuse eye expansion. Reductions in retinal dopamine and DOPAC were proportional to the eye growth and refraction effects. CONCLUSIONS: Localized image degradation can cause myopia with predominantly axial expansion, myopia with more diffuse vitreous chamber expansion, or eye expansion without myopia. Robust expansion of the equatorial diameter alone was not observed. The associated alterations in retinal dopamine metabolism are consistent with a hypothesized role of dopaminergic amacrine cells in the visual regulation of eye growth. Besides refraction and overall size, visual blur can affect eye shape; but the goggle responses do not correspond to a simple summation of blur signals across the retina. Therefore, other mechanisms seemingly are needed to account for the full range of refractions and ocular shapes seen in chicks and, by analogy, in humans.

Emmetropisation under continuous but non-constant light in chicks.

It has been suggested that ambient lighting at night influences eye growth and might play a causal role in human myopia. To test this hypothesis, we reared newly hatched chicks under 12 hr light-dark or light-dim cycles with a light phase intensity of 1500 microW/cm(2) and variable dim phase intensities between 0.01 and 500 microW/cm(2). Other chicks were reared under constant light conditions with intensities between 1 and 1500 microW/cm(2). After three weeks, the chicks were examined by refractometry, ultrasound and caliper measurements of enucleated eyes. To relate ocular parameters with a retinal neurotransmitter likely involved in eye growth control, retinal and vitreal levels of dopamine and its principal metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), were measured by high performance liquid chromatography with electrochemical detection in the light, dark and dim phases. Diurnal fluctuations in axial length and choroidal thickness also were measured twice daily by partial coherence interferometry (PCI) in chicks under light-dark and the two brightest light-dim conditions. The eyes of chicks reared under most light-dim conditions had refractions and ocular dimensions comparable to those reared under light-dark conditions. At dim phase light intensities of 10 microW/cm(2) and above, the day-night changes in retinal dopamine metabolism were not observed. The daily fluctuations of axial length and choroidal thickness were altered with rearing under the two brightest dim light intensities, compared to the light-dark condition. Rearing under constant light with intensities ranging between 1 and 1500 microW/cm(2) produced a shallow anterior chamber and other eye alterations previously described for constant light rearing even though rearing under continuous light that fluctuated between these same intensities generally permitted normal eye growth. Thus, continuous but fluctuating light exerts different developmental effects on the eye than constant non-fluctuating light. Light-dim rearing may be more relevant to daily human light exposures than other laboratory lighting conditions and may provide an opportunity to study developmental interactions of visual quality (e.g. blur, defocus, etc.) and features of the light-dark cycle under conditions that perturb daily rhythms in dopamine metabolism and ocular dimensions. Such studies also could provide mechanistic insights into whether and how daily rhythms in retinal dopamine metabolism, axial length or choroidal thickness modulate refractive development.

GABA, experimental myopia, and ocular growth in chick.

PURPOSE: To learn whether gamma-aminobutyric acid (GABA) participates in retinal mechanisms that influence refractive development. METHODS: White leghorn chicks, some of which wore a unilateral goggle to induce myopia, received daily intravitreal injections of agonists or antagonists to the major GABA receptor subtypes. Eyes were studied with refractometry, ultrasound, and calipers. Retinas of other chicks wearing unilateral goggles were assayed for GABA content. RESULTS: Antagonists to GABA(A) or GABA(A0r) (formerly known as GABA(C)) receptors inhibited form-deprivation myopia. GABA(A) antagonists showed greater inhibition of myopic growth in the equatorial than the axial dimension. A GABA(A0r) antagonist displayed parallel inhibition in the axial and equatorial dimensions. A GABA(A0r) agonist but not GABA(A) agonists altered the myopic refraction of goggled eyes. GABA(B) receptor antagonists, more so than an agonist, also slowed development of myopia, inhibiting axial growth more effectively than equatorial expansion of goggled eyes. When administered to nongoggled eyes, GABA(A) or GABA(A0r) agonists or antagonists also altered eye growth, chiefly stimulating it. Only a GABA(A) agonist induced a myopic refraction. Several of these agents stimulated eye growth in the axial, but not the equatorial, dimension. Retinal GABA content was slightly reduced in goggled eyes. CONCLUSIONS: GABA(A), GABA(A0r), and GABA(B) receptors modulate eye growth and refractive development. The anatomic effects of these drugs reinforce the notion that eye shape and not just eye size is regulated. A retinal site of action is consistent with the known ocular localizations of GABA and its receptors and with the altered retinal biochemistry in form-deprived eyes.