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Self-referencing H + -selective electrodes were used to measure extracellular H +  fluxes from Müller (glial) cells isolated from the tiger salamander retina. A novel chamber enabled stable recordings using H + -selective microelectrodes in a self-referencing format using bicarbonate-based buffer solutions. A small basal H +  flux was observed from the end foot region of quiescent cells bathed in 24 mM bicarbonate-based solutions, and increasing extracellular potassium induced a dose-dependent increase in H +  flux. Barium at 6 mM also increased H +  flux. Potassium-induced extracellular acidifications were abolished when bicarbonate was replaced by 1 mM HEPES. The carbonic anhydrase antagonist benzolamide potentiated the potassium-induced extracellular acidification, while 300 μM DIDS, 300 μM SITS, and 30 μM S0859 significantly reduced the response. Potassium-induced extracellular acidifications persisted in solutions lacking extracellular calcium, although potassium-induced changes in intracellular calcium monitored with Oregon Green were abolished. Exchange of external sodium with choline also eliminated the potassium-induced extracellular acidification. Removal of extracellular sodium by itself induced a transient alkalinization, and replacement of sodium induced a transient acidification, both of which were blocked by 300 μM DIDS. Recordings at the apical portion of the cell showed smaller potassium-induced extracellular H +  fluxes, and removal of the end foot region further decreased the H +  flux, suggesting that the end foot was the major source of acidifications. These studies demonstrate that self-referencing H + -selective electrodes can be used to monitor H +  fluxes from retinal Müller cells in bicarbonate-based solutions and confirm the presence of a sodium-coupled bicarbonate transporter, the activity of which is largely restricted to the end foot of the cell.    NEW &amp; NOTEWORTHY The present study uses self-referencing H + -selective electrodes for the first time to measure H +  fluxes from Müller (glial) cells isolated from tiger salamander retina. These studies demonstrate bicarbonate transport as a potent regulator of extracellular levels of acidity around Müller cells and point toward a need for further studies aimed at addressing how such glial cell pH regulatory mechanisms may shape neuronal signaling.

Extracellular H+ fluxes from tiger salamander Müller (glial) cells measured using self-referencing H+-selective microelectrodes

Extracellular H⁺ fluxes from tiger salamander Müller (glial) cells measured using self-referencing H⁺-selective microelectrodes