Figure 5.

Glutamate-evoked morphological alterations of retinal glial cells are mediated by Na⁺ and Cl^- fluxes. The cross-sectional areas of the glial cell profiles in the IPL are given as percentage of control (100%). A,Na⁺-free or low-Cl^- extracellular solutions reversed the morphological effect of glutamate. The K⁺ channel blockers TEA (10 mm) and Ba²⁺ (1 mm), the Na-K-2Cl cotransport blocker furosemide (5 mm), and the Cl^- channel blockers flufenamic acid (500 μm), NPPB (100 μm), and picrotoxin (200 μm) did not inhibit the glutamate effect. The low-Cl^- extracellular solutions were made by exchanging NaCl with either sodium gluconate or sodium methylsulfate. B, Ca²⁺-free extracellular solution or a solution that was supplemented with TTX (1 μm) plus Cd²⁺ (100 μm) did not alter the glutamate-evoked effects on glial cell morphology. C, Effect of solutions with different osmolarities on the cross-sectional area of glial cell trunks. The osmolarity was changed by alterations of the NaCl concentration in the extracellular solution. D, Effect of an extracellular solution that was diluted to 60% ionic strength. E, Addition of taurine (20 mm) to the extracellular solution did not change the glutamate-evoked morphological alterations. F, Nocodazol (10 μg/ml; preincubation for 2 hr at room temperature), a microtubuli destabilizing drug, did not alter the glutamate effect on the glial cell morphology. Similarly, cytochalasin D (1 μg/ml; preincubation for 15 min), which disrupts the actin cytoskeleton, and ML7 (50 μm; preincubation for 1.5 hr), an inhibitor of the myosin light-chain kinase, did not inhibit the action of glutamate. The effects of glutamate (1 mm) and ions were measured after a 10 min exposure. Recovery was measured after 15 min washout. Means ± SEM of three to six experiments. Significant differences versus control: ^•p < 0.05; ^••p < 0.01; ^•••p < 0.001. Significant effects of the blocker and of washout: ^○p < 0.05.