scholarly journals K+ Channels Are Responsible for an Inwardly Rectifying Current in the Plasma Membrane of Mesophyll Protoplasts of Avena sativa

1992 ◽  
Vol 98 (3) ◽  
pp. 1087-1097 ◽  
Author(s):  
Joseph Kourie ◽  
Mary Helen M. Goldsmith
Keyword(s):  
Plasma Membrane ◽  
Avena Sativa ◽  
Mesophyll Protoplasts ◽  
K Channels ◽  
Inwardly Rectifying

Voltage-Dependence of Extracellular Ca2+-Induced Modification in Properties of the Inward Rectifying K+ Channels in the Plasma Membrane of Mesophyll Protoplasts of Avena sativa

1996 ◽  
Vol 23 (3) ◽  
pp. 349 ◽  
Author(s):  
J Kourie
Keyword(s):  
Plasma Membrane ◽  
Time Constant ◽  
Avena Sativa ◽  
Voltage Dependence ◽  
Membrane Current ◽  
Time Dependent ◽  
Mesophyll Cells ◽  
K Channels ◽  
Current Passing ◽  
K Current

Data obtained using the whole-celi configuration of the patch-clamp technique reveal that characteristics of the inward rectifying K+ current across the plasma membrane of protoplasts isolated from mesophyll cells of leaves of oat (Avena sativa) are modified by increasing concentrations or removing the extracellular Ca2+. The whole-cell membrane current reveals two components. The first component an initial current II* which is the sum of two currents: (a) a linear ohmic leak current passing through non-gated channels, liNGC, and (b) a rectifying inward K+ current passing through inward rectifying gated K+ channels, IKi, that are instantaneously open. The second component of the membrane current at the steady state Iss is a time-dependent K+ current IKss defined as Iss-IiNGC and passes through inward rectifying gated K+ channels. The tail K+ current, IKT, is also defined as IT-IiNGC. Raising external calcium concentration, [Ca2+]o, from 0.1 mM to 10 mM blocked the inward rectifying currents IKi, IKss and IKT. The voltage-dependence of the activation time constant (τa) for time-dependent KC current IKss was not altered significantly by increasing [Ca2+]o whereas the deactivation time constant (τd) of the IKT increased from 16 ms to 30 ms at a Vm of -100 mV. Removal of [Ca2+]o increased the amplitude and altered the characteristics of the inward rectifying K+ current. Ten minutes after the removal of [Ca2+]o the increase in IKi was 3.5-fold larger than the increase in IKss. Furthermore, removing [Ca2+]o hastened the activation of IKss and the deactivation of IKT. However, the deactivation time constant (Td) remained dependent on membrane voltage (Vm). Extracellular Ca2+ may modulate the function of mesophyll cells by regulating K+ transport through the inward rectifying K+ channels and this may have significant implications for photosynthesis and cell expansion.

K+ Channels of Müller Glial Cells in Retinal Disorders

2018 ◽  
Vol 17 (4) ◽  
pp. 255-260 ◽  
Author(s):  
Feng Gao ◽  
Lin-Jie Xu ◽  
Yuan Zhao ◽  
Xing-Huai Sun ◽  
Zhongfeng Wang
Keyword(s):  
Müller Cells ◽  
Major Type ◽  
Delayed Rectifier ◽  
Muller Cells ◽  
Bkca Channels ◽  
K Channels ◽  
Functional Changes ◽  
Physiological Properties ◽  
Retinal Disorders ◽  
Inwardly Rectifying

Background & Objective: Müller cell is the major type of glial cell in the vertebrate retina. Müller cells express various types of K+ channels, such as inwardly rectifying K+ (Kir) channels, big conductance Ca2+-activated K+ (BKCa) channels, delayed rectifier K+ channels (KDR), and transient A-type K+ channels. These K+ channels play important roles in maintaining physiological functions of Müller cells. Under some retinal pathological conditions, the changed expression and functions of K+ channels may contribute to retinal pathogenesis. Conclusion: In this article, we reviewed the physiological properties of K+ channels in retinal Müller cells and the functional changes of these channels in retinal disorders.

scholarly journals Characterization of the R162W Kir7.1 mutation associated with snowflake vitreoretinopathy

2013 ◽  
Vol 304 (5) ◽  
pp. C440-C449 ◽  
Author(s):  
Wei Zhang ◽  
Xiaoming Zhang ◽  
Hui Wang ◽  
Anil K. Sharma ◽  
Albert O. Edwards ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Expression System ◽  
Dominant Negative ◽  
Dominant Negative Effect ◽  
Xenopus Laevis Oocyte ◽  
Cation Selectivity ◽  
Negative Effect ◽  
Dominant Disease ◽  
Vitreoretinal Degeneration ◽  
Inwardly Rectifying

KCNJ13 encodes Kir7.1, an inwardly rectifying K+ channel that is expressed in multiple ion-transporting epithelia. A mutation in KCNJ13 resulting in an arginine-to-tryptophan change at residue 162 (R162W) of Kir7.1 was associated with snowflake vitreoretinal degeneration, an inherited autosomal-dominant disease characterized by vitreous degeneration and mild retinal degeneration. We used the Xenopus laevis oocyte expression system to assess the functional properties of the R162W (mutant) Kir7.1 channel and determine how wild-type (WT) Kir7.1 is affected by the presence of the mutant subunit. Recordings obtained via the two-electrode voltage-clamp technique revealed that injection of oocytes with mutant Kir7.1 cRNA resulted in currents and cation selectivity that were indistinguishable from those in water-injected oocytes, suggesting that the mutant protein does not form functional channels in the plasma membrane. Coinjection of oocytes with equal amounts of mutant and WT Kir7.1 cRNAs resulted in inward K+ and Rb+ currents with amplitudes that were ∼17% of those in oocytes injected with WT Kir7.1 cRNA alone, demonstrating a dominant-negative effect of the mutant subunit. Similar to oocytes injected with WT Kir7.1 cRNA alone, coinjected oocytes exhibited inwardly rectifying Rb+ currents that were more than seven times larger than K+ currents, indicating that mutant subunits did not alter Kir7.1 channel selectivity. Immunostaining of Xenopus oocytes or Madin-Darby canine kidney cells expressing mutant or WT Kir7.1 demonstrated distribution of both proteins primarily in the plasma membrane. Our data suggest that the R162W mutation suppresses Kir7.1 channel activity, possibly by negatively impacting gating by membrane phosphadidylinositol 4,5-bisphosphate.

scholarly journals Distinct inwardly rectifying K+ channels mediate agonist-inhibition of hormone secretion between α and β cells of pancreatic islet

1999 ◽  
Vol 79 ◽  
pp. 92
Author(s):  
Yukiko Yoshimoto ◽  
Yoshiyuki Horio ◽  
Yuji Fukuyama ◽  
Atsushi Inanobe ◽  
Uchida Wataru ◽  
...  
Keyword(s):  
Pancreatic Islet ◽  
Hormone Secretion ◽  
Β Cells ◽  
K Channels ◽  
Inwardly Rectifying

Detergents, dimeric G beta gamma, and eicosanoid pathways to muscarinic atrial K+ channels

1990 ◽  
Vol 258 (5) ◽  
pp. H1507-H1514 ◽  
Author(s):  
A. Yatani ◽  
K. Okabe ◽  
L. Birnbaumer ◽  
A. M. Brown
Keyword(s):  
Cold Spring Harbor ◽  
K Channel ◽  
Direct Effects ◽  
K Channels ◽  
Nonspecific Effects ◽  
Gamma Subunits ◽  
Cold Spring ◽  
Inwardly Rectifying ◽  
Channel Currents ◽  
Zwitterionic Detergent

Control experiments for the direct effects of G protein beta gamma-subunits (G beta gamma) on muscarinic atrial K+ channel [K+ (ACh)] currents have produced different results (Nature Lond. 327: 21-22, 1987; Nature Lond. 325: 296-297, 1987; Cold Spring Harbor Symp. Quant. Biol. 53: 365-373, 1989). A recent view is that stimulation is indirect via phospholipase by (PLA2) and arachidonic acid (AA) metabolites (Nature Lond. 337: 504-505, 1989). On reexamination we found that 1) the zwitterionic detergent 3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulfonate (CHAPS) used to suspend beta gamma stimulates atrial K+ (ACh) currents by itself, and the effects are concentration and Mg2+ dependent; 2) CHAPS stimulates atrial ATP-sensitive K+ channel and inwardly rectifying K+ channel currents; 3) blockers of eicosanoid pathways have nonspecific effects on atrial K+, Ca2+, and Na+ channels. We have confirmed that detergent-free, hydrophilic G beta gamma-subunits inhibit K+ (ACh) currents. Stimulatory effects of dimeric G beta gamma could not be separated from stimulatory effects of detergent, and blockers of PLA2 or lipoxygenase pathways do not clearly establish the significance of these pathways to atrial K+ (ACh) currents.

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