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Abstract #8521 Published in IGR 5-1
Effects of β-adrenergic blockers on glutamate-induced calcium signals in adult mouse retinal ganglion cells
Zhang J; Wu SM; Gross RBrain Research 2003; 959: 111-119
Betaxolol, a selective β1-adrenoceptor antagonist, is an antiglaucoma drug commonly used to lower the intraocular pressure (IOP) in treatment of glaucoma. Recent evidence has also shown that it attenuates ligand- and voltage-gated currents in retinal ganglion cells, which may lead to reduction of intracellular calcium and prevention of glutamate-induced ganglion cell damage in glaucoma. In the present study, the authors examined the effectiveness of betaxolol and other β-adrenergic blockers on glutamate-induced calcium signals. Dissociated adult mouse retinal ganglion cells were immunolabelled with antibody CD90.2 and loaded with Fura-2AM. Calcium signals were recorded with optical recording techniques. Low doses of glutamate cause an increase in intracellular calcium that may result in pathological changes in ganglion cells. The action of glutamate could be reversibly suppressed by β-adrenergic blockers and the order of inhibitory potency is (s)(-)-propranolol>betaxolol>>timolol, with average IC50 of 78.05, 235.7 and 2167.05, μM, respectively. Betaxolol compressed the dose-response curve of glutamate. The EC50 of glutamate was shifted from 6.19 to 23.53 μM, indicating that betaxolol acts as a non-competitive inhibitor of glutamate response in retinal ganglion cells. These data are consistent with previous reports that betaxolol and other β-adrenergic blockers may exert its neuroprotective action by suppression of glutamate-induced intracellular calcium increase in retinal ganglion cells.
Dr. J. Zhang, Department of Ophthalmology, Cullen Eye Institute, Baylor College of Medicine, Houston, TX 77030, USA. jianz@bcm.tmc.edu
Classification:
11.8 Neuroprotection (Part of: 11 Medical treatment)
