Blocking of Ca-dependent outward current in molluscan neuron somatic membrane by raised intracellular pH

1983 ◽  
Vol 14 (4) ◽  
pp. 324-328
Author(s):  
P. A. Doroshenko ◽  
A. E. Martynyuk
Keyword(s):  
Intracellular Ph ◽  
Outward Current ◽  
Somatic Membrane ◽  
Molluscan Neuron

Membrane potential oscillations in molluscan “burster” neurones

1979 ◽  
Vol 81 (1) ◽  
pp. 93-112
Author(s):  
R. W. Meech
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Intracellular Ph ◽  
Action Potentials ◽  
Outward Current ◽  
Ionized Calcium ◽  
Isolated Cells ◽  
Potential Oscillations ◽  
Inward Current ◽  
Membrane Potential Oscillations

Membrane potential oscillations can be induced in molluscan neurones under a variety of artificial conditions. In the so-called ‘burster’ neurones oscillations are generated even in isolated cells. A likely mechanism for ‘bursting’ involves the following ionic currents: 1. A transient inward current carried by Na+ and Ca2+. This current is responsible for the upstroke of the action potentials. 2. A delayed outward current carried by K+. This current is voltage-sensitive and is responsible for the downstroke of the action potential during the early part of the burst. It becomes progressively inactivated during the burst. Its amplitude depends on the intracellular pH. 3. A rapidly developing outward current carried by K+ which is inactivated at potentials close to action potential threshold. This current tends to hold the membrane in the hyperpolarized state and is involved in spacing the action potentials. 4. A prolonged inward current which may not inactivate. It is probably carried by both Na+ and Ca2+. This current is responsible for the depolarizing phase of the burst but also contributes to the action potential. 5. A slowly developing outward current, carried by K+. This current appears as a result of a slow increase in intracellular ionized calcium and is responsible for the hyperpolarizing phase of the burst. Note that a transient increase in this current may also contribute to the falling phase of the action potential during the later stages of the burst. It is also sensitive to intracellular pH. One of the more significant features of this system of producing membrane potential oscillations is that the frequency of the bursts depends on the rate at which the intracellular ionized calcium returns to its resting level. This process depends on the metabolic state of the animal which can thereby exert a considerable influence on the electrical activity of burster neurones.

scholarly journals A Highly Temperature-sensitive Proton Current in Mouse Bone Marrow–derived Mast Cells

1997 ◽  
Vol 109 (6) ◽  
pp. 731-740 ◽  
Author(s):  
Miyuki Kuno ◽  
Junko Kawawaki ◽  
Fusao Nakamura
Keyword(s):  
Bone Marrow ◽  
Mast Cells ◽  
Intracellular Ph ◽  
Time Course ◽  
Reversal Potential ◽  
Outward Current ◽  
Temperature Sensitive ◽  
Mouse Bone Marrow ◽  
Bafilomycin A1 ◽  
Ph Homeostasis

Proton (H+) conductive pathways are suggested to play roles in the regulation of intracellular pH. We characterized temperature-sensitive whole cell currents in mouse bone marrow–derived mast cells (BMMC), immature proliferating mast cells generated by in vitro culture. Heating from 24 to 36°C reversibly and repeatedly activated a voltage-dependent outward conductance with Q10 of 9.9 ± 3.1 (mean ± SD) (n = 6). Either a decrease in intracellular pH or an increase in extracellular pH enhanced the amplitude and shifted the activation voltage to more negative potentials. With acidic intracellular solutions (pH 5.5), the outward current was detected in some cells at 24°C and Q10 was 6.0 ± 2.6 (n = 9). The reversal potential was unaffected by changes in concentrations of major ionic constituents (K+, Cl−, and Na+), but depended on the pH gradient, suggesting that H+ (equivalents) is a major ion species carrying the current. The H+ current was featured by slow activation kinetics upon membrane depolarization, and the activation time course was accelerated by increases in depolarization, elevating temperature and extracellular alkalization. The current was recorded even when ATP was removed from the intracellular solution, but the mean amplitude was smaller than that in the presence of ATP. The H+ current was reversibly inhibited by Zn2+ but not by bafilomycin A1, an inhibitor for a vacuolar type H+-ATPase. Macroscopic measurements of pH using a fluorescent dye (BCECF) revealed that a rapid recovery of intracellular pH from acid-load was attenuated by lowering temperature, addition of Zn2+, and depletion of extracellular K+, but not by bafilomycin A1. These results suggest that the H+ conductive pathway contributes to intracellular pH homeostasis of BMMC and that the high activation energy may be involved in enhancement of the H+ conductance.

Investigation of the TEA-resistant outward current in the somatic membrane of perfused nerve cells

1980 ◽  
Vol 11 (5) ◽  
pp. 341-348
Author(s):  
P. A. Doroshenko ◽  
P. G. Kostyuk ◽  
A. Ya. Tsyndrenko
Keyword(s):  
Outward Current ◽  
Nerve Cells ◽  
Somatic Membrane

Inactivation of calcium currents in the molluscan neuron somatic membrane

1983 ◽  
Vol 14 (5) ◽  
pp. 387-392
Author(s):  
P. A. Doroshenko ◽  
P. G. Kostyuk ◽  
A. E. Martynyuk
Keyword(s):  
Calcium Currents ◽  
Somatic Membrane ◽  
Molluscan Neuron

Changes in intracellular pH affect calcium currents in Paramecium caudatum

1982 ◽  
Vol 216 (1203) ◽  
pp. 209-224 ◽  
Keyword(s):  
Membrane Potential ◽  
Intracellular Ph ◽  
Outward Current ◽  
Calcium Currents ◽  
Resting Membrane Potential ◽  
Ca Channel ◽  
Paramecium Caudatum ◽  
Membrane Excitability ◽  
Ca Current ◽  
Intracellular Alkalinization

The relation between intracellular pH and membrane excitability was studied in the holotrich ciliate Paramecium caudatum . Intracellular pH (pH j ) was measured with recessed-tip ion-sensitive microelectrodes (Thomas 1974) and electrical properties were examined by current stimulation and conventional two-electrode voltage clamp. Under normal conditions the resting pH i of Paramecium was 6.80 ± 0.05. Intracellular alkalinization enhanced the early Ca current, while internal acidification depressed the Ca current. Both effects occurred in a voltage-independent manner. The late outward current was relatively unaffected by these alterations. Results obtained with replacement of extracellular Ca 2+ by Ba 2+ also support a direct effect of pH i on current through the Ca channel. Intracellular alkalinization to pH 7.15 converted graded, quasi-regenerative Ca responses elicited by injected current pulses into all-or-none action potentials. This change to all-or-none behaviour is presumed to be due to the increase in Ca current and a consequent change in the balance of inward and outward currents. Extracellular pH changes had little effect on pH i , resting membrane potential or the current-voltage relations. The intracellular pH was also independent of shifts in membrane potential. The results are consistent with a model in which Ca channel permeability is blocked by intracellular protonation of a single titratable site having an apparent dissociation constant of 6.2.

Two selective filters in the calcium channel of the molluscan neuron somatic membrane

1984 ◽  
Vol 15 (4) ◽  
pp. 314-319 ◽  
Author(s):  
P. G. Kostyuk ◽  
S. L. Mironov ◽  
Ya. M. Shuba
Keyword(s):  
Calcium Channel ◽  
Somatic Membrane ◽  
Molluscan Neuron

Mechanisms of intracellular pH regulation during postischemic reperfusion of diabetic rat hearts

Diabetes ◽  
1995 ◽  
Vol 44 (2) ◽  
pp. 196-202 ◽  
Author(s):  
N. Khandoudi ◽  
M. Bernard ◽  
P. Cozzone ◽  
D. Feuvray
Keyword(s):  
Intracellular Ph ◽  
Ph Regulation ◽  
Diabetic Rat ◽  
Intracellular Ph Regulation ◽  
Postischemic Reperfusion ◽  
Rat Hearts
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