title: Complex rectification of Müller cell Kir currents.
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.
authors.affiliation: Department of Biochemistry, Universidad Central del Caribe, School of Medicine, Bayamón, PR.
authors.forename: Yuriy V
authors.initials: YV
authors.lastname: Kucheryavykh
authors.forename: Yaroslav M
authors.initials: YM
authors.lastname: Shuba
authors.forename: Sergei M
authors.initials: SM
authors.lastname: Antonov
authors.forename: Mikhail Y
authors.initials: MY
authors.lastname: Inyushin
authors.forename: Luis
authors.initials: L
authors.lastname: Cubano
authors.forename: Wade L
authors.initials: WL
authors.lastname: Pearson
authors.forename: Harley
authors.initials: H
authors.lastname: Kurata
authors.forename: Andreas
authors.initials: A
authors.lastname: Reichenbach
authors.forename: Rüdiger W
authors.initials: RW
authors.lastname: Veh
authors.forename: Colin G
authors.initials: CG
authors.lastname: Nichols
authors.forename: Misty J
authors.initials: MJ
authors.lastname: Eaton
authors.forename: Serguei N
authors.initials: SN
authors.lastname: Skatchkov
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D004594:Electrophysiology; D009457:Neuroglia / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology*; D024661:Potassium Channels, Inwardly Rectifying / Q000187:drug effects / Q000502:physiology*; D011894:Rana pipiens; D051381:Rats; D020318:Rats, Long-Evans; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins / Q000378:metabolism; D012160:Retina / Q000166:cytology / Q000502:physiology*; D000098854:Kcnj10 Channel
chemical_list: D000098854:Kcnj10 Channel; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D011994:Recombinant Proteins; D011188:Potassium