Wei Li, Chief and Senior Investigator at the National Eye Institute/National Institutes of Health, Retinal Neurophysiology Section will be delivering a seminar on “Living In The Cold – Hibernation And Retinal Neurobiology” on Wednesday, December 18th at 12:00 Noon in the Moran Eye Center auditorium.
Abstract: We are interested in understanding how the retina adapts to extreme metabolic conditions, such as those experienced by hibernating animals. We believe that metabolism is one of the core issues pertaining to the health and pathological change in the retina. By studying hibernating animals (the ground squirrel), we hope to identify strategies that can help the retina better cope with metabolic stresses that feature in retinal disease. In this presentation, I will discuss several adaptive features of the ground squirrel retina during hibernation.
A very cool paper was published in JAMA yesterday that is a result of Google Research asking if machine learning and computer vision could improve retinal fundoscopic examinations of patients with diabetic retinopathy. The outcome of course is increased patient screening for physicians with limited resources.
Vladimir Kefalov, Professor of Ophthalmology and Visual Sciences at Washington University in St. Louis will be delivering a seminar on “Calcium Homeostasis in Mammalian Rod and Cone Photoreceptors” on Wednesday, May 11th at 12:00 Noon in the Moran Eye Center auditorium.
Abstract: Calcium plays an important role in the function and health of photoreceptors. Calcium modulates the phototransduction cascade and controls the response sensitivity, response kinetics, and adaptation. Abnormal calcium homeostasis, associated with mutations in multiple phototransduction proteins, has also been suggested to cause retinal degeneration and blindness. This talk will present the results of our recent studies on the mechanisms for extruding calcium from mammalian photoreceptors. We have identified novel mechanisms for regulating calcium in both rods and cones. The implications of our findings for the function and survival of mammalian photoreceptors will also be addressed
Bruch’s membrane is a highly specialized and multi-laminar structure in our retinas that forms the basis for mediating interactions between the retinal pigment epithelium and blood flow from the choroid. I’ve not seen many good images online, so figured this image from mouse would be a good addition showing the relationship of the basal surface of the RPE with Bruch’s membrane.
This is a 58 year old white female with a retinal astrocytic hamartoma on her right optic nerve. Retinal astrocytic hamartomas are glial tumors of the retinal nerve fiber layer arising from retinal astrocytes.
This animated GIF file illustrates the height of the hamartoma and is another example of where animated gifs can be a fantastic teaching tool.
The left and right stereo images shown were taken with a Zeiss FF-4 Fundus camera by James Gilman of the Moran Eye Center.
We at Webvision would like to wish you the very best this holiday season. As in past years, we like to post an image from retinal science that is somehow evocative of the Holiday Season and this year, Gabe Luna from the Steve Fisher / Geoff Lewis laboratory delivers a stunning image of astrocytes in a retinal flat mount, but with a twist… We think you’ll be seeing more of Gabe’s beautiful imagery, but for now, here is his description of how he made this image:
“I used a GFAP-GFP mouse to identify all the astrocytes in the retina and manually (at the time it was manual) annotate their coordinates, then we used a probabilistic random-walk algorithm to go to each “cell center” and perform a segmentation result of that one astrocyte. Once all the 5,000 or so cells are segmented as a greyscale image of the individual cell, then they are assigned various hues that are spectrally distinct and the montage is re-assembled into one large image. The image there is a grossly down-sized image of the original. The original was a seamless mosaic of 412 individual z-stacks of about 15 planes at 1 micron intervals, using a 40x oil immersion lens.”
Abstract: Excessive light exposure is known to harm the retina and exacerbates disease progression in many retinal disorders. In addition, certain genetic mutations affec6ng components in the phototransduction cascade serve as a source of “equivalent light” and cause retinal degenera6on. How light exerts its harmful effect on the retina is not well understood. Mouse models can be used to isolate distinct light damage pathways. Dr. Chen will discuss recent findings on mechanisms of retinal damage caused by environmental and genetic sources of “equivalent light”.
We’ve talked about jumping spiders before here on Webvision as they are an amazing animal with very well developed vision. However, their retinas and visual pathways are very different from the vertebrate retinas in that they use image defocusing for depth perception rather than parallax like humans and other vertebrates do. Figuring out spider vision has been a long standing effort by a small group of scientists and one of the problems of observing spiders is figuring out how they scan. The movie above however shows a transparent jumping spider with the pigment cells in its eyes/retinas moving while they scan an image. There is another pretty impressive movie here, showing a microscopic view into the retina of a living jumping spider.
The Paul Kayser International Award in Retina Research was created by the Directors of Retina Research Foundation and endowed by the Trustees of The Kayser Foundation to honor and perpetuate the memory of long-time friend and dedicated benefactor of RRF, Paul Kayser. Through this award both organizations are demonstrating the conviction they shared with Mr. Kayser that blindness caused by retinal disease is a global concern and must be addressed accordingly. It is thus the purpose of this award to foster greater awareness of the need for intensive study of the retina, its role in the visual process, and the retinal diseases that threaten and/or destroy eyesight by recognizing outstanding achievement and sustaining meritorious scientific investigations worldwide.
Dr. Marc was chosen as the recipient of this award for his lifetime body of work in retinal research, discovering the structure and function of the retina through novel technologies and approaches that have pushed our understanding of the retina forward.
Purpose: Converging evidence suggests that large- and intermediate-scale neural networks throughout the nervous system exhibit small world’ design characterized by high local clustering of connections yet short path length between neuronal modules (Watts & Strogatz 1998 Nature; Sporns et al.2004 Trends in Cog Sci). It is suspected that this organizing principle scales to local networks (Ganmor et al. 2011 J Neurosci; Sporns 2006 BioSystems) but direct observation of synapses and local network topologies mediating small world design has not been achieved in any neuronal tissue. We sought direct evidence for synaptic and topological substrates that instantiate small world network architectures in the ON inner plexiform layer (IPL) of the rabbit retina. To test this we mined ≈ 200 ON cone bipolar cells (BCs) and ≈ 500 inhibitory amacrine cell (AC) processes in the ultrastructural rabbit retinal connectome (RC1).
Methods: BC networks in RC1 were annotated with the Viking viewer and explored via graph visualization of connectivity and 3D rendering (Anderson et al. 2011 J Microscopy). Small molecule signals embedded in RC1 e.g. GABA glycine and L-glutamate combined with morphological reconstruction and connectivity analysis allow for robust cell classification. MacNeil et al. (2004 J Comp Neurol) BC classification scheme used for clarity.
Results: Homocellular BC coupling (CBb3::CBb3 CBb4::CBb4 CBb5::CBb5) and within-class BC inhibitory networks (CBb3 → AC –| CBb3 CBb4 → AC –| CBb4 CBb5 → AC –| CBb5) in each ON IPL strata form laminar-specific functional sheets with high clustering coefficients. Heterocellular BC coupling (CBb3::CBb4 CBb4::CBb5 CBb3::CBb5) and cross-class BC inhibitory networks (CBb3 → AC –| CBb4 CBb4 → AC –| CBb3 CBb4 → AC –| CBb5 CBb5 → AC –| CBb4 CBb3 → AC –| CBb5 CBb5 → AC –| CBb3) establish short synaptic path lengths across all ON IPL laminae.
Conclusions: The retina contains a greater than expected number of synaptic hubs that multiplex parallel channels presynaptic to ganglion cells. The results validate a synaptic basis (ie. direct synaptic connectivity) and local network topology for the small world architecture indicated at larger scales providing neuroanatomical plausibility of this organization for local networks and are consistent with small world design as a fundamental organizing principle of neural networks on multiple spatial scales.
Purpose: To elucidate mechanisms underlying the dendrite developmental plasticity of retinal ganglion cells, we examined the role of glutamate receptors on retinal ganglion cell dendrite elongation and filopodia elimination.
Methods: We used the JamB genetically labeled subtype of RGCs as our working model. JamB-CreER:YFP ganglion cell dendritic arbors were imaged in whole mount retina using confocal microscopy. Dendrite length, area, branching, and filopodia number were traced and measured using Neurolucida. Visual inputs were blocked by dark-rearing pups after P5. Glutamatergic activity was blocked using daily intraocular injections of AP5 and CNQX from P9 to P13 or genetic ablation of the NMDA receptor in these RGCs.
Results: To test the role of visual inputs on dendrite development, we dark-reared mice from P5 to P30 and found a modest effect on filopodia elimination in JamB RGCs. Anticipating that spontaneous glutamatergic activity in the retina may also contribute to RGC filopodia elimination, we blocked spontaneous glutamatergic activity by daily intraocular injections of AP5 and CNQX from P9 to P13. This led to an increase in filopodia density due to decreased dendrite length but no change in filopodia number. We confirmed this result by examining NMDAR knockout JamB cells (JamB-CreER:YFP:Grin1-/-). As expected, Grin1-/- JamB RGCs have decreased dendrite outgrowth like the pharmacologic blockade. However, filopodia elimination in these cells was significantly decreased as well, suggesting that NMDA and non-NMDA glutamate receptors might regulate the RGC dendritic development in a differential manner. This effect was dramatic at P13. To test if this effect persists into adulthood, we examined Grin1-/- JamB RGCs at P30 and found that they are indistinguishable from wild-type JamB RGCs, suggesting that a compensatory mechanism exists to drive dendrite elongation and filopodia elimination in the absence of the NMDA receptor.
Conclusions: Our study demonstrated that ganglion cell dendrite outgrowth and pruning of filopodia require glutamatergic activity and visual input that act via NMDA and possibly non-NMDA glutamate receptors.