This paper in the Journal of Comparative Neurology by J. Scott Lauritzen, James R. Anderson, Bryan W. Jones, Carl B. Watt, Shoeb Mohammed, John V. Hoang and Robert E. Marc is another effort out of the Marc Laboratory For Connectomics that continues to define complete neural circuits to completeness.
This paper is another elucidation of data from the first Rabbit Retinal Connectome volume (RC1) that reveals that the division between the ON and the OFF inner plexiform layer (IPL) is not structurally absolute. ON cone bipolar cells make noncanonical axonal synapses onto specific targets and receive amacrine cell synapses in the nominal OFF layer, creating novel motifs, including inhibitory crossover networks. Automated transmission electron microscopic imaging, molecular tagging, tracing, and rendering of ∼400 bipolar cells reveals axonal ribbons in 36% of ON cone bipolar cells, throughout the OFF IPL. The targets include γ-aminobutyrate (GABA)-positive amacrine cells (γACs), glycine-positive amacrine cells (GACs), and ganglion cells. Most ON cone bipolar cell axonal contacts target GACs driven by OFF cone bipolar cells, forming new architectures for generating ON–OFF amacrine cells. Many of these ON–OFF GACs target ON cone bipolar cell axons, ON γACs, and/or ON–OFF ganglion cells, representing widespread mechanisms for OFF to ON crossover inhibition. Other targets include OFF γACs presynaptic to OFF bipolar cells, forming γAC-mediated crossover motifs. ON cone bipolar cell axonal ribbons drive bistratified ON–OFF ganglion cells in the OFF layer and provide ON drive to polarity-appropriate targets such as bistratified diving ganglion cells (bsdGCs). The targeting precision of ON cone bipolar cell axonal synapses shows that this drive incidence is necessarily a joint distribution of cone bipolar cell axonal frequency and target cell trajectories through a given volume of the OFF layer. Such joint distribution sampling is likely common when targets are sparser than sources and when sources are coupled, as are ON cone bipolar cells.
Figure Above: The first Rabbit Retinal Connectome volume (RC1), constructed via automated transmission electron microscopy (ATEM) and computational molecular phenotyping (CMP), spans the mid-inner nuclear layer (INL) at section 001 to the ganglion cell layer (GCL) at section 371, shown in a mirror image below. RC1 is a short cylinder ≈ 250 μm in diameter and ≈ 30 μm high containing 341 ATEM sections and 11 intercalated CMP sections. The cylinder is capped at top and bottom with 10-section CMP series allowing molecular segmentation of cells, and an activity marker, 1-amino-4-guanidobutane (AGB), to mark cells differentially stimulated via glutamatergic synapses. ATEM section 001 is a horizontal plane section through the INL visualized with GABA.glycine.glutamate → red.green.blue transparency mapping and a dark gold alpha channel (ANDed taurine + glutamine channels). ATEM section 371 is a horizontal plane section through the GCL visualized with GABA.AGB.glutamate → red.green.blue transparency mapping.
An interesting article was published in Experimental Eye Research by Marijana Samardzija, Hedwig Wariwoda, Cornelia Imsand, Philipp Huber, Severin R. Heynen, Andrea Gubler and Christian Grimm that examines survival pathways that are induced in the retinas of rd10 mice. Dynamics of retinal degeneration in the rd10 mouse was also examined including an analysis of retinal vasculature and kinetics. The study is fairly comprehensive including crude anatomical approaches, biochemistry, real-time PCR, Western blotting and immunofluorescence. They recapitulate some of the studies that have examined development of the rd10 mouse up to pnd15, but then explored the phases of initial retinal degeneration and explored survival mechanisms and pathways (Lif, Edn2, Fgf2, Mt1, Mt2, p-JAK2, CASP1 and GFAP) in the cells that remain. It would have been interesting to follow these results at later stages of degeneration. The authors mention remodeling, but only in passing which was too bad as there are some really interesting aspects of cell survival there. Regardless, its an interesting paper worthy of having a look at.
Pat D’Amore, Senior Scientist and Director of Research at the Schepens Eye Research Institute/Massachusetts Eye and Ear. Professor of Ophthalmology and Pathology Harvard Medical School will be delivering a seminar at the John A. Moran Eye Center Auditorium on Tuesday, January 29, 2013 from 12:00-1:00 pm
Abstract: VEGF has a well established role in vascular development and pathology; however, its possible function in the adult is just being investigated. Our observations point to critical roles for VEGF in various adult tissues, most notably the eye. These findings have important implications for chronic VEGF blockage such as occurs with the long-term use of VEGF neutralizing therapies.
An interesting paper by Adi Schejter, Limor Tsur, Nairouz Farah, Inna Reutsky-Gefen, Yishay Falick, and Shy Shoham published an interesting paper that shows in vivo fluorescent images with cellular resolution using optogenetic probes expressed in retinal ganglion cells by adapting a simple endoscope as a low cost fundoscopic imaging system.
The authors were able to resolve really nice, high quality images that reveal the entire retina, showing ganglion cells as well as the ganglion cell fibers expressing a channelrhodopsin2-e YFP construct.
Thanks to friend of Webvision, Steve Fliesler for sending this along.
Here on Webvision, our goal is retinal education and even though Webvision is hosted here at the Moran Eye Center, we nevertheless try to include as much of the wider community as possible in posts and in content, though we will point out work that comes of of the Moran Eye Center from time to time. So, while we compiling chapters for information as well as posts to the front page here that we hope contain informative items relevant to the retina and the retinal research community, it is important from time to time to step back and ask why it is that we study the retina and get a bigger picture view of what role all of this biology plays in peoples lives.
Continue reading “Moran Eye Center International Outreach”
Barry Knox from Upstate University of New York, Departments of Neuroscience and Physiology, Biochemistry and Molecular Biology and Ophthalmology will be delivering a talk on Mechanisms Of Retinal Degeneration Caused By Mutant Rhodopsin: Applications Of Live Rod Imaging, January 22nd, 2013 in the John A. Moran Eye Center Auditorium.
Last year we started a tradition here on Webvision of summarizing some statistics of traffic to Webvision to give you some idea of who the users and visitors are. While 2011 was a year of major infrastructure change to Webvision with a complete replacement of the database backend and a move to hosting with a WordPress based platform, 2012 was a year of steady growth, updates to many existing chapters and the addition of 2 new chapters on Retinal Ganglion Cell Dendritic Structure And Synaptic Connections by Ning Tian, and Glycine Receptor Diversity in the Mammalian Retina by Silke Haverkamp and a chapter on Visual Evoked Potentials by Don Creel.
Continue reading “Webvision Year In Review, 2012”