N-methyl-D-aspartate-induced excitotoxicity in adult rat retina is antagonized by single systemic injection of MK-801

Intravitreal injection of N-methyl-D-aspartate (NMDA) produced a substantial damage to the adult rat retina that was largely restricted to inner retinal layers, including the ganglion cell layer (GCL), inner nuclear layer (INL), inner, and outer plexiform layers. This retinal damage was significantly reduced by a systemic injection of a low dose of MK-801 (0.5 mg/kg), a potent NMDA-receptor antagonist. This neuroprotection was dose dependent and was most effective when the antagonist was given 1 h before NMDA insult. An intraperitoneal injection of 0.5 mg/kg MK-801 provided a virtually complete protection to the retina to the NMDA-induced toxicity, as indicated quantitatively by the number of DiI-filled retinal ganglion cells, the number of cells in the GCL and INL that undergo DNA fragmentation, and the edematous changes in retinal thickness. A post-lesion administration of MK-801 was still able to provide an effective neuroprotective effect to the retina, but this protection was lost when MK-801 was given 4 h after NMDA exposure. The current results indicate a therapeutic potential of systemic application of MK-801 in protecting the adult rat retina from neurologic disorders related to excessive activation of NMDA receptors.     

The development of the retina of the albino rat

Morphogenesis of the retina of the Sprague-Dawley albino rat was studied by light microscopy from day 11 of gestation until 225 days after birth. A quantitative analysis during development of retinal volume, thickness of the entire neural retina and thickness of each of the retinal layers, both posteriorly and peripherally, was made. The results indicate that initially a single neuroblastic layer forms and continually thickens by mitosis at its outer border. The retinal layers then form in sequence, moving from the inner retinal border outward and always beginning posteriorly and then spreading peripherally. The transient layer of Chievitz does not appear. All adult layers are present by eight days after birth and each layer thins after reaching its maximal thickness. Total thickness of the retina excluding pigmented epithelium, is greatest on postnatal day 5, but retinal volume only reaches a peak on postnatal days 7 to 12. The nerve fiber, inner plexiform, outer plexiform and bacillary layers all continue to increase in thickness after the ganglion cell and inner and outer nuclear layers reach their maximal width and are beginning to become thinner.     

A two-compartment model of the human retina

PURPOSE: In this article we question a basic concept in retinal pathology, which views the retina as composed primarily of neural elements, in a single compartment. METHODS: We suggest an alternative approach, centering on the epithelial-glial elements of the retina, dividing the retina into two distinct compartments. The framework of these two compartments is composed of two epithelial-like monostratified cell layers facing each other by their apical surfaces. This model is in agreement with the embryological development of the retina. RESULTS: Each compartment is composed of a monostratified cell layer in which neural elements are embedded and each is supplied by a different blood supply. The inner compartment, also referred to as the Muller cell compartment, extends between the inner and outer limiting membranes. The outer, or RPE, compartment extends between the outer limiting and Bruch's membranes. The border between the two compartments is formed by the outer limiting membrane (OLM). One simplified example utilizing the two-compartment concept is as follows: inner compartment edema (inner blood-retinal barrier breakdown) may manifest as cystoid edema, but not as serous retinal detachment, while outer compartment edema (outer blood-retinal barrier breakdown) may manifest as serous retinal detachment but not as cystoid edema, as long as the integrity of the OLM is maintained. CONCLUSION: A two-compartment approach to the structure of the retina, centering on non-neural elements, may enhance our understanding of some retinal pathologies. Various retinal diseases, mainly of vascular origin, are limited to one of the two compartments.     

Labelling of retinal microglial cells following an intravenous injection of a fluorescent dye into rats of different ages

Retinal microglia were selectively and sequentially labelled in different layers of the retina of postnatal rats following a single intravenous injection of the fluorescent dye, rhodamine isothiocyanate (RhIc). The fluorescent cells were doubly immunostained with OX-42 and ED-1 antibodies that recognise complement type 3 (CR3) receptors and macrophage antigen, respectively. RhIc was first detected in the retinal blood vessels 5 min after injection. At 1 h, a variable number of microglia in the inner layers of the retina, namely, the nerve fibre and ganglion cell layers appeared to emit weak fluorescence. Labelled microglial cells in the inner nuclear and outer plexiform layers were not detected until 1 and 2 d had elapsed following RhIc injection. The number of labelled retinal microglia was progressively increased with time, peaking at 4 d after RhIc injection. The frequency of RhIc labelled cells also increased with age, with the largest number of cells occurring in 7-d-old rats but declined thereafter. In 11 d or older rats, RhIc was confined to the retinal blood vessels. It is concluded that when injected into the circulation, RhIc could readily gain access into the retina tissues due to an inefficient blood-retina barrier in early postnatal stages. It became impeded with maturation of the blood-retina barrier, which was established between 11 and 13 d of age. RhIc that inundated the retinal tissues was thoroughly sequestered by the resident microglial cells. It is therefore suggested that the latter could play a protective role against serum-derived substances that may be deleterious to the developing retina.     

Generation of retinal cells in the wallaby, Setonix brachyurus (quokka)

We have examined the generation of retinal cells in the wallaby, Setonix brachyurus (quokka). Animals received a single injection of tritiated thymidine between postnatal days 1-85 and retinae were examined at postnatal day 100. Retinae were sectioned, processed for autoradiography and stained with Cresyl Violet. Ganglion cells were labelled by injection of horseradish peroxidase into the optic tracts and primary visual centres. Other cells were classified according to their morphology and location. Retinal cell generation takes place in two phases. During the first phase, which concludes by postnatal day 30, cells destined to lie in all three cellular layers of the retina are produced. In the second phase, which starts by postnatal day 50, cell generation is almost entirely restricted to the inner and outer nuclear layers. Cells produced in the first phase are orthotopic and displaced ganglion cells, displaced and orthotopic amacrine cells, horizontal cells and cones. Glia in the ganglion cell layer, orthotopic amacrine cells, bipolar and horizontal cells. Muller glia, and rods are generated in the second phase. Cells became heavily labelled with tritiated thymidine in the central retina before postnatal day 7, over the entire retina (panretinal) by postnatal day 7 and from postnatal day 18, only in the periphery. The second phase of cell generation is initiated at P50, in a region extending from the optic nerve head to mid-temporal retina. Subsequently, cells are generated in annuli, centred on mid-temporal retina, which are seen at progressively more peripheral locations. Therefore, cell addition to the inner and outer nuclear layers continues for longer in peripheral than in mid-temporal retina. We suggest that such later differential cell addition to the inner and outer nuclear layers contributes to an asymmetric increase in retinal area. This non-uniform growth presumably results in more expansion of the ganglion cell layer peripherally than in mid-temporal retina and may play a role in establishing density gradients of ganglion cells.     

Histopathologic and ultrastructural findings of photocoagulation lesions produced by transpupillary diode laser in the rabbit retina.

Transpupillary retinal photocoagulations were performed on ten eyes of five pigmented rabbits using a diode laser (Nidek Co., LTD, Aichi, Japan) emitting infrared radiation at 800 nm wavelength. A histological and an ultrastructural study on the treated eyes were done at 1, 3, 5, and 7 days after retinal photocoagulations. The purpose of this study was to observe the sequential changes in the retina and the choroid following transpupillary diode laser retinal photocoagulations at the parameters of laser power which produced a grayish white retinal discoloration with distinct white center. It seemed that the lesion was grade 3 retinal photocoagulation by Tso et al''s classification. It appeared that the parameters necessary to produce grade 3 photocoagulation lesions were 160 mW power, and 0.2 second duration at 200 microns size. In general, with an agreement to other reports, histologic study of the diode laser lesions showed that the outer retina was damaged more severely than the inner retina. However, on day 1 after laser treatment, the alterations were more profound in the inner retina than in the outer retina and an occasional swelling of the axons in the nerve fiber layer was observed on the ultrastructural study. The results observed have not been found in other previous studies and suggest that the inner retina might be injured directly by 800 nm wavelength diode laser radiations. Thus we could conclude that 800 nm wavelength diode radiation might be absorbed by melanin pigment and also by other chromophores contained in inner retinal tissues. Further studies must follow to verify the laser-tissue interactions in diode laser retinal photocoagulations.     

Retinal response of Macaca mulatta to picosecond laser pulses of varying energy and spot size

We investigate the relationship between the laser beam at the retina (spot size) and the extent of retinal injury from single ultrashort laser pulses. From previous studies it is believed that the retinal effect of single 3-ps laser pulses should vary in extent and location, depending on the occurrence of laser-induced breakdown (LIB) at the site of laser delivery. Single 3-ps pulses of 580-nm laser energy are delivered over a range of spot sizes to the retina of Macaca mulatta. The retinal response is captured sequentially with optical coherence tomography (OCT). The in vivo OCT images and the extent of pathology on final microscopic sections of the laser site are compared. With delivery of a laser pulse with peak irradiance greater than that required for LIB, OCT and light micrographs demonstrate inner retinal injury with many intraretinal and/or vitreous hemorrhages. In contrast, broad outer retinal injury with minimal to no choriocapillaris effect is seen after delivery of laser pulses to a larger retinal area (60 to 300 microm diam) when peak irradiance is less than that required for LIB. The broader lesions extend into the inner retina when higher energy delivery produces intraretinal injury. Microscopic examination of stained fixed tissues provide better resolution of retinal morphology than OCT. OCT provides less resolution but could be guided over an in vivo, visible retinal lesion for repeated sampling over time during the evolution of the lesion formation. For 3-ps visible wavelength laser pulses, varying the spot size and laser energy directly affects the extent of retinal injury. This again is believed to be partly due to the onset of LIB, as seen in previous studies. Spot-size dependence should be considered when comparing studies of retinal effects or when pursuing a specific retinal effect from ultrashort laser pulses.     

人胎视网膜发生的光镜和电镜观察

本文在光镜下观察40例人胎视网膜的发生,在电镜下观察15例人胎视网膜视细胞、双极细胞、节细胞的发育。结果表明:胚胎第9周时神经上皮可分内、外成神经细胞层。第10周时内、外成神经细胞层之间的Chievitz带消失;第11周时节细胞从内成神经细胞层内迁;第13周节细胞与内成神经细胞之间出现内网层;第16周始双极细胞从外成神经细胞层中内迁形成外网层和内核层。第20周后视网膜各层形成。而视细胞、双极细胞、节细胞的超微结构于胎儿8个月后才发育完善。其结构与成人基本相同。     

高血压大鼠视网膜溶酶体酶组织化学研究

目的：探讨溶酶体酶在高血压视网膜网变发生过程中的作用。方法：应用光镜定量酶组织化学方法对ＷＫＹ大鼠和自发性高血压大鼠视网膜原酸性磷酸的分布和活性变化进行定量观察。结果：视网膜各层酸性磷酸酶活性岂强到弱依次是（Ｆ检验，Ｐ〈０．０５）；（１）色素上皮层；（２）视杆维层内节和外网层（两层间活性无显著性差异）；（３）内网层；（４）节细胞层和神经纤维层，（５）外核层和内核层（两层间活性无显著性差异）杆锥层外     

基于光学相干层析的视网膜图像分割

利用光学相干层析（optical coherence tomography,OCT）技术可以得到清晰的视网膜层状结构,实现视网膜层状结构自动分割功能是解决OCT技术应用于视网膜疾病诊断的一项基础问题。本文通过图像平滑、峰值探测、Snake模型、贪婪算法和样条插值等综合技术,对OCT视网膜图像进行分割,自动提取层状结构轮廓并获取视网膜厚度分布图。将以上算法应用于24例正常人眼底图像,并与专家手动标记轮廓提取的厚度相比,结果证实上述视网膜自动测量算法与专家人工标记取得较好一致性。本文提出的测量算法有望应用于视网膜变异性评估。     

Light-induced retinal damage involves tyrosine 33 phosphorylation, mitochondrial and nuclear translocation of WW domain-containing oxidoreductase in vivo

WW domain-containing oxidoreductase WOX1, also named WWOX or FOR, is a known proapoptotic protein and a candidate tumor suppressor. Stress stimuli activate WOX1 via tyrosine 33 (Tyr33) phosphorylation and translocation to the mitochondria and nuclei in vitro. Here, the potential role of WOX1 in light-induced retinal degeneration in vivo was investigated. WOX1 is expressed primarily in the inner retina at perinatal stages, whereas an enhanced expression of WOX1, along with its Tyr33 phosphorylation (p-WOX1), is shown specifically in the retinal ganglion cells in adults. Prolonged exposure of mature rats to constant, low-intensity light (500 lux) for 1-2 months resulted in substantial death of photoreceptors and the presence of activated microglia, astrocytes and Muller glial in the outer retina. However, the inner retina was not or barely affected. In the damaged inner and outer nuclear layers of rat retina, WOX1 and p-WOX1 were overly expressed. Also, WOX1 colocalized with fragments of opsin-positive cones. In rd mice with an inherited retinal deficiency, upregulation of WOX1 and p-WOX1 in degenerated retina was observed with age. By electron microscopy, a large number of immunogold particles of WOX1 and p-WOX1 were found in the damaged mitochondria and condensed nuclei of degenerating photoreceptors, indicating that WOX1 undergoes activation and translocation to these organelles. In contrast, little or no WOX1-positive particles were found in the Golgi apparatus. In conclusion, activated WOX1 is likely to exert apoptosis of neuronal cells in the outer retina during the light-induced injury and in mice with an inherited retinal defect.     

An ultrastructural analysis of the development of foetal rat retina transplanted to the occipital cortex, a site lacking appropriate target neurons for optic fibres

Summary Foetal retina was removed from donor rats at 15 days of gestation and transplanted to the occipital cortex of neonatal host rats. The purpose of this procedure was to examine the development of retinal neurons and photoreceptors, and document synaptic patterns during maturation of the transplanted retina in an environment lacking a normal target for optic axons. Host animals were sacrificed at 5, 10, 15, 20 and 30 days and samples of cortex containing the transplant were subjected to a light and electron microscopic analysis. During early stages of development, (5 days) the retina assumes a radial orientation with the scleral (outer) surface located centrally and the vitreal (inner) surface occupying the periphery. Numerous mitotic figures are found at the centre of the transplant and columns of primitive neuroblasts appear to radiate out from this zone. By 10 to 15 days after transplantation the retinal tissue contains numerous small rosettes each of which displays a histotypic organization with recognizable layers of sensory cells and their centrally-projecting processes, an outer limiting membrane, made up of a network of zonulae adherentes, and a rudimentary outer and inner plexiform layer which delineate the cells of the inner nuclear layer. Ultrastructural analysis of such rosettes confirmed the presence of typical bipolar, amacrine, horizontal and ganglion cells, but revealed that while the plexiform layers were occupied by numerous processes from these neurons, few if any, of these exhibited synaptic vesicles.By 20 to 30 days following transplantation sensory cells have completely differentiated, giving rise to prominent inner and outer segments which display typical cilia, centrioles and basal bodies, together with numerous stacked lamellae of photoreceptors which were contorted, presumably due to growth in an abnormal site. It should be further emphasized that these structures developed in the absence of pigment cells. Synaptic development ensues during this period to form characteristic dyads within the outer and inner plexiform layers. Additionally, clusters of amacrine to amacrine contacts occurred in the inner plexiform layer and were found to be increased relative to other types of junctions. In general, synaptogenesis takes place in the outer and inner plexiform layers and all categories of retinal synapses are established, but the process was found to be significantly delayed in comparison to normal retina at the same stage of development.Quantitative analysis revealed a reduced number of presumptive ganglion cells in proportion to the other categories of neurons. Optic fibres remained small and failed to myelinate. It is suggested that lack of an appropriate target for optic axons induced this alteration and may be indirectly related to the delay in the onset of synaptic development.     

Rhodopsin和S-opsin在MNU诱导的大鼠视网膜损伤过程中的表达变化

目的:观察在N-甲基-N亚硝酸脲(MNU)诱导的大鼠视网膜外核层细胞损伤过程中视紫质(rhodopsin)和蓝光视蛋白(blue-sensitive opsin/S-opsin)在视网膜中的表达变化,分析其与MNU诱导的视网膜损伤的关系。方法:将30只SPF级50 d龄雌性SD大鼠随机分为正常对照组和MNU模型1、3、7、10 d组,每组各6只大鼠。模型组以腹腔注射MNU(40 mg/kg)建立MNU模型;正常对照组大鼠腹腔注射生理盐水(5 mL/kg)。右眼冰冻切片行苏木素-伊红(HE)染色判断视网膜损伤程度。通过逆转录-聚合酶链反应(RT-PCR)和免疫荧光检测各组视网膜中rhodopsin和S-opsin的mRNA及蛋白表达情况。结果:病理检测确定造模结果与以往实验一致,各组病理分级之间的差异显著(2=16.838,P0.01)。RT-PCR检测结果表明,与正常对照组相比,各MNU模型组rhodopsin和S-opsin的mRNA表达水平随MNU作用时间增加而逐渐降低且差异均显著(rhodopsin 1 d组P0.05;S-opsin 1 d组P0.01;3、7、10 d组rhodopsin和S-opsin均P0.01)。免疫荧光检测结果显示,在正常大鼠视网膜rhodopsin主要在光感受器细胞外段表达,MNU作用后rhodopsin主要在外核层表达,少量在内核层表达,并随MNU作用时间增加而逐渐表达降低。S-opsin在正常视网膜各层均有表达,在各模型组随MNU作用时间增加S-opsin的表达逐渐降低,在外核层和光感受器细胞内、外段尤为明显。结论:MNU诱导的视网膜外核层细胞损伤可降低rhodopsin和S-opsin的表达,并与MNU选择性引起光感受器细胞丧失有关。     

Cytochrome oxidase activity in the rat retina following unilateral thalamic lesion

The present study has investigated the cytochrome oxidase (CO) activity in retinas of normal rats and rats which received central lesions at birth or young adult stage. The results show that a thalamic lesion which injured the retinal ganglion cell axons in young adult rats led to severe loss of CO activity in the ganglion, inner and outer plexiform layers in the retina contralateral to the lesion as compared to those of normal rats. In contrast, distinct CO-reactive bands and cells were clearly observed in corresponding laminae in retinas in which almost the entire population of retinal ganglion cells was eliminated by a neonatal thalamic lesion. These results indicate that retinal ganglion cells contribute significantly to the CO activity observed in the inner retinal laminae under normal but not under abnormal conditions, and suggest that considerable changes in the activity of the remaining neurons and possibly reorganization of neural circuitry within the retina in rats which received neonatal lesions has taken place, as revealed by CO histochemistry.     

Ocular development in the oman shark, Iago omanensis (Triakidae), Gulf of Aqaba, Red Sea

Ocular ontogenesis was studied in embryos of the placental viviparous shark, Iago omanensis, abundant in the Gulf of Aqaba, Red Sea, at depths of 150-1500 meters. Samples of gravid females were collected bi-monthly, and their embryos extracted. The eyes of 220 of those embryos of various dimensions were dissected and routinely prepared for histological and electron microscopic studies. The initial signs of eyes appear in embryos of 8 mm total length (TL). The primordial zone of germinal neural cells appears in 12 mmTL embryos and at 26 mm separation of the visual layer of the retina and the plexiform layers is initiated. From this stage on until 60 mmTL the nuclear and plexiform parts of the retina continue to develop and outer segments of the visual cells begin to form. Concomitant with ripening of the inner and outer plexiform layers, the tapetal layers of melanocytes and tapetal platelets of reflecting guanine also begin to ripen. The tapetum in Iago is of the cellular type. In embryos of 140-145 mmTL (6-7 months old), as they approach term, the visual cells, their synaptic connections and the intermediate cell types of the retina are all full developed. The melanocytes, rich in pigmentation, and sacs of tapetal platelets, penetrate deeply between the lamellated outer segments of the visual cells. Data are provided on growth parameters of the retinal cell layers and growth of the eyes during embryonic development. According to the position of the nuclei of the visual cells, the retina of Iago appears to be duplex, with rods and cones.     

Functional neuroarchitecture of the retina: hypothesis on the dysfunction of retinal dopaminergic circuitry in Parkinson's disease

Recent morphologic and functional techniques for the study of nerve cells, such as intracellular injection and neurotransmitter immunohistochemistry, allow a new approach to the functional architecture of the retinal circuitry. Two types of dopaminergic cells are described: amacrine cells and interplexiform cells. These latter cells, which send processes to both the inner and outer plexiform layers, form a feedback loop acting at the level of horizontal cell coupling. Two molecules localized in such cells, dopamine and GABA, have antagonistic effects on horizontal cell coupling and regulate the diameter of their receptive fields which code for contrast. Changes in the ERG, VEPs and contrast sensitivity occur in Parkinsonian patients and are identical to those observed in animal models whose dopaminergic retinal system has been destroyed, thus suggesting a degenerative process of this system in Parkinson's disease. The observation of dopamine neurons, labelled by their tyrosine hydroxylase immunoreactivity, in the retina of 5 patients, led to the observation of reduced dopamine innervation in the central retina of Parkinsonian patients.     

Retinal development in the lamprey (Petromyzon marinus L.): Premetamorphic ammocoete eye

Development of the retina of the ammocoete begins early in embryogenesis, with the formation of the optic vesicle, but development of the rudimentary eye is suspended and remains arrested during larval life. Prior to the onset of metamorphosis, the retina of the ammocoete is completely undifferentiated, with the exception of a small area (Zone II) surrounding the optic nerve head, where all of the adult retinal layers are found. The photoreceptors in this area have developed to include synaptic contacts as well as inner and outer segments. The pigment epithelium in this area, too, has differentiated to include well-formed melanin granules, myeloid bodies and endoplasmic reticulum and is closely associated with the receptor cell outer segments. With the approach of metamorphosis, differentiation of the remainder of the retina (Zone I) begins, taking place in a radial fashion from the optic nerve head. Differentiating pigment epithelial cells adjacent to the differentiated retinal zone begin to accumulate melanin granules. In the neural retina, junctional complexes are established in the form of an external limiting membrane, and connecting cilia project into the optic ventricle. Photoreceptor differentiation begins with the formation of a mitochondria-filled ellipsoid within the inner segment. Development and differentiation of the ammocoete retina is unique to vertebrates in that only a small area of differentiated retina is present during the larval stage. The remainder of the retina differentiates and becomes functional during metamorphosis.     

Retinal degeneration in experimental Creutzfeldt-Jakob disease

Mice with experimental Creutzfeldt-Jakob disease (CJD) develop a progressive retinal degeneration after a prolonged incubation period. Sections of the eyes stained with hematoxylin and eosin revealed pathologic changes in the optic nerve and a marked degeneration of photoreceptor cell inner and outer segment areas. Both peripheral and central retina, normally 10 cells thick, were reduced to one photoreceptor cell or less in thickness. Ultrastructural analysis revealed total loss of outer segment and most inner segment elements. Only Müller cell microvilli and macrophages remained in the subretinal space. Macrophages were also visible in the remnant photoreceptor cell layer. The inner nuclear layer and pigment epithelial cell layers appeared normal. Müller cell hypertrophy was evident but was not accompanied by spongiform vacuolation. Several of the degenerative changes of the eye in mice with experimental Creutzfeldt-Jakob disease differ from those observed for scrapie in rodents. The pathologic similarities between the retinal degenerations occurring in mice with experimental Creutzfeldt-Jakob disease and those found in some forms of human retinal degeneration are provocative. These similarities raise the question whether or not other retinal degenerative diseases might be caused by infectious agents such as prions or slow viruses.     

Lectin binding to the human retina

Formalin-fixed, paraffin-embedded tissue sections of the human retina were stained with different fluorescein isothiocyanate-conjugated lectins. The lectins used were concanavalin A (Con A), Triticum vulgaris (WGA), glycine maximum (SBA), Dolichos biflorus (DBA), Ulex europaeus (UEA I), Arachis hypogaea (PNA), and Ricinus communis (RCA I). Con A stained both the inner and outer segments of the rods and cones, whereas WGA stained the inner and outer segments of the rods and the outer segments of the cones. PNA selectively stained only the inner segments of the cones. In addition, Con A and WGA stained neuron cytoplasm and nerve fibers in different layers of the retina. The results obtained differ in some important aspects from those previously obtained in the frog and monkey retina; this finding may be due to species differences. The results of lectin staining in the normal human retina may form the basis for future studies of retinal diseases.     

Ultramicroscopical immunolocalization of PAX6 in the adult chicken retina

Cell type-specific PAX6 protein expression was examined in all retinal layers of the normal chicken retina. The most intense PAX6 immunostaining was found in the ganglion cell and inner nuclear layers, and in lower amounts in the optic nerve fiber, the inner plexiform and the photoreceptor layers. PAX6 immunostaining was variable in terms of its subcellular localization, even within one cell. PAX6 immunostaining was mainly localized in nuclear heterochromatin of the ganglion cell and inner nuclear layers whereas in the outer nuclear layer, PAX6 immunostaining was only observed in the intercellular space and the cytoplasm. In photoreceptors, the myoid portion of the inner segment showed PAX6 immunostaining, but the ellipsoid portion and the outer segment did not. The ultrastructural distribution pattern of PAX6 in the adult chicken retina suggests that normal expression of PAX6 is variable even in subcellular structures in the same cell type.