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PubMed1981

Thermosensitivity of the membrane potential of normal and simian virus 40-transformed hamster lymphocytes.

The effects of temperature in the fever range (37-42 degrees) on the membrane potentials of normal and simian virus 40-transformed hamster lymphocytes were analyzed. The transmembrane distributions of radiolabeled triphenylmethylphosphonium and thiocyanate were measured, and they provide upper and lower limits for the normal cell membrane potential at 37 degrees of -48 +/- 6 (S.D.) and -31 +/- 5 mV and for the tumor cells, -36 +/- 4 and -19 +/- 2 mV. The mitochondrial contribution to the triphenylmethylphosphonium-measured membrane potential, 5 to 10 mV for both splenocytes and simian virus 40-transformed lymphocytes, was estimated by utilizing antimycin A and carbonylcyanide-m-chlorophenylhydrazone to inhibit generation of a mitochondrial membrane potential. Incubation for 1 to 2 hr at 38-42 degrees resulted in a 6- to 15-mV depolarization of normal cells and a 2- to 6-mV hyperpolarization of tumor cells. Both depolarization and hyperpolarization were fully reversible by subsequent incubation at 37 degrees and insensitive to antimycin A and carbonyl-cyanide-m-chlorophenylhydrazone. The membrane potential of normal splenocytes when measured with triphenylmethylphosphonium at 37 degrees was depolarized by 35% with 1 mM ouabain and thermally induced depolarization was blocked. The membrane potential of tumor cells at 37 degrees was insensitive to ouabain; however, the hyperpolarization at 40 degrees was inhibited. The membrane potential of normal lymphocytes stimulated with phytohemagglutinin was depolarized relative to that of nonstimulated control cells and assumed the thermal response characteristics of tumor cells.

Animals↗

PubMed2005

Membrane potential across low-water-content charged membranes: Effect of ion pairing.

In the present paper, we systematically examined the ion-pairing effect in low-water-content charged membranes. Cation- and anion-exchange membranes with various water contents and homogeneous fixed-charge distribution were prepared by radical copolymerization and then characterized by membrane potential measurements. The experimental results were analyzed by our recently developed theoretical model (Yamamoto, R.; Matsumoto, H.; Tanioka, A. J. Phys. Chem. B 2003, 107, 10615), which is based on the Donnan equilibrium, the Nernst-Planck equation for ion flux, and the Fuoss formalism for ion-pair formation between the fixed-charge group and the counterion in the membrane. The theoretical predictions agreed well with the experimental results for both cation- and anion-exchange membranes. This supported the belief that the ion-pairing effect was substantial in a low-water-content membrane system. Our theoretical analysis also showed the following results: (i) the dielectric constant in the membrane, epsilon(r), was smaller than the value in bulk water, (ii) the center-to-center distance of the ion pair, a, was independent of the water content of the membranes, and (iii) the charge effectiveness of all membranes, Q, was small (<0.35).

Journal Article↗

PubMed2002

[Changes in mitochondrial membrane potentials and its exponential relation with phosphatidylserine translocation in the plasma membrane as markers in the initial events of apoptosis: evaluation in different spermatic fractions].

OBJECTIVE: To determine the integrity of the plasmatic membrane through phosphatidylserine (PS) translocation in two spermatic fractions and their correlation with the spermatic mitochondrial membrane potential. MATERIAL AND METHODS: The analysis of both spermatic fractions was carried out through a discontinuous gradient separation with Percoli, in order to obtain two samples with high and low mobility (90-40%). Twelve patients were recruited for the initial evaluation of seminal parameters. Mitochondrial membrane integrity was determined using a second antibody (Mitosensor), and was analyzed by fluorescence microscopy, evaluating an average of 200 cells. A 450-490 nm excitation filter was used for this analysis. Cytoplasmatic assessment was carried out by anexine V bonding to PS, in order to determine the initial events of cellular death. Non parameter tests were used in order to determine the differences between mitochondrial potentials and plasmatic membrane processes. Linear correlation tests were used for the anexine V and Mitosensor ratios. RESULTS: Due to the study's design, some differences were observed regarding the displacement parameters and the presence of apoptosis, both, in the plasmatic membrane and in mitochondrial membrane potentials. A positive correlation between both, mitochondrial and cytoplasmic membrane functions was also found. CONCLUSIONS: This is the first study performing a comparative analysis between mitochondrial membrane function and cytoplasmatic PS expression as early cellular death markers. The male infertility population is probably associated with an increase in this kind of apoptosis processes.

Apoptosis↗

PubMed1984

Contributions of electrogenic pumps to resting membrane potentials: the theory of electrogenic potentials.

Pumped and transported components of ionic flux have been added to passive electrodiffusive components. This permits the derivation of equations for the resting membrane potential that take account of electrogenic mechanisms in which the transport mechanism or pump itself produces a net ionic current. Such equations are general in that they apply to non-steady-state conditions in which intracellular ionic concentrations are changing. The equations developed allow calculation of resting membrane potentials in terms of ionic concentrations, membrane permeability to ions, and kinetic relations for pumped ionic fluxes. When applied to skeletal muscle fibers, the equations predict a buffering effect of the Na/K pump on the membrane potential over a wide range in the values [K]i and [Na]i such that a fairly constant membrane potential occurs under conditions in which the passive ionic fluxes themselves would produce increasing degrees of depolarization. A plot of the membrane potential versus log [K]o with an electrogenic Na pump present gives a curve with slopes both greater than and less than 58 mV per 10-fold concentration change. Over a middle range of [K]o values, the slope is 58 mV. The slope of Em versus log [K]o curves is, therefore, not a very sensitive test for the presence of an electrogenic pump. For the same internal ionic concentrations, less electrogenic increment in membrane potential is observed the higher the value of [K]o, and the more depolarized the membrane. This is due to a rectification present in the pump current-voltage curve, which requires that more pump current be present to produce a given membrane hyperpolarization at depolarized values of the potential than at hyperpolarized values of the potential. A gain in Na and a loss of K by the fibers affects the rectification curve in such a way that less pump current is required to produce the same degree of hyperpolarization. This mechanism ensures that adequate internal negativity will be maintained at high values of [Na]i and [K]o where saturation of the pumping rates might be expected. In the non-steady state of Na extrusion, the condition for which these equations were developed, it is clearly possible for the Na pump to generate potentials considerably higher than those generated under steady-state conditions. For steady-state conditions, both skeletal muscle and squid giant axon Na pumps generate additional internal negativity amounting to a few millivolts.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1970

The spatial variation of membrane potential near a small source of current in a spherical cell.

A theoretical analysis is presented of the change in membrane potential produced by current supplied by a microelectrode inserted just under the membrane of a spherical cell. The results of the analysis are presented in tabular and graphic form for three wave forms of current: steady, step function, and sinusoidal. As expected from physical reasoning, we find that the membrane potential is nonuniform, that there is a steep rise in membrane potential near the current microelectrode, and that this rise is of particular importance when the membrane resistance is low, or the membrane potential is changing rapidly. The effect of this steep rise in potential on the interpretation of voltage measurements from spherical cells is discussed and practical suggestions for minimizing these effects are made: in particular, it is pointed out that if the current and voltage electrodes are separated by 60 degrees , the change in membrane potential produced by application of current is close to that which would occur if there were no spatial variation of potential. We thus suggest that investigations of the electrical properties of spherical cells using two microelectrodes can best be made when the electrodes are separated by 60 degrees .

Cell Membrane↗

PubMed1984

Characterization of the plasma and mitochondrial membrane potentials of alveolar type II cells by the use of ionic probes.

The lipophilic cation triphenylmethylphosphonium (TPMP+) and the potassium analog Rb+, were used to monitor the membrane potential (delta psi) of freshly isolated rabbit type II alveolar epithelial cells. Type II cells were found to accumulate TPMP+ rapidly at 37 degrees C in Hanks' balanced-salt solution with 5 microM tetraphenyl boron, but this accumulation was partially due to non-membrane potential dependent binding of TPMP+ to the cell. Lysophosphatidylcholine (lysoPC) was found to abolish delta psi and permitted correction for bound TPMP+ or Rb+. TPMP+ remaining in the cell following correction for binding represents the sum of mitochondrial and plasma membrane potential dependent accumulation. The accumulation of Rb+ by the type II cell was found to be independent of the mitochondrial membrane potential and indicated a trans-plasma membrane Rb+ distribution potential of -62.9 +/- 4 mV. A similar value was obtained by estimating the plasma membrane potential dependent accumulation of TPMP+ in type II cells whose mitochondria were depolarized with carbonylcyanide m-chlorophenylhydrazone (CCCP). The release of TPMP+ due to CCCP treatment also permitted an estimation for the trans-mitochondrial membrane potential of -141.8 +/- 10 mV. These techniques of membrane potential measurements were found to be sensitive to changes in delta psi induced by a number of inhibitors and ionophores. The ability to measure the membrane potential of the type II pneumocyte, and the changes caused by various agents, should be useful in characterizing the functional responses of this pulmonary surfactant producing cell.

Animals↗

PubMed1967

Temperature effects on pacemaker generation, membrane potential, and critical firing threshold in Aplysia neurons.

Temperature increases cause a regular and reproducible increase in the frequency of generation of pacemaker potentials in most Aplysia neurons specialized for this type of activity which can only be explained as a direct stimulating effect of temperature upon the ionic mechanisms responsible for pacemaker potentials. At the same time all cells in the visceral ganglion undergo a membrane potential hyperpolarization of approximately 1-2 mv/ degrees C warmed. In spite of the marked variation in resting membrane potential the critical firing threshold remains at a constant membrane potential level at all temperatures in the absence of accommodative changes. The temperature-frequency curves of all types of cells are interpreted as a result of the interaction between the effects of temperature on the pacemaker-generating mechanism and resting membrane potential. Previous observations on the effects of temperature on excitability of mammalian neurons suggest that other types of neurons may undergo similar marked shifts in resting membrane potential with temperature variation.

Action Potentials↗

PubMed1988

Studies of axon-glial cell interactions and periaxonal K- homeostasis--I. The influence of Na+, K+, Cl- and cholinergic agents on the membrane potential of the adaxonal glia of the crayfish medial giant axon.

The ionic basis for the low (-40 mV) resting membrane potential of glial cells surrounding the giant axons of the crayfish and their hyperpolarization by cholinergic agents (to -55 mV) was studied using standard electrophysiological techniques, ionic substitutions and pharmacological agents. The resting membrane potential of the glial cell was depolarized by increasing [K+]o, but the response was not Nernstian. Na+ depletion caused a small depolarization of the glial resting membrane potential, whereas Cl- depletion resulted in a hyperpolarization comparable to that seen with carbachol at various [K+]o. Both furosemide (1 mM) and bumetanide (0.1 mM) produced an 8-10 mV hyperpolarization as compared to 15-17 mV seen with Cl- depletion or carbachol. Carbachol has no further effect on the potential following furosemide treatment or Cl- depletion. After carbachol administration or Cl- depletion the resting membrane potential of the glial cell responded to [K+]o in a more Nernstian manner. The data indicate that the low resting membrane potential of glial cells is due to a combination of a low [K+]i and an outwardly-directed (depolarizing) Cl- electrochemical gradient. Carbachol acts to decrease Cl- conductance, resulting in the hyperpolarization of the glial cell membrane and a decrease in the outwardly-directed K+ electrochemical gradient by approximately two-thirds. We hypothesize that this mechanism for modulation of the glial cell membrane potential and the K+ electrochemical gradient serves to enhance the uptake of K+ by the glial cell transport system.

Animals↗

PubMed1988

The binding of IgG1 containing immune complexes to the FcR of allogenically activated T cells induces changes in the membrane potential and the cell surface charge.

The effect on membrane potential and cell surface charge of binding immune complexes containing IgG1 and IgG2a monoclonal antibodies to Fc receptors was studied in resting and allogenically activated murine T cells. IgG1 complexed by antigen or heat aggregation induced electrophysiological changes on activated T cells. A biphasic alteration of membrane potential was detected by measurement of the intra- and extracellular distribution of the fluorescent dye, DiOC6. A short-lived hyperpolarization, detectable for 4-6 min after adding the respective ligand, was followed by a longer lasting depolarization. The cell surface charge, measured by cell electrophoresis, was also changed. This alteration was detected 2-4 hr after addition of immune complexes and disappeared by the 8th hr of incubation. Monoclonal antibody 2.4.G2, reactive with mouse FcR, induced a similar membrane potential response on activated T cells, but did not affect the cell surface charge. Monomeric IgGs and complexes of IgG2a did not modify these parameters. FcR ligands had no effect on the studied characteristics of resting T cells.

Animals↗

PubMed1975

A model for conformational coupling of membrane potential and proton translocation to ATP synthesis and to active transport.

Acceptance of a membrane potential and/or a proton gradient as a possible means of transmitting energy from oxidations to ATP synthesis rests in part on a satisfactory hypothesis for how the potential or proton gradient could drive ATP synthesis. Recognition that energy input may drive ATP synthesis by change in binding of reactants at the catalytic site has led to the suggestions presented in this paper. These are that in oxidative phosphorylation and photophosphorylation, the requisite conformational changes may be coupled to exposure of charged groups to different sides of the membrane. The cycle of charged group exposure or movement may be driven by the membrane potential or, through protonation and deprotonation, may be coupled to proton translocation across the membrane. Effects of proton gradient and membrane potential may be additive. Similar conformational coupling suggestions may explain proton translocation coupled to ATP cleavage and active transport of metabolites coupled to membrane potential, proton gradients of ATP cleavage.

Adenosine Triphosphate↗

PubMedDate not supplied

Carbon monoxide effect on the membrane potential of cells in nervous tissue cultures.

The effects of carbon monoxide (CO) on the membrane potential of neurons and glial cells were investigated using organotropic cultures of the cerebellum of newborn rats in two experimental groups. Group I comprised cultures maintained during 2, 3 and 4 weeks and exposed only once to CO during 30 minutes. In group II 3-week cultures were exposed twice to CO with a 30-minute interval between exposures. The gaseous environment of the cultures contained air with 10% of CO. The results of measurements of membrane potentials carried out immediately after exposure and 24 hours later were subjected to conventional statistical analysis. After one exposure to CO the membrane potential of the neurons and glial cells decreased, and after 24 hours it rose, without, however, reaching the value observed in the cells kept in standard cultures. Immediately after two exposures of 30 minutes each a significant fall of the membrane potential was observed in the neurons and glial cells, while 24 hours later the measurements of the resting potential in all cells showed zero value. The experiments with two exposures to CO for 10 minutes each demonstrated a fall in the membrane potential of neurons and glia, and after 24 hours this potential rose only in glial cells. The results of these investigations are compared with those reported in the literature and the mechanism of disturbances of cell membrane polarization during cytotoxic hypoxia is discussed.

Animals↗

PubMed1985

Intracellular microelectrode studies of Necturus antral mucosa. Effect of aspirin on cell membrane potentials.

Intracellular microelectrode techniques were used to determine the effects of luminal aspirin on epithelial cell membrane potentials of Necturus antral mucosa. In this tissue, prolonged stable intracellular impalements were obtained with 15-50-M omega microelectrodes filled with 3 M KCl. In acidic mucosal solution (pH 4.0) the addition of aspirin at 5.0 mM resulted in a significant decrease of apical cell membrane potential (Vmc) from -36.8 +/- 2.2 to -22.2 +/- 2.1 mV (p less than 0.001) and basolateral cell membrane potentials (Vcs) from -38.8 +/- 1.7 to -25.3 +/- 2.1 mV (p less than 0.001). Upon removal of aspirin from the mucosal solution, both cell membranes hyperpolarized for a brief period before returning to their original potentials. In neutral mucosal solutions (pH 7.0), addition of aspirin (5.0 mM) resulted in a significant increase in apical cell membrane potential (Vmc) from -40.0 +/- 2.4 to -46.8 +/- 3.3 mV (p less than 0.001) and basolateral cell membrane potential (Vcs) from -41.5 +/- 2.0 to -49.7 +/- 2.5 mV (p less than 0.001). This hyperpolarization of the cell was associated with an increase in transmucosal potential from -1.5 +/- 1.8 to -2.9 +/- 1.8 mV (p less than 0.001) and an increase in the ratio of apical to basolateral membrane resistances from 2.2 +/- 0.4 to 3.1 +/- 0.7 (p less than 0.05). These changes in membrane potentials and the ratio of membrane resistances may be caused by a change in ionic conductance of the cell membranes induced by aspirin.

Animals↗

PubMed1980

Antagonistic effect of insulin on glucagon-evoked hyperpolarization. A correlation between changes in membrane potential and gluconeogenesis.

In the perfused rat liver, administration of glucagon causes a hyperpolarization of the liver cell membrane and increases gluconeogenesis. Insulin, a hormone which is known to antagonize the effect of glucagon on gluconeogenesis also blocks the hyperpolarizing effect of glucagon. Because of this inhibitory effect of insulin of the glucagon-evoked hyperpolarization, a systematic study of possible correlation between changes in membrane potential and gluconeogenesis was undertaken. The membrane potential was changed by valinomycin, tetracaine, or by varying the ionic composition of the perfusate. A highly significant correlation between changes in membrane potential and the rate of gluconeogenesis was noticed. The possibility was raised that changes in membrane potential might exert an influence on metabolic process by a yet unknown mechanism.

Animals↗

PubMed1991

Effects of hydrogen peroxide and hypochlorite on membrane potential of mitochondria in situ in rat heart cells.

Hydrogen peroxide (H2O2) and hypochlorite (HOCl) cause a variety of cellular dysfunctions. In this study we examined the effects of these agents on the electrical potential gradient across the inner membrane of mitochondria in situ in isolated rat heart myocytes. Myocytes were prepared by collagenase digestion and incubated in the presence of H2O2 or HOCl. Transmembrane electrical gradients were measured by distribution of [3H]triphenylmethylphosphonium+, a lipophilic cation. The particulate fraction was separated from the cytosolic compartment first by permeabilization using digitonin, followed by rapid centrifugal sedimentation through a bromododecane layer. We found that the mitochondrial membrane potential (161 +/- 7 mV, negative inside) was relatively well maintained under oxidant stress, i.e., the potential was decreased only at high concentrations of HOCl and H2O2 and gradually with time. The membrane potential of isolated rat heart mitochondria was affected similarly by H2O2 and HOCl in a concentration- and time-dependent manner. High concentrations of oxidants also reduced the cellular ATP level but did not significantly change the matrix volume. When the extra-mitochondrial free calcium concentration was increased in permeabilized myocytes, the transmembrane potential was decreased proportionally, and this decrease was potentiated further by H2O2. These results support the view that heart mitochondria are equipped with well-developed defense mechanisms against oxidants, but the action of H2O2 on the transmembrane electrical gradient is exacerbated by an increase in cytosolic calcium.

Animals↗

PubMed1984

Plasma membrane potential of Lettré cells does not depend on cation gradients but on pumps.

The plasma membrane potential of Lettré cells has been determined with the optical indicator oxonol-V and found to be -57 mV at 37 degrees C (range -20 to -80 mV depending on the physiological condition of the cells). Increasing extracellular K+ does not depolarize cells: even in the presence of 155 mM K+ the potential is -41 mV; membrane potential is also insensitive to the chemical gradient of Na+, Mg2+, Ca2+ or Cl-. Ouabain depolarizes the cells; H+ efflux from cells is stimulated by extracellular Na+. We propose that in Lettré cells the plasma membrane potential is generated by electrogenic cation pumps. The balancing fluxes of Na+ and K+ are mainly through electroneutral cation exchanges (Na+/K+ and Na+/H+) and the magnitude of the potential is limited by organic anion leaks. Such a mechanism may operate in other biological membranes also.

Animals↗

PubMed2002

Mitochondrial membrane potential is reduced in peripheral natural killer cells following partial hepatectomy.

The mechanism underlying immunosuppression after partial hepatectomy remains unclear. Hepatectomy induces lymphopenia, which is related to immunomodulation. The aim of this study was to determine whether peripheral blood lymphocytes (PBL) are susceptible to mitochondria-mediated apoptosis after hepatic resection. We compared the changes in mitochondrial membrane potential in lymphocytes from hepatectomized patients with metastatic liver tumor with the corresponding changes in lymphocytes from cholechystectomized patients, because changes in mitochondrial membrane potential have been reported to frequently occur during the early stages of apoptosis. Mitochondrial membrane potential, subpopulation, and apoptosis of lymphocytes were estimated with flow cytometry. Hepatectomy significantly (P<0.001) reduced postoperative mitochondrial membrane potential, while cholecystectomy slightly decreased it. Apoptosis of lymphocytes was increased on post-hepatectomy day, and this increase was correlated with the extent of mitochondrial membrane potential reduction. The major subset of lymphocytes with low mitochondrial membrane potential consisted of CD56(+) natural killer (NK) cells, and NK cell activity and cell counts significantly decreased after hepatectomy. Mitochondrial membrane potential of PBL was reduced after hepatectomy, and some lymphocytes underwent apoptosis through the mitochondrial pathway, which was one of the causes for lymphopenia. NK cells were more responsible for the decrease of mitochondrial membrane potential after hepatectomy than other lymphocytes, and the reduction in mitochondrial membrane potential in NK cells appeared to reflect modulation of the innate immune system.

Apoptosis↗

PubMed1991

Polymorphonuclear leukocyte heterogeneity of Fc receptor expression and membrane potential in human neonates.

In order to clarify the relationship among polymorphonuclear neutrophil (PMN)-related phenomena, i.e. the Fc receptor expression, the ionic condition of the plasma membrane and chemotactic response, we determined percentage of EA rosette-forming PMN (RFN), membrane potential and PMN chemotaxis in 15 neonates. RFN was assessed by the whole blood method as well as the purified PMN. Membrane potential was examined using the lipophilic fluorescent cyanine dye, 3,3'-dipentyloxacarbocyanine [di-O-C5(3)] and flow cytometry. Both parameters were measured with resting PMN. Numbers of RFN by the two methods have a significant correlation (p less than 0.01, r = 0.881, n = 15). Number of RFN by the whole blood method had a significant correlation with membrane potential (p less than 0.01, r = 0.703, n = 14). Furthermore, number of RFN and membrane potential were significantly correlated with PMN chemotaxis, respectively (p less than 0.01, r = 0.781, n = 14; p less than 0.01, r = 0.695, n = 10). When we examined the effect of beta-adrenergic agents and prostaglandin E1 on number of RFN, membrane potential and PMN chemotaxis, and attempted to confirm the interrelation among these parameters, we observed that PMN chemotaxis was markedly depressed so were both number of RFN and membrane potential. These findings indicate that impaired PMN chemotaxis may in part be related to a decrease in both rosette formation capacity of PMN and membrane potential.

Alprostadil↗

PubMed1992

Ca2+ transport by digitonin-permeabilized Leishmania donovani. Effects of Ca2+, pentamidine and WR-6026 on mitochondrial membrane potential in situ.

The use of low concentrations of digitonin allowed the quantitative determination of the mitochondrial membrane potential of Leishmania donovani promastigotes in situ using safranine O. L. donovani mitochondria were able to build up and retain a membrane potential of a value comparable with that of mammalian mitochondria. The response of promastigotes mitochondrial membrane potential to phosphate, carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP), valinomycin and Ca2+ indicates that these mitochondria behave similarly to vertebrate mitochondria with regard to the properties of their electrochemical proton gradient. When L. donovani promastigotes were permeabilized with digitonin in a reaction medium containing MgATP, succinate and 3.5 microM free Ca2+, they lowered the medium Ca2+ concentration to the submicromolar level (0.05-0.1 microM). The presence of 1 microM-FCCP decreased by about 75% the initial rate of Ca2+ sequestration by these permeabilized cells. This FCCP-insensitive Ca2+ uptake, probably by the endoplasmic reticulum, was completely inhibited by 500 microM-vanadate. On the other hand, when vanadate instead of FCCP was present, the initial rate of Ca2+ accumulation was decreased by about 25% and the Ca2+ set point was increased to 0.7 microM. The succinate-dependence and FCCP-and Ruthenium Red-sensitivity of the Ca2+ uptake detected in the presence of vanadate indicate that this uptake is probably by the mitochondria. This interpretation was further supported by the Ruthenium Red-sensitive decrease in the mitochondrial membrane potential caused by Ca2+ addition. The anti-leishmanial cationic drugs pentamidine and WR-6026 also induced a rapid collapse of the mitochondrial inner membrane potential of L. donovani promastigotes.

Aminoquinolines↗