These retinal images are from an 84 year old white male who presented to the Moran Eye Center in 2008. He was diagnosed and followed for dry age-related macular degeneration (AMD) with serial autofluorescent photographs showing progression of geographic atrophy of the RPE from 2008 to 2014.
These images were prepared by James Gilman of the Moran Eye Center.
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.
This abstract was presented today at the 2015 Association for Research in Vision and Opthalmology (ARVO) meetings in Denver, Colorado by Rebecca L. Pfeiffer, Bryan W. Jones and Robert E. Marc.
Purpose: Müller cells (MCs) play a critical role in glutamate (E) metabolism and carbon skeleton cycling in retina. MCs demonstrate changes in metabolism and morphology during retinal degeneration. The timing, extent, regulation, and impacts of these changes are not yet known. We evaluated metabolic phenotypes of MCs and evaluated their capacity to transport glutamate during degeneration.
Methods: Retinas were harvested from wild-type (WT) and rhodopsin Tg P347L rabbits, divided into chips mounted on filters, and incubated in Ames medium with 5 mM D-aspartate (D-Asp), D-glutamate (D-Glu), or D-glutamine (D-Gln) for 10 min at 35 deg to explore transport and metabolism. Chips were fixed in mixed aldehydes and resin embedded for computational molecular phenotyping (CMP) of a range of L- and D-amino acid markers and selected proteins including glutamine synthetase (GS) (J Comp Neurol. 464:1, 2003).
Results: CMP revealed wide variations in metabolite levels across individual MCs from Tg P347L retinas, generating chaotic patterns. GS decreased significantly while glutamine levels (Q) increased, although to varying degrees. Remarkably, E levels were variable and much higher in some MCs than normal, but did not correlate (inversely) with GS levels. Transport experiments using D-Glu, D-Asp, and D-Gln showed that alterations in MC metabolites are not the product of defective transporters, in contrast to previous reports. These results are also inconsistent with conventional models of GS-based E-Q metabolism and microenvironmental regulation of MC phenotypes.
Conclusions: These observations suggest three conclusions. (1) Although degeneration of the retina is certainly the trigger, MC phenotype changes are not a coherent response to the surrounding microenvironment but are, rather, uncoordinated individual MC responses. (2) Although GS is accepted as the primary enzyme responsible for the conversion of E to Q in the normal retina, alternative pathways appear unmasked in the degenerate state. (3) It has been previously hypothesized that MCs in retinal degenerations exhibit deficient E transport. Our experiments show no transport deficiency. This indicates that chaotic metabolite levels emerge from changes in individual MC metabolic processing.
We are on our way to ARVO, 2015 in Denver, Colorado to participate in the largest gathering of vision scientists and clinicians in the world. It’s the annual meeting of researchers presenting and discussing all things vision and ophthalmology.
If you are going to be at ARVO and want to meet up, leave us a comment here or send a Tweet to @Webvision1.
Look forward to seeing you there.