Volume regulation of murine T lymphocytes relies on voltage-dependent and two-pore domain potassium channels

2011 ◽  
Vol 1808 (8) ◽  
pp. 2036-2044 ◽  
Author(s):  
Nicole Bobak ◽  
Stefan Bittner ◽  
Joseph Andronic ◽  
Susanne Hartmann ◽  
Friederike Mühlpfordt ◽  
...  
2013 ◽  
Vol 1828 (2) ◽  
pp. 699-707 ◽  
Author(s):  
Joseph Andronic ◽  
Nicole Bobak ◽  
Stefan Bittner ◽  
Petra Ehling ◽  
Christoph Kleinschnitz ◽  
...  

2005 ◽  
Vol 12 (7) ◽  
pp. 808-813 ◽  
Author(s):  
Rafael Godínez Fernández ◽  
Joaquín Azpiroz Leehan ◽  
Reyna Fierro Pastrana ◽  
Rocío Ortíz Muñiz

ABSTRACT Severe malnutrition in children is frequently associated with infectious diseases. Animal models have been useful for studying the effects of malnutrition. One of the immunosuppressive mechanisms of malnutrition is inhibition of the activation of T lymphocytes. The voltage-dependent K(V) potassium channels are vital for the activation of T lymphocytes. The blockade of K(V) channels inhibits the activation of T lymphocytes. Malnutrition could affect the suitable synthesis of K(V) channels in T lymphocytes, producing changes in the magnitude and/or dependency of the voltage of the K+ current. We reported a significant decrease in the K+ current and activation to a 20 mV more positive membrane potential in T lymphocytes of rats with severe malnutrition. These results indicate that the diminution in the K+ conductance by alteration of K(V) channels in severe malnutrition is one of the mechanisms that inhibit the activation of T lymphocytes.


1991 ◽  
Vol 266 (12) ◽  
pp. 7583-7587
Author(s):  
M P Kavanaugh ◽  
M D Varnum ◽  
P B Osborne ◽  
M J Christie ◽  
A E Busch ◽  
...  

2014 ◽  
Vol 453 (4) ◽  
pp. 754-760 ◽  
Author(s):  
Paulina Burgos ◽  
Rafael Zúñiga ◽  
Pedro Domínguez ◽  
Fernando Delgado-López ◽  
Leigh D. Plant ◽  
...  

1981 ◽  
Vol 78 (1) ◽  
pp. 43-61 ◽  
Author(s):  
I Inoue

A spike that is the result of calcium permeability through potassium channels was separated from the action potential is squid giant axons internally perfused with a 30 mM NaF solution and bathed in a 100 mM CaCl2 solution by blocking sodium channels with tetrodotoxin. Currents through potassium channels were studied under voltage clamp. The records showed a clear voltage-dependent inactivation of the currents. The inactivation was composed of at least two components; one relatively fast, having a time constant of 20--30 ms, and the other very slow, having a time constant of 5--10 s. Voltage clamp was carried out with a variety of salt compositions in both the internal and external solutions. A similar voltage-dependent inactivation, also composed of the two components, was recognized in all the current through potassium channels. Although the direction and intensity of current strongly depended on the salt composition of the solutions, the time-courses of these currents at corresponding voltages were very similar. These results strongly suggest that the inactivation of the currents in attributable to an essential, dynamic property of potassium channels themselves. Thus, the generation of a potassium-channel spike can be understood as an event that occurs when the equilibrium potential across the potassium channel becomes positive.


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