Fig. 8

Glutamate permeability of the glial maxi-anion channel and the pharmacological profile of the net glutamate release from astrocytes in hypotonic or ischemic conditions. a chloride currents recorded in symmetric conditions with both pipette and bath containing normal Ringer solution (146 mM Cl⁻). b Glutamate currents through an astrocytic maxi-anion channel. Traces were recorded in asymmetrical conditions in which all chloride in the bath (intracellular) solution was replaced with 146 mM glutamate. Arrowheads indicate the zero current level. c Unitary I–V relationships for the maxi-anion channel in symmetrical chloride conditions (open circles) and in asymmetrical conditions in which all chloride in the bath (intracellular) solution was replaced with 146 mM glutamate (open triangles). Each symbol represents the mean (the error bar is smaller than the symbol size). The slope conductance for symmetrical conditions is 403.9 ± 1.7 pS. The solid line for asymmetrical conditions is a polynomial fit with a reversal potential of −38.9 ± 1.2 mV for 146 mM glutamate. d Effects of phloretin (100 μM), tamoxifen (50 μM) and Gd³⁺ (50 μM) plus phloretin (100 μM) on the net release of glutamate from astrocytes induced by hypotonic or ischemic stimulation (for 15 min). Each column represents the mean ± SEM (vertical bar). *P < 0.05 compared with control. Modified from Liu et al. [5]