December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Adrenergic Modulation of Glutamate-Induced Calcium Signals in Dissociated Mouse Retinal Ganglion Cells
Author Affiliations & Notes
  • RL Gross
    Department of Ophthalmology Baylor College of Medicine Houston TX
  • J Zhang
    Houston TX
  • SM Wu
    Houston TX
  • Footnotes
    Commercial Relationships   R.L. Gross, None; J. Zhang , None; S.M. Wu , None. Grant Identification: NIH EY04446, EY02520 (Vision Core), the Retina Research Foundation (Houston), and Research to Preven
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2205. doi:
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      RL Gross, J Zhang, SM Wu; Adrenergic Modulation of Glutamate-Induced Calcium Signals in Dissociated Mouse Retinal Ganglion Cells . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2205.

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

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Abstract: : Purpose:Glutamate-induced neurotoxic actions are thought to be associated with elevation of intracellular calcium. The objective of this project is to understand how adrenergic agents modulate glutamate-induced increase of intracellular calcium in mouse retinal ganglion cells and how they may protect ganglion cells from glutamate-induced damage. Methods:Enzymatically dissociated adult mouse (strain C57BL/6J) retinal ganglion cells were identified with monoclonal antibody against Thy1.2 and Cy3-conjugated secondary antibody. The dissociated neurons were loaded with Fura-2AM, and calcium signals were recorded with a cooled CCD camera attached to an inverted microscope. Results:In a previous study we have demonstrated that dissociated mouse ganglion cells can be identified by their Thy1.2 immuno-positive fluorescence. Application of glutamate increased the intracellular calcium level in retinal ganglion cells in a dose dependent manner. The EC50 for glutamate was 6.19µM (n=12). ß-adrenergic blockers, (s)(-)-propanolol, betaxolol and timolol compressed the dose-curve and shifted the EC50 to higher dose ranges, suggesting that they act as non-competitive blockers of the glutamate responses. The relative efficacy for inhibiting 20µM glutamate-induced calcium signals is (s)(-)-propanolol≷betaxolol≷≷timolol with average IC50 of 78.05µM, 235.7µM and 2167.05µM, respectively. The inhibitory actions persisted in the presence of H9, a PKA blocker and isopropanolol, a ß-receptor agonist, indicating that the down regulation of glutamate-induced calcium increase in mouse ganglion cells is possibly not mediated by activation of ß-adrenergic receptors or the PKA pathway. Conclusion:Glutamate-induced elevation of intracellular calcium in mouse retinal ganglion cells can be reversibly suppressed by ß-adrenergic blockers with relative efficacy of (s)(-)-propanolol ≷betaxolol ≷≷timolol. In addition to lowering intraocular pressure, ß-blockers may be potentially neuroprotective against ganglion cell damage induced by elevated glutamate levels in glaucomatous retinas.

Keywords: 415 ganglion cells • 489 neuroprotection • 514 pharmacology 

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