scholarly journals Mutational Analysis of theShab-encoded Delayed Rectifier K+Channels inDrosophila

1999 ◽  
Vol 274 (31) ◽  
pp. 22109-22113 ◽  
Author(s):  
Priti Hegde ◽  
Gang-Gou Gu ◽  
Dong Chen ◽  
Stephen J. Free ◽  
Satpal Singh
Keyword(s):  
Mutational Analysis ◽  
Delayed Rectifier ◽  
K Channels

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.

Pseudomonas fluorescens lipopolysaccharide inhibits both delayed rectifier and transient A-type K+ channels of cultured rat cerebellar granule neurons

2003 ◽  
Vol 983 (1-2) ◽  
pp. 185-192 ◽  
Author(s):  
Sana Mezghani-Abdelmoula ◽  
Sylvie Chevalier ◽  
Olivier Lesouhaitier ◽  
Nicole Orange ◽  
Marc G.J. Feuilloley ◽  
...  
Keyword(s):  
Pseudomonas Fluorescens ◽  
Cerebellar Granule Neurons ◽  
Delayed Rectifier ◽  
Granule Neurons ◽  
Cerebellar Granule ◽  
K Channels ◽  
Type K

Inhibition of the cloned delayed rectifier K+ channels, Kv1.5 and Kv3.1, by riluzole

Neuroscience ◽  
2005 ◽  
Vol 133 (4) ◽  
pp. 1007-1019 ◽  
Author(s):  
H.S. Ahn ◽  
J.-S. Choi ◽  
B.H. Choi ◽  
M.-J. Kim ◽  
D.-J. Rhie ◽  
...  
Keyword(s):  
Delayed Rectifier ◽  
K Channels

scholarly journals Changes in the expression of potassium channels during mouse T cell development.

1986 ◽  
Vol 164 (6) ◽  
pp. 1846-1861 ◽  
Author(s):  
D McKinnon ◽  
R Ceredig
Keyword(s):  
T Cell ◽  
T Lymphocytes ◽  
Cell Lineage ◽  
Electrophysiological Recording ◽  
K Channel ◽  
Delayed Rectifier ◽  
Developmentally Regulated ◽  
K Channels ◽  
Channel Expression ◽  
Low Levels

In this report we have combined the whole-cell electrophysiological recording technique with flow microfluorometry to isolate phenotypically defined thymocytes and T lymphocytes. Results obtained showed that J11d-/Lyt-2-/L3T4- cells express none or very few delayed rectifier K+ channels, whereas most other Lyt-2-/L3T4- cells, as well as typical cortical thymocytes (Lyt-2+/L3T4+), do express K+ channels. Mature (Lyt-2+/L3T4- or Lyt-2-/L3T4+) thymocytes, which are heterogeneous for J11d expression, were also found to be heterogeneous for K+ channel expression. Consistent with this finding was the observation that the cortisone-resistant subpopulation of thymocytes, which express low levels of J11d, were enriched for cells expressing low levels of K+ channels. Mature phenotype peripheral T lymphocytes expressed very low levels of K+ channels, but upon activation with Con A were found to express high levels of K+ channels. The results suggest that K+ channel expression in T cells is developmentally regulated. Increased expression of the channel is induced in response to mitogenic signals throughout the T cell lineage. Expression of the channel, therefore, serves as a useful marker in defining steps in the T cell differentiation pathway.

scholarly journals Charybdotoxin selectively blocks small Ca-activated K channels in Aplysia neurons.

1987 ◽  
Vol 90 (1) ◽  
pp. 27-47 ◽  
Author(s):  
A Hermann ◽  
C Erxleben
Keyword(s):  
Single Channel ◽  
Delayed Rectifier ◽  
Pacemaker Activity ◽  
Dependent Manner ◽  
Open Probability ◽  
Apparent Dissociation Constant ◽  
External Application ◽  
K Channels ◽  
Voltage Dependent ◽  
K Current

The action of charybdotoxin (ChTX), a peptide component isolated from the venom of the scorpion Leiurus quinquestriatus, was investigated on membrane currents of identified neurons from the marine mollusk, Aplysia californica. Macroscopic current recordings showed that the external application of ChTX blocks the Ca-activated K current in a dose- and voltage-dependent manner. The apparent dissociation constant is 30 nM at V = -30 mV and increases e-fold for a +50- to +70-mV change in membrane potential, which indicates that the toxin molecule is sensitive to approximately 35% of the transmembrane electric field. The toxin is bound to the receptor with a 1:1 stoichiometry and its effect is reversible after washout. The toxin also suppresses the membrane leakage conductance and a resting K conductance activated by internal Ca ions. The toxin has no significant effect on the inward Na or Ca currents, the transient K current, or the delayed rectifier K current. Records from Ca-activated K channels revealed a single channel conductance of 35 +/- 5 pS at V = 0 mV in asymmetrical K solution. The channel open probability increased with the internal Ca concentration and with membrane voltage. The K channels were blocked by submillimolar concentrations of tetraethylammonium ions and by nanomolar concentrations of ChTX, but were not blocked by 4-aminopyridine if applied externally on outside-out patches. From the effects of ChTX on K current and on bursting pacemaker activity, it is concluded that the termination of bursts is in part controlled by a Ca-activated K conductance.

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