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Andreas Bringmann, Bernd Biedermann, Ute Schnurbusch, Volker Enzmann, Frank Faude, Andreas Reichenbach; Age- and Disease-Related Changes of Calcium Channel–Mediated Currents in Human Müller Glial Cells. Invest. Ophthalmol. Vis. Sci. 2000;41(9):2791-2796.
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purpose. To determine whether the expression of voltage-gated Ca2+ channels in human Müller glial cells changes during normal aging
and in cells from patients with proliferative vitreoretinopathy (PVR).
methods. Müller cells were enzymatically isolated from retinas of healthy
donors and from excised retinal pieces of patients with PVR, and the
whole-cell, voltage-clamp technique was used to characterize the
current densities of transient, low-voltage–activated calcium channels
and of sustained, high-voltage–activated calcium channels,
respectively. To obtain maximal currents through both channel types,
Na+ ions were used as the charge carrier.
results. During normal aging, Müller cells developed a hypertrophy, as
indicated by an increase of the cell membrane capacitance. The mean
membrane capacitance of cells from aged donors (≥ 60 years old) was
elevated by 25% compared with cells from younger donors. The
hypertrophy was not accompanied by a changed density of
low-voltage–activated currents, whereas the density of the
high-voltage–activated currents was enhanced by 76%. The density of
the high-voltage–activated currents increased in correlation with the
increase of the cell membrane capacitance and with the age of the
donors. In the case of PVR, Müller cells displayed a strong
hypertrophy accompanied by a downregulation of both current types by
conclusions. Both normal aging and PVR cause a gliotic reactivity of human
Müller cells, as indicated by their hypertrophy. The type of
reactivity, however, differs between the two conditions. Normal aging
is accompanied by an increased expression of voltage-gated
Ca2+ channels, whereas in PVR Ca2+ channel
expression is decreased.
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