Age-dependent changes in the regulation mechanisms for intracellular calcium ions in ganglion cells of the mouse retina

Authors

  • Miriam Mann,

    1. Department of Ophthalmology II, Augenklinik Abt. II, Forschungsstelle Experimentelle Ophthalmologie, Röntgenweg 11, 72076 Tübingen, Germany
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  • Wadood Haq,

    1. Department of Ophthalmology II, Augenklinik Abt. II, Forschungsstelle Experimentelle Ophthalmologie, Röntgenweg 11, 72076 Tübingen, Germany
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  • Thomas Zabel,

    1. Department of Ophthalmology II, Augenklinik Abt. II, Forschungsstelle Experimentelle Ophthalmologie, Röntgenweg 11, 72076 Tübingen, Germany
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  • Elke Guenther,

    1. Department of Ophthalmology II, Augenklinik Abt. II, Forschungsstelle Experimentelle Ophthalmologie, Röntgenweg 11, 72076 Tübingen, Germany
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  • Eberhart Zrenner,

    1. Department of Ophthalmology II, Augenklinik Abt. II, Forschungsstelle Experimentelle Ophthalmologie, Röntgenweg 11, 72076 Tübingen, Germany
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  • Thomas Ladewig

    1. Department of Ophthalmology II, Augenklinik Abt. II, Forschungsstelle Experimentelle Ophthalmologie, Röntgenweg 11, 72076 Tübingen, Germany
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Dr Thomas Ladewig, as above.
E-mail: ladewig.thomas@uni-tuebingen.de

Abstract

The purpose of this study was to investigate the role of intracellular calcium buffering in retinal ganglion cells. We performed a quantitative analysis of calcium homeostasis in ganglion cells of early postnatal and adult mice by simultaneous patch-clamp recordings in sliced tissue and microfluorometric calcium measurements with Fura-2. Endogenous calcium homeostasis was quantified by using the ‘added buffer’ approach which uses amplitudes and decay time constants of calcium transients to give a standard for intracellular calcium buffering. The recovery phase of depolarization-induced calcium transients was well approximated by a mono-exponential function with a decay time constant that showed a linear dependence on dye concentration. Endogenous calcium binding ratios were found to be 575 (n = 18 cells) in early postnatal and 121 (n = 18 cells) in adult retinal ganglion cells. With respect to ganglion cell degeneration at early postnatal stages, our measurements suggest that neuroprotection of a majority of developing ganglion cells partially results from a specialized calcium homeostasis based on high buffering capacities. Furthermore, the dramatic decrease of the intracellular calcium buffering capacity during ganglion cell development may enhance their vulnerability to neurodegeneration.

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