Previous studies in retinal glial (Mu ¨ller) cells have suggested that (1) the dominant membrane currents are mediated by K ϩ inward-rectifier (Kir) channels (Newman and Reichenbach, Trends Neurosci 19:307-312, 1996), and (2) rectification of these Kir channels is due largely to a block of outward c
Complex rectification of Müller cell Kir currents
✍ Scribed by Yuriy V. Kucheryavykh; Yaroslav M. Shuba; Sergei M. Antonov; Mikhail Y. Inyushin; Luis Cubano; Wade L. Pearson; Harley Kurata; Andreas Reichenbach; Rüdiger W. Veh; Colin G. Nichols; Misty J. Eaton; Serguei N. Skatchkov
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 613 KB
- Volume
- 56
- Category
- Article
- ISSN
- 0894-1491
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✦ Synopsis
Abstract
Although Kir4.1 channels are the major inwardly rectifying channels in glial cells and are widely accepted to support K^+^‐ and glutamate‐uptake in the nervous system, the properties of Kir4.1 channels during vital changes of K^+^ and polyamines remain poorly understood. Therefore, the present study examined the voltage‐dependence of K^+^ conductance with varying physiological and pathophysiological external [K^+^] and intrapipette spermine ([SP]) concentrations in Müller glial cells and in tsA201 cells expressing recombinant Kir4.1 channels. Two different types of [SP] block were characterized: “fast” and “slow.” Fast block was steeply voltage‐dependent, with only a low sensitivity to spermine and strong dependence on extracellular potassium concentration, [K^+^]~o~. Slow block had a strong voltage sensitivity that begins closer to resting membrane potential and was essentially [K^+^]~o~‐independent, but with a higher spermine‐ and [K^+^]~i~‐sensitivity. Using a modified Woodhull model and fitting i/V curves from whole cell recordings, we have calculated free [SP]~in~ in Müller glial cells as 0.81 ± 0.24 mM. This is much higher than has been estimated previously in neurons. Biphasic block properties underlie a significantly varying extent of rectification with [K^+^] and [SP]. While confirming similar properties of glial Kir and recombinant Kir4.1, the results also suggest mechanisms underlying K^+^ buffering in glial cells: When [K^+^]~o~ is rapidly increased, as would occur during neuronal excitation, “fast block” would be relieved, promoting potassium influx to glial cells. Increase in [K^+^]~in~ would then lead to relief of “slow block,” further promoting K^+^‐influx. © 2008 Wiley‐Liss, Inc.
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