Sodium-pump potentials and currents in guinea-pig ventricular muscles and myocytes

1999 ◽  
Vol 77 (5) ◽  
pp. 339-349 ◽  
Author(s):  
Yuji Kasamaki ◽  
An Chi Guo ◽  
Lesya M Shuba ◽  
Toshitsugu Ogura ◽  
Terence F McDonald

When guinea-pig papillary muscles were depolarized to ca. -30 mV by superfusion with K+-free Tyrode's solution supplemented with Ba2+, Ni2+, and D600, addition of Cs+ transiently hyperpolarized the membrane in a reproducible manner. The size of the hyperpolarization (pump potential) depended on the duration of the preceding K+-free exposure; peak amplitudes (Epmax) elicited by 10 mM Cs+ after 5-, 10-, and 15-min K+-free exposures were 12.9, 17.7, and 23.2 mV, respectively. Pump potentials were unaffected by external Cl- but suppressed by cardiac glycosides, hyperosmotic conditions, and low-Na+ solution. Using Epmax as an indicator of Na+ pump activation, the half-maximal concentration for activation by Cs+ was 12-16.3 mM. At 6 mM, Cs+ was three times less potent than Rb+ or K+ and five times more potent than Li+. From these findings, and correlative voltage-clamp data from myocytes, we calculate that (i) a pump current of 7.8 nA/cm2 generates an Epmax of 1 mV and (ii) resting pump current in normally polarized muscle (~0.16 µA/cm2) is five times smaller than previously estimated.Key words: sodium pump, cesium, rubidium, sodium pump current.

1999 ◽  
Vol 81 (4) ◽  
pp. 1478-1485 ◽  
Author(s):  
Christopher A. del Negro ◽  
Chie-Fang Hsiao ◽  
Scott H. Chandler

Outward currents influencing bursting dynamics in guinea pig trigeminal motoneurons. To initiate and maintain bursts (and plateau potentials) in the presence of serotonin, guinea pig trigeminal motoneurons utilize L-type Ca2+ and persistent Na+ inward currents. However, the intrinsic currents that contribute to burst termination and determine the duration of the interburst interval are unknown. Therefore we investigated the roles of outward currents, whose slow activation is coupled to cytosolic cation (Ca2+ and Na+) accumulation. First we examined a Ca2+-dependent K+ current ( I K-Ca) with apamin and Ba2+-substituted, low-Ca2+ solution. Blockade of I K-Ca lengthened burst duration and cycle time but did not abolish bursting. Next we studied the Na+/K+-ATPase pump current ( I p) with cardiac glycosides. In the presence of apamin or low-Ca2+/Ba2+ solution, blocking I p (with ouabain or strophanthidin) decreased both burst duration and cycle time and ultimately transformed bursting into tonic spiking. We conclude that I K-Ca and I p contribute to burst termination in trigeminal motoneurons. These currents influence temporal bursting properties such as burst duration and cycle time and may help determine the phasic activity of motoneurons during rhythmic oral-motor behaviors.


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