May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
Analysis of Glial and Neural Retinal Response in Short–term Human Retinal Detachment (RD)
Author Affiliations & Notes
  • D.G. Charteris
    Moorfield Eye Hospital, London, United Kingdom
  • C.S. Sethi
    Moorfield Eye Hospital, London, United Kingdom
  • G.P. Lewis
    Neuroscience Research Institute, University of California, Santa Barbara, CA
  • S.K. Fisher
    Neuroscience Research Institute, University of California, Santa Barbara, CA
  • D. McLeod
    Academic Dept of Ophthalmology, Manchester Royal Eye Hospital, Manchester, United Kingdom
  • Footnotes
    Commercial Relationships  D.G. Charteris, None; C.S. Sethi, None; G.P. Lewis, None; S.K. Fisher, None; D. McLeod, None.
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 2033. doi:
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      D.G. Charteris, C.S. Sethi, G.P. Lewis, S.K. Fisher, D. McLeod; Analysis of Glial and Neural Retinal Response in Short–term Human Retinal Detachment (RD) . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2033.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: To analyse the intra–retinal and peri–retinal responses of glial and neural elements of the human retina in short–term human RD Methods: The eye of a patient who died approximately 10 days after developing symptoms of acute RD was analysed. Retinal tissue from the area of RD was immunostained with antibodies to retinal glia (GFAP), photoreceptors (rhodopsin, M & S cone opsins), horizontal cells (calbindin D), synaptic protein (synaptophysin) and RPE cells (cellular retinaldehyde binding protein). Sections were incubated in secondary antibodies conjugated to Cy2 or Cy3 and viewed using a BioRad 1024 confocal microscope. Results: In an area of detachment where there was macroscopic evidence of retinal breaks there was extensive glial cell hypertrophy which formed a confluent scar around the break edge. In this area there was marked loss of neural retinal elements including photoreceptor inner and outer segments and relocalistion of rhodopsin to rod cell bodies. Rod axon extensions to the ganglion cell layer were found in this area. In areas of detachment removed from the retinal break pathological changes were less extensive with residual (though disorganised) rod and cone outer segments. Photoreceptor inner segments were preserved and there was relocalisation of opsins to photoreceptor cell bodies. Irregular synaptophysin immunostaining was seen in the outer plexiform layer. There was marked glial (GFAP) upregualtion and evidence of ILM disruption suggesting early glial epiretinal membrane (ERM) formation. Conclusions: A range of glial and neural retinal pathology is seen in short–term RD which appears to be related to duration – the changes being more severe around retinal breaks. Glial scarring was marked in relation to retinal breaks. In areas of more acute detachment neural elements remained present but there was evidence of early neural circuitry change (synaptic remodelling) and early ERM formation. The observed pathology is consistent with that found previously in animal models.

Keywords: pathology: human • retinal detachment • photoreceptors 

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