Premium
Complex rectification of Müller cell Kir currents
Author(s) -
Kucheryavykh Yuriy V.,
Shuba Yaroslav M.,
Antonov Sergei M.,
Inyushin Mikhail Y.,
Cubano Luis,
Pearson Wade L.,
Kurata Harley,
Reichenbach Andreas,
Veh Rüdiger W.,
Nichols Colin G.,
Eaton Misty J.,
Skatchkov Serguei N.
Publication year - 2008
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20652
Subject(s) - spermine , biophysics , potassium , biology , potassium channel , glutamate receptor , membrane potential , electrophysiology , conductance , neuroglia , resting potential , patch clamp , neuron , neuroscience , slice preparation , microbiology and biotechnology , central nervous system , biochemistry , chemistry , receptor , physics , organic chemistry , condensed matter physics , enzyme
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.