Mammalian retinal glial (Müller) cells express large-conductance Ca2+-activated K+ channels that are modulated by Mg2+ and pH and activated by protein kinase A
✍ Scribed by Andreas Bringmann; Frank Faude; Andreas Reichenbach
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 225 KB
- Volume
- 19
- Category
- Article
- ISSN
- 0894-1491
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✦ Synopsis
The cell-attached and excised patch configurations of the patch clamp technique were used to characterize Ca 21 -activated maxi-K 1 channels in freshly isolated Mu ¨ller glial cells. The cells were dissociated from postmortem adult human and porcine retinas. The maxi-K 1 channels in Mu ¨ller cells of both species display a single channel conductance of 175 pS in cell-attached and inside-out patches (125/110 mM K 1 ). The channels are activated by membrane depolarization and by elevation of intracellular Ca 21 . In the presence of 10 25 , 10 24 , and 10 23 M intracellular free Ca 21 , the halfactivation voltages are 17.2, 226.6, and 247.5 mV, respectively. The half-activation-[Ca 21 ] at 110 mV is 8.1 µM, and the Hill coefficient of Ca 21 binding is 1.7. Ba 21 exerts a voltage-dependent block of the open-state probability. The maxi-K 1 channels of Mu ¨ller cells are activated by raising of the intracellular pH as well as by Mg 21 ions at the cytosolic face of the channels. Phosphorylation of the channel after cytosolic addition of the catalytic subunit of a cAMP dependent protein kinase in the presence of Mg-ATP caused a shift of the activation curve to negative membrane potentials. Between 240 and 280 mV membrane potentials, the open-state probability rose to 190.3% of the control value (100%) after phosphorylation of the channel. Therefore, phosphorylation enhances sensitivity of the channels to Ca 21 and voltage. The maxi-K 1 channels may provide a link between second messenger systems and membrane conductance of retinal Mu ¨ller cells and may have an important function in repolarization of the Mu ¨ller cell membrane and, therefore, in the maintainance of the retinal spatial K 1 buffering mechanisms.