Topic
Inner nuclear layer
About: Inner nuclear layer is a research topic. Over the lifetime, 1722 publications have been published within this topic receiving 74180 citations.
Papers published on a yearly basis
1 / 2
Papers
TL;DR: It is proposed that hypoxia caused by the onset of neuronal activity is detected by strategically located populations of neuroglia, first astrocytes, then Muller cells, and in response they secrete VEGF, inducing formation of the superficial and deep layers of retinal vessels, respectively.
Abstract: We have studied the role of the hypoxia-inducible angiogenic growth factor vascular endothelial growth factor (VEGF) in the induction and control of vessel growth in the developing retina of rats and cats, using in situ hybridization techniques. VEGF is expressed successively in two layers of neural retina, the innermost (axon) layer and the inner nuclear layer (INL). In the axon layer, VEGF is expressed transiently by astrocytes as they spread across the layer, closely preceding the formation of superficial vessels. In the INL, VEGF is expressed transiently by somas at the middle of the layer (presumably Muller cells), closely preceding the formation of the deep layer of retinal vessels. We propose that hypoxia caused by the onset of neuronal activity is detected by strategically located populations of neuroglia, first astrocytes, then Muller cells. In response they secrete VEGF, inducing formation of the superficial and deep layers of retinal vessels, respectively. As the vessels become patent, they relieve the hypoxic stimulus, so vessel formation is matched to oxygen demand. This hypothesis was tested experimentally in three ways. Expression of the high affinity flk-1 receptor for VEGF was demonstrated in newly formed retinal vessels, confirming that the secreted VEGF acts on the vessels, in a paracrine fashion. Direct hypoxic regulation of VEGF expression by macroglia was demonstrated in primary cultures of astrocytes and in cells of a glioma line. Hypoxic regulation of VEGF expression in the intact developing retina was demonstrated by showing that oxygen-enriched atmospheres that inhibit vessel formation also suppress endogenous VEGF production.
1,064 citations
TL;DR: Retinal remodeling is not plasticity, but represents the invocation of mechanisms resembling developmental and CNS plasticities and together, neuronal remodeling and the formation of the glial seal may abrogate many cellular and bionic rescue strategies.
861 citations
TL;DR: This review summarizes the main functional relationships between retinal glial cells and neurons, presenting a general picture of the retina recently modified based on experimental observations.
717 citations
TL;DR: Evidence in this study suggests that in human age-related macular degeneration, RPE, photoreceptors, and inner nuclear layer cells die by apoptosis.
Abstract: Objective To investigate apoptosis in human age-related macular degeneration (AMD). Methods Postmortem retinas with AMD and normal retinas were studied by terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) to identify dying cells, and by immunocytochemistry with cell-specific antibodies to identify rods and cones. Sections were also labeled for Fas, a cell surface receptor that triggers apoptosis in other cell types. The maculas with AMD had geographic atrophy (GA) or exudative AMD. Results Maculas with AMD had statistically significant increases in TUNEL-positive cells in the inner choroid, retinal pigment epithelium (RPE), photoreceptors, and inner nuclear layers compared with normal retinas. In eyes with GA, TUNEL-positive rod and RPE cell nuclei were present near edges of RPE atrophy. Photoreceptors in the maculas of eyes with AMD were strongly Fas-positive, while normal photoreceptors were only weakly labeled. Conclusions Evidence in this study suggests that in human AMD, RPE, photoreceptors, and inner nuclear layer cells die by apoptosis. Most TUNEL-positive RPE and photoreceptor cells were at edges of atrophy, correlating with clinically observed expansion of atrophic areas with vision loss in patients with GA. Increased Fas labeling in AMD photoreceptors indicates that the Fas/Fas ligand system may be involved in photoreceptor apoptosis. This information is essential for developing rational therapy for AMD.
558 citations
TL;DR: Remodeling in human and rodent retinas is independent of the initial molecular targets of retinal degenerations, including defects in the retinal pigmented epithelium, rhodopsin, or downstream phototransduction elements, and suggests that the neural retina may be more plastic than previously believed.
Abstract: Many photoreceptor degenerations initially affect rods, secondarily leading to cone death. It has long been assumed that the surviving neural retina is largely resistant to this sensory deafferentation. New evidence from fast retinal degenerations reveals that subtle plasticities in neuronal form and connectivity emerge early in disease. By screening mature natural, transgenic, and knockout retinal degeneration models with computational molecular phenotyping, we have found an extended late phase of negative remodeling that radically changes retinal structure. Three major transformations emerge: 1) Muller cell hypertrophy and elaboration of a distal glial seal between retina and the choroid/retinal pigmented epithelium; 2) apparent neuronal migration along glial surfaces to ectopic sites; and 3) rewiring through evolution of complex neurite fascicles, new synaptic foci in the remnant inner nuclear layer, and new connections throughout the retina. Although some neurons die, survivors express molecular signatures characteristic of normal bipolar, amacrine, and ganglion cells. Remodeling in human and rodent retinas is independent of the initial molecular targets of retinal degenerations, including defects in the retinal pigmented epithelium, rhodopsin, or downstream phototransduction elements. Although remodeling may constrain therapeutic intervals for molecular, cellular, or bionic rescue, it suggests that the neural retina may be more plastic than previously believed.
492 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 6 |
| 2024 | 10 |
| 2023 | 30 |
| 2022 | 50 |
| 2021 | 29 |
| 2020 | 26 |