Inorganic mercury interacts with thiols at the nucleotide and cationic binding sites of the ouabain-sensitive cerebral electrogenic sodium pump

2011 ◽  
Vol 58 (7) ◽  
pp. 776-784 ◽  
Author(s):  
T.I. Omotayo ◽  
J.B.T. Rocha ◽  
E.O. Ibukun ◽  
I.J. Kade
Keyword(s):  
Binding Sites ◽  
Sodium Pump ◽  
Inorganic Mercury ◽  
Electrogenic Sodium Pump

Mammalian cold receptor afferents: role of an electrogenic sodium pump in sensory transduction

1974 ◽  
Vol 73 (1) ◽  
pp. 156-160 ◽  
Author(s):  
Friedrich-Karl Pierau ◽  
Peter Torrey ◽  
David O. Carpenter
Keyword(s):  
Sodium Pump ◽  
Sensory Transduction ◽  
Cold Receptor ◽  
Electrogenic Sodium Pump

An Investigation of the Electrogenic Sodium Pump in Snail Neurones, Using the Constant-Field Theory

1969 ◽  
Vol 51 (1) ◽  
pp. 181-201
Author(s):  
R. B. MORETON
Keyword(s):  
Field Equation ◽  
Sodium Pump ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Constant Field ◽  
Sodium Ions ◽  
Intracellular Potassium ◽  
Electrogenic Sodium Pump ◽  
Snail Neurones ◽  
Intracellular Potassium Concentration

1. Sodium ions injected into giant neurones of Helix aspersa by diffusion from low-resistance microelectrodes caused hyperpolarization of the cells. Under these conditions the behaviour of the resting potential could be described by a modified ‘constant-field’ equation, including a term representing the effect of a potassiumsensitive, electrogenic sodium pump. 2. Exposure to potassium-free solution, ouabain or cyanide abolished the hyperpolarization, and caused a gradual fall in the intracellular potassium concentration, as estimated from the constant-field equation. 3. Assuming that this fall was due to replacement of intracellular potassium by injected sodium ions, it was possible to calculate the rates of injection and pumping of sodium ions, and, using the measured membrane resistance of the cell, the hyperpolarization which the sodium pump could cause, if it were electrogenic. 4. This was related to the observed hyperpolarization, supporting the view that the latter was caused by stimulation of the electrogenic sodium pump.

Activation of electrogenic sodium pump in hippocampal CA1 neurons following glutamate-induced depolarization

1986 ◽  
Vol 56 (2) ◽  
pp. 507-522 ◽  
Author(s):  
S. M. Thompson ◽  
D. A. Prince
Keyword(s):  
Pyramidal Neurons ◽  
Sodium Pump ◽  
Equilibrium Potential ◽  
Ca1 Neurons ◽  
Electrogenic Sodium Pump ◽  
Hippocampal Ca1 ◽  
Voltage Dependent ◽  
Specific Antagonist ◽  
Conductance Increase

Intracellular recordings were obtained from guinea pig hippocampal CA1 pyramidal neurons maintained in vitro. Focal applications of glutamate produced depolarizations followed by prolonged hyperpolarizations. The mechanisms underlying this postglutamate hyperpolarization (PGH) were investigated. PGH did not reverse polarity with hyperpolarization to potentials at or near the presumed K+ equilibrium potential. A transient increase in conductance was associated with the PGH; control values returned well before the termination of PGH. Application of Mn2+, an antagonist of voltage-dependent calcium conductance, blocked synaptic transmission and the afterhyperpolarization (AHP) that follows a directly evoked train of action potentials but did not diminish the PGH or the transient conductance increase. Intracellular application of the calcium chelator ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid blocked AHP but did not affect PGH. Reductions in temperature from 37 to 27-32 degrees C reduced the amplitude of PGH and prolonged its duration but increased the amplitude and duration of AHP. The transient conductance increase associated with PGH was unaffected. Application of strophanthidin, a specific antagonist of Na+-K+-ATPase, reversibly blocked PGH and led to large increases in the amplitude and duration of the AHP. It is concluded that PGH is produced by activation of the electrogenic sodium pump by glutamate-induced excitation. As such, PGH is a useful physiological assay of electrogenic sodium transport. In addition, maintenance of the Na+ gradient by the sodium pump is important for the buffering of Ca2+ influx.

scholarly journals Photoreception in Limulus: Role of an Electrogenic Sodium Pump?

Science ◽  
1969 ◽  
Vol 164 (3884) ◽  
pp. 1188-1189 ◽  
Author(s):  
G. Duncan ◽  
S. L. Bonting ◽  
T. G. Smith ◽  
J. E. Brown ◽  
W. K. Stell ◽  
...  
Keyword(s):  
Sodium Pump ◽  
Electrogenic Sodium Pump

Monovalent Ion Specificity of the Electrogenic Sodium Pump in Vascular Smooth Muscle

1981 ◽  
Vol 166 (3) ◽  
pp. 457-461 ◽  
Author(s):  
R. C. Webb ◽  
W. E. Lockette ◽  
P. M. Vanhoutte ◽  
D. F. Bohr
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Sodium Pump ◽  
Ion Specificity ◽  
Electrogenic Sodium Pump ◽  
Monovalent Ion

Electrogenic sodium-dependent glycine transport in sheep reticulocytes

1978 ◽  
Vol 56 (6) ◽  
pp. 545-551 ◽  
Author(s):  
Stephen Benderoff ◽  
Rose M. Johnstone ◽  
Rhoda Blostein
Keyword(s):  
Membrane Potential ◽  
Sodium Pump ◽  
Marked Decrease ◽  
Massive Bleeding ◽  
Atp Content ◽  
Chemical Gradient ◽  
Electrogenic Sodium Pump ◽  
Sodium Dependent ◽  
Glycine Transport ◽  
Measurable Change

Na+-dependent glycine transport has been studied in reticulocyte-enriched fractions of blood obtained after massive bleeding of sheep. The activity is dependent on the sodium electrochemical potential and the membrane potential. The sodium chemical gradient was varied by changing either external or internal Na+ and the membrane potential, by addition of valinomycin. Similar results were obtained with resealed reticulocyte ghosts. Under conditions optimal for sodium pumping (intracellular Na+ > 50 mM), ouabain inhibited glycine uptake prior to any measurable change in the cellular Na+ suggesting that in these cells an electrogenic sodium pump is sufficiently active to contribute to the membrane potential. Na+-dependent glycine transport undergoes a marked decrease during Song-term incubation at 37 °C. During this time, the cells maintain their integrity and ATP content but undergo maturation as evidenced in the decrease in cells with reticulocyte morphology.

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