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Ronald L. Gross, Steve H. Hensley, Fan Gao, Xiong-Li Yang, Sun-Chuan Dai, Samuel M. Wu; Effects of Betaxolol on Light Responses and Membrane Conductance in Retinal Ganglion Cells. Invest. Ophthalmol. Vis. Sci. 2000;41(3):722-728.
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purpose. To examine the physiological effects of betaxolol, aβ 1-adrenergic receptor blocker commonly used in the
treatment of glaucoma, on retinal ganglion cells and to evaluate its
potential to elicit responses consistent with a neuroprotective agent
against ganglion cell degeneration.
methods. Single-unit extracellular recording, electroretinogram (ERG),
intracellular and whole-cell patch-clamp recording techniques were made
from flatmounted, isolated retina, superfused eyecup, and living
retinal slice preparations of the larval tiger salamander.
results. Bath application of 20 μM betaxolol reduced the glutamate-induced
increase of spontaneous spike rate in retinal ganglion cell by
approximately 30%. The glutamate-induced postsynaptic current recorded
under voltage-clamp conditions was reduced by 50 μM betaxolol, and
the difference current-voltage (I-V) relation
(IControl -Ibetaxolol) was N-shaped and
AP5-sensitive, characteristic of N-methyl-d-aspartate receptor–mediated
current. Application of 50 μM betaxolol reversibly reduced the
voltage-gated sodium and calcium currents by approximately one third of
their peak amplitudes. The times-to-action of betaxolol on ganglion
cells are long (15–35 minutes for 20–50 μM betaxolol), indicative
of modulation through slow biochemical cascades. Betaxolol, up to 100μ
M, exerted no effects on horizontal cells or the ERG, suggesting
that the primary actions of this β1 blocker are
restricted to retinal ganglion cells.
conclusions. These physiological experiments provide supporting evidence that
betaxolol acts in a manner consistent with preventing retinal ganglion
cell death induced by elevated extracellular glutamate or by increased
spontaneous spike rates under pathologic conditions. The physiological
actions of betaxolol lead to reducing neurotoxic effects in ganglion
cells, which are the most susceptible retinal neurons to
glutamate-induced damages under ischemic and glaucomatous conditions.
Therefore, betaxolol has the potential to be a neuroprotective agent
against retinal degeneration in patients with disorders mediated by
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