| pubmed-article:8146026 | pubmed:abstractText | There is ample evidence that retinal radial glial (Müller) cells play a crucial role in retinal ion homeostasis. Nevertheless, data on the particular types of ion channels mediating this function are very rare and incomplete; this holds especially for mammalian Müller cells. Thus, the whole-cell variation of the patch-clamp technique was used to study voltage-dependent currents in Müller cells from adult rabbit retinae. The membrane of Müller cells was almost exclusively permeable to K+ ions, as no significant currents could be evoked in K(+)-free internal and external solutions, external Ba2+ (1 mM) reversibly blocked most membrane currents, and external Cs+ ions (5 mM) blocked all inward currents. All cells expressed inwardly rectifying channels that showed inactivation at strong hyperpolarizing voltages (> or = -120 mV), and the conductance of which varied with the square root of extracellular K+ concentration ([K+]e). Most cells responded to depolarizing voltages (> or = -30 mV) with slowly activating outward currents through delayed rectifier channels. These currents were reversibly blocked by external application of 4-aminopyridine (4-AP, 0.5 mM) or tetraethylammonium (TEA, > 20 mM). Additionally, almost all cells showed rapidly inactivating currents in response to depolarizing (> or = -60 mV) voltage steps. The currents were blocked by Ba2+ (1 mM), and their amplitude increased with the [K+]e. Obviously, these currents belonged to the A-type family of K+ channels. Some of the observed types of K+ channels may contribute to retinal K+ clearance but at least some of them may also be involved in regulation of proliferative activity of the cells. | lld:pubmed |
