PURPOSE: To evaluate the morphological changes in Muller cells of an induced diabetic rat model with carbonic anhydrase histochemical staining. METHODS: Retinae of three normal rats and four streptozotocin-induced diabetic rats were used. The morphological changes in the Muller cells of these retinae were observed using enzyme histochemical staining. RESULTS: The numbers of positive staining Muller cells in diabetic rats retinae were significantly lower than those of the normal rats. In addition, the shape of the Muller cell bodies in the streptozotocin-induced diabetic rat model's retina changed from polygonal to abnormally flat. Furthermore, the staining of the Muller cells' segment in the outer nuclear layer of the diabetic rat's retinae were weaker, and some Muller cell segments were not stained at all. CONCLUSIONS: The numbers of Muller cells in diabetic rats' retinae were significantly lower than those of the normal rats. In addition, the features of Muller cell bodies of the diabetic rats were changed morphologically.
Animals ; Carbonic Anhydrases ; Ependymoglial Cells* ; Models, Animal ; Rats* ; Retina*

Retinal detachment was studied in a rabbit model of penetrating ocular injuries with retinal laceration. In experimental group, to study its effect on the prevention of retinal detachment, cryopexy was performed at the site of penetrating ocular injury. No retinal detachment was found when the injury was made in 3 mm radial incision from corneoscleral limbus. When the injury was extended to the equator of the globe, namely 6 mm radial incision from corneoscleral limbus, the incidence of retinal detachment was 35%. But when the incision was made circumferentially 6 mm through the retina near ora serrata ie, 3 mm from the limbus, the incidence was 65%. The higher incidence of retinal detachment following injuries located at the ora serrata is probably due to the involvement of the vitreous base. However, there was no significant difference in the incidence of retinal detachment between control and experimental groups. And the cryotherapy can release viable retinal pigment epithelial cells into the vitreous cavity which can cause proliferative vitreoretinopathy. Therefore, the cryotherapy should be limited in posterior penetraring ocular injuries. The histopathologic examination of proliferative vitreoretinopathy in rabbit eyes with posterior penetrating ocular injuries revealed Muller cells, fibroblast and retinal pigment epithelial cells as main cellular components. Through this experiment, cryopexy was proved to be little effect in prevention of retinal detachment in rabbit eyes with perforating eye injuries.
Cryotherapy ; Ependymoglial Cells ; Epithelial Cells ; Eye Injuries ; Fibroblasts ; Incidence ; Lacerations* ; Retina ; Retinal Detachment ; Retinaldehyde* ; Vitreoretinopathy, Proliferative

Our current understanding of the ultrastructure of the retina has been gained using transmis sion electron microscopy (TEM) of thin sections. Scanning electron microscopy was proven to be a very valuable adjunct to TEM in retinal research. The present study describes the surface features of the retina. The complex shape of Muller cells varies in different layers of the retina. The Muller cell processes surround the cell bodies in the ganglion cell Iayer and form a part of the inner limiting membrane. The external limiting membrane consists of tight junctions between the beginning of the photo receptors and the Muller cells. The Muller cells extend beyond the external limiting membrane to embrace the photoreceptors. The course of the fibers of the outer plexiform layer is almost parallel to the surface of the macula. The interphotoreceptor space has a reticular structure.
Ependymoglial Cells ; Ganglion Cysts ; Humans* ; Membranes ; Microscopy, Electron ; Microscopy, Electron, Scanning* ; Retina* ; Retinaldehyde ; Tight Junctions

PURPOSE: Vascular cells may not be the only cells affected by diabetes in the retina. In particular, b-wave abnormalities of the electroretinogram in diabetic patients with absentor minimal microangiopathy have suggested to possible dysfunction of Muller cells. METHODS: This study was performed to investigate the morphological changes of Muller cell in human diabetic retinopathy. Thirteen human retinas were obtained from donor eyes. These eyes were enucleated immediately after death. Five eyes were used as normal controls without specific medical history. Eight eyes were obtained from diabetes patients and four eyes of them had diabetic retinopathy in gross finding. RESULTS: In normal control group, Muller cells were observed in nerve fiber layer and inner nuclear layer of the retina. The Muller cells were found to have stained strong positive reaction and polygonal pattern. In the group of diabetic history without diabetic retinopathy, Muller cells had similar pattern with control group. But, in diabetic retinopathy, Muller cells had lightly positive pattern in inner nuclear layer and nuclei were oval, compared with polygonal shape in normal retina. CONCLUSIONS: These findings suggested that Muller cells might have functional and morphological changes in diabetic retinopathy, and these changes can induce the diabetic microvascular abnormalities.
Carbonic Anhydrases ; Diabetic Retinopathy* ; Ependymoglial Cells ; Humans* ; Nerve Fibers ; Retina ; Tissue Donors

PURPOSE: The histiogenesis of retinoblastoma, the most common intraocular malignancy of childhood, has been investigated from the early times. But in spite of this effort, its origin has been controversial. This study was performed to investigated the cell of origin for retinoblastoma using enzyme histomchemistry for carbonic anhydrase. METHODS: We obtained enucleated eye that was diagnosed as retinoblastoma and its section was stained for hematoxylin-eosin for diagnosis of retinoblastoma. We used enzyme histomchemistry for carbonic anhydrase distinguishing Muller's cells, red-and green-sensistive cones from neuro-retinal cells. RESULTS: They were disagnosed as relatively well-differentiated retinoblastoma by hematoxylin-eosin staining and composed of tumor cells with numerous rosette. Neither numeric nor morphologic changes of Muller cells that are suspected of malignant features in enzyme histochemistry for carbonic anhydrase was found. CONCLUSIONS: The cells of retinoblastoma were originated from the two layers, inner nuclear and ganglion cell layer. The enzyme histochemistry for carbonic anhydrase is the one of the useful methods to investigate the origin of retinoblastoma although more cases is needed to assess.
Carbonic Anhydrase I ; Carbonic Anhydrases ; Diagnosis ; Ependymoglial Cells ; Ganglion Cysts ; Retinoblastoma*

Carbonic anhydrase, an enzyme catalysing the reversible hydration of carbon dioxide, is present in the Muller cells.Because the enzyme is not present in other uroretinal cells in the retina, it can be used as a marker for Muller cells.Carbonic anhydrase activity was demonstrated bnzymehistochemically in human and rabbit Muller cells to know a relation of metabolic functions and carbonic anhydrase activity.Human retinas were obtained from donor eyes.The eyes were enucleated immediately after death forenzymatic activity. In human retina, heavy staining was found in the inner nuclear layer and nerve fiber layer, moderate staining in the outer nuclear layer and weak or no staining in the plexiform layers.In rabbit retina, heavy staining was found in the nerve fiber layer and nuclear layers and weak reaction in the two plexiform layers. These findings suggest that Muller cells may participate in CO2 homeostasis mechanism of carbonic anhydrase in the retina.
Carbon Dioxide ; Carbon* ; Carbonic Anhydrases ; Ependymoglial Cells ; Homeostasis ; Humans ; Metabolism ; Nerve Fibers ; Retina ; Tissue Donors

In the vertebrate retina, Müller cells are principal glial cells which stretch across the whole thickness of the retina and contact with the somata and processes of all retinal neurons, thus forming an anatomical and functional link between glial cells and retinal neurons. Numerous studies have shown that Müller cells express various neurotransmitter receptors, transporters, ion channels and enzymes that are relative to cellular activities. In addition, the cells also release factors, such as D-serine and glutamate etc., to regulate the neuron excitability. Therefore, retinal Müller cells may play more curious roles in addition to supporting the retinal neurons. The information exchange and interaction between Müller cells and neurons may regulate and maintain retinal neuronal functions. In the glaucomatous retina, Müller cells are reactivated (gliosis). Reactivated Müller cells undergo a variety of changes in cellular physiology, biochemistry and morphological features. Meanwhile, the reactivated Müller cells may produce and release cytotoxic factors, such as nitric oxide (NO), tumor necrosis factor-α (TNF-α), reactive oxygen species (ROS) and prostaglandin E2 (PGE2), thus involving in the induction of retinal ganglion cell apoptosis and death. Here, we reviewed the physiological properties of retinal Müller cells, and the functional changes of Müller cells in the glaucomatous retina.
Ependymoglial Cells ; pathology ; physiology ; Glaucoma ; physiopathology ; Humans ; Neurons ; physiology ; Retina ; cytology

Heterozygous loss-of-function variants of FOXP4 are associated with neurodevelopmental disorders (NDDs) that exhibit delayed speech development, intellectual disability, and congenital abnormalities. The etiology of NDDs is unclear. Here we found that FOXP4 and N-cadherin are expressed in the nuclei and apical end-feet of radial glial cells (RGCs), respectively, in the mouse neocortex during early gestation. Knockdown or dominant-negative inhibition of Foxp4 abolishes the apical condensation of N-cadherin in RGCs and the integrity of neuroepithelium in the ventricular zone (VZ). Inhibition of Foxp4 leads to impeded radial migration of cortical neurons and ectopic neurogenesis from the proliferating VZ. The ectopic differentiation and deficient migration disappear when N-cadherin is over-expressed in RGCs. The data indicate that Foxp4 is essential for N-cadherin-based adherens junctions, the loss of which leads to periventricular heterotopias. We hypothesize that FOXP4 variant-associated NDDs may be caused by disruption of the adherens junctions and malformation of the cerebral cortex.
Mice ; Animals ; Ependymoglial Cells/physiology* ; Cadherins ; Neurons/metabolism* ; Cerebral Cortex/metabolism* ; Cell Differentiation ; Cell Movement

PURPOSE: Blood vessels within the retina are surrounded by Muller cells, and it is known that Muller cells may be related with the pathogenesis of diabetic retinopathy based on this histologic structure. Argon laser photocoagulation is routinely performed in the treatment of diabetic retinopathy by inhibiting neovascularization and edema, but its mechanism remains unclear. Muller cell changes were demonstrated utilizing carbonic anhydrase immunohistochemical staining to know a relation between argon laser photocoagulation and the effect of Muller cells in the rabbit retina. METHODS: Author used 16 rabbit retinas which were obtained from 8 rabbits. Exposure time and spot size were kept 0.15 second and 500 microgram. 150~350 mW of power intensity was needed to produce moderate degree coagulation in rabbit retina. RESULTS: We observed retina and its histological changes at 1 week, 2 weeks, 3 weeks and 4 weeks after photocoagulation by using carbonic anhydrase staining. The differences in the morphological changes in Muller cells and retina layers were observed between moderate and severe degree coagulation. With severe degree coagulation, the loss of all the retinal layers was observed. On the other hand, with moderate degree coagulation, proliferated pigment epithelial cells and chorioretinal adhesion were observed with loss of photoreceptor and outer nuclear layer. Muller cells were observed by carbonic anhydrase staining with proliferated Muller cells with increased nuclei and proliferated process. CONCLUSIONS: These findings suggest that Muller cells might be important in the scar formation by argon laser photocoagulation and that the proliferaration of Muller cells play a certain role in the therapeutic mechanism.
Argon* ; Blood Vessels ; Carbonic Anhydrases ; Cicatrix ; Diabetic Retinopathy ; Edema ; Ependymoglial Cells ; Epithelial Cells ; Hand ; Light Coagulation* ; Rabbits ; Retina ; Retinaldehyde

Radial glial cells (RGCs) which function as neural stem cells are known to be non-excitable and their proliferation depends on the intracellular calcium (Ca²⁺) level. It has been well established that Inositol 1,4,5-trisphosphate (IP3)-mediated Ca²⁺ release and Ca²⁺ entry through various Ca²⁺ channels are involved in the proliferation of RGCs. Furthermore, RGCs line the ventricular wall and are exposed to a shear stress due to a physical contact with the cerebrospinal fluid (CSF). However, little is known about how the Ca²⁺ entry through mechanosensitive ion channels affects the proliferation of RGCs. Hence, we hypothesized that shear stress due to a flow of CSF boosts the proliferative potential of RGCs possibly via an activation of mechanosensitive Ca²⁺ channel during the embryonic brain development. Here, we developed a new microfluidic two-dimensional culture system to establish a link between the flow shear stress and the proliferative activity of cultured RGCs. Using this microfluidic device, we successfully visualized the artificial CSF and RGCs in direct contact and found a significant enhancement of proliferative capacity of RGCs in response to increased shear stress. To determine if there are any mechanosensitive ion channels involved, a mechanical stimulation by poking was given to individual RGCs. We found that a poking on radial glial cell induced an increase in intracellular Ca²⁺ level, which disappeared under the extracellular Ca²⁺-free condition. Our results suggest that the shear stress by CSF flow possibly activates mechanosensitive Ca²⁺ channels, which gives rise to a Ca²⁺ entry which enhances the proliferative capacity of RGCs.
Brain ; Calcium Channels* ; Calcium* ; Cerebrospinal Fluid ; Ependymoglial Cells* ; Inositol 1,4,5-Trisphosphate ; Ion Channels ; Lab-On-A-Chip Devices ; Microfluidics ; Neural Stem Cells