May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
The Glutamate Transporter GLT–1C Is Expressed by Retinal Ganglion Cells in Both Glaucoma and AMD
Author Affiliations & Notes
  • D.V. Pow
    Biomedical Sciences, University of Newcastle, Newcastle, Australia
  • L.T. Macnab
    Biomedical Sciences, University of Newcastle, Newcastle, Australia
  • E. WoldeMussie
    Biological Sciences, Allergan Inc, Irvine, CA
  • R.K. P. Sullivan
    Biomedical Sciences, University of Newcastle, Newcastle, Australia
  • Footnotes
    Commercial Relationships  D.V. Pow, None; L.T. Macnab, None; E. WoldeMussie, Allergan Inc, E; R.K.P. Sullivan, None.
  • Footnotes
    Support  NHMRC (Australia)
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 891. doi:https://doi.org/
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      D.V. Pow, L.T. Macnab, E. WoldeMussie, R.K. P. Sullivan; The Glutamate Transporter GLT–1C Is Expressed by Retinal Ganglion Cells in Both Glaucoma and AMD . Invest. Ophthalmol. Vis. Sci. 2006;47(13):891. doi: https://doi.org/.

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

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Abstract
 
Purpose:
 

To determine whether retinal ganglion cells express a marker indicative of over–stimulation by glutamate in animals and humans with degenerative retinal conditions including glaucoma and macular degeneration.

 
Methods:
 

Rat and human tissues were examined by immunocytochemistry using an antibody to the glutamate transporter splice variant GLT–1C which was raised and characterised in our laboratories, as well as other glutamate transporters such as GLAST. Human tissues were obtained from Lions Eye Banks in Florida, USA and Australia, with diagnoses as normal, with AMD or affected by glaucoma being provided by the eye banks. Human tissues were compared with rat tissues subject to experimental induction of glaucoma.

 
Results:
 

Retinal ganglion cells in normal retinae from humans and rats did not express detectable levels of the glutamate transporter GLT–1. However in eyes affected by AMD or glaucoma there was prominent expression of the GLT–1C splice variant of GLT–1 in ganglion cells across the entire retina. GLAST immunoreactivity in glaucomatous eyes appeared to be indistinguishable from that in control eyes but aberrations were noted in AMD.

 
Conclusions:
 

Both rat and human retinal ganglion cells express the glutamate transporter GLT–1C in response to conditions that may be associated with the excitotoxic stimulation of retinal ganglion cells. In accord with prior studies from other labs, normal retinal ganglion cells did not express detectable levels of GLT–1. It has previously been shown that other cells such as brain astrocytes up–regulate GLT–1 expression in response to raised extracellular glutamate. We suggest that elevated extracellular glutamate may mediate the up–regulation of GLT–1C expression in retinal ganglion cells in response to retinal insults.  

 
Keywords: excitatory neurotransmitters • ganglion cells • neuroprotection 
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