In vitro activity: Betaxolol is able to protect retinal neurons. Betaxolol attenuates the NMDA-induced influx of 45Ca2+ while β-adrenoreceptor agonists are ineffective. The glutamate-induced release of LDH is almost completely prevented when betaxolol (10 μM) is included. Betaxolol (100 μM) is very effective in preventing the hypoxia-induced release of LDH from cortical cultures.

Cell Assay: Dissociated cortical cells from 16–18-day-old fetal rats are grown, in 35 mm dishes, in DMEM supplemented with L-glutamine (4 mM), glucose (6 g/L), penicillin (100 U/mL), streptomycin (100 μg/mL) and 10% hormonal supplemented medium consisting of transferrin (1 mg/mL), insulin (250 μg/mL) putrescine (600 μM), sodium selenite (0.3 μM), progesterone (0.2 μM) and estradiol (0.1 pM) for 7 days in an atmosphere of 5% CO2/95% O2 at 37 °C. The cultures are then transferred to a culture medium which lacks the hormonal supplemented medium. L-glutamate is added to the medium and incubated for a further 4 hours under normoxic conditions. Betaxolol are added to the cultures at the same time as L-glutamate. In other experiments the cultures are subjected to anoxic conditions, 95% N2/5% CO2, for 5 hours at 37 °C. Betaxolol is added prior to anoxia. Reoxygenation is then achieved by replacing the cells in normoxic conditions (95% O2/5% CO2) for 3 hours. Cellular injury is assessed by measuring lactate dehydrogenase (LDH) release into the cell culture supernatant after hypoxia/reoxygenation or glutamate exposure. LDH activity is assayed spectrophotometrically by following NADH metabolism for 2 minutes at 340 nm.

Exp Eye Res. 2003 Apr;76(4):505-16; Exp Eye Res. 1999 Sep;69(3):331-42.