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PubMedDate not supplied

A role for plasma membrane potential in doxorubicin--induced cytotoxicity.

Using a modifier of membrane function, we have shown that plasma membrane potential plays an important role in doxorubicin (DOX) - induced cytotoxicity through its connection with cell metabolism and through its effect on drug accumulation. Membrane potential of K562 cells, measured using 3, 3'-dihexyl-oxacarbocyanine (DiOC6 (3)), was increased in the presence of non-toxic cepharanthin or N-1379 and decreased in the presence of non-toxic K252a. Correlated with the level of the potential, DOX efficacy was enhanced by cepharanthin or N-1379 and decreased by K252a associated with an increase or decrease of the percentage of cells in S-phase and of intracellular DOX accumulation.

Alkaloids↗
PubMed1988

Membrane potential modulates photocycling rates of bacterial rhodopsins.

Effects of membrane potential on photochemical reactions of three retinal-containing chromoproteins in Halobacterium halobium, sensory rhodopsin I (sR-I), bacteriorhodopsin, and halorhodopsin, are described. Each of the three exhibits a decreased rate of thermal decay of its principal intermediate when photoactivated in an artificially energized compared to a deenergized membrane. The similar response of the three pigments suggests a voltage-dependent conformational change common to their respective photocycles. Spectral and kinetic properties of the sR-I photochemical reaction cycle were measured in phototactic H. halobium cells, and differences from in vitro photocycle kinetics were attributable to the electrical membrane potential present in vivo. In vivo sR-I photocycling rates were reproduced in envelope vesicle preparations in the presence of a valinomycin-induced potassium diffusion potential.

Halobacterium↗
PubMed1987

Liposomes as a model for olfactory cells: changes in membrane potential in response to various odorants.

Various odorants were found to depolarize azolectin liposomes. The results obtained are as follows. (1) Changes in the membrane potential of azolectin liposomes in response to various odorants were monitored by measuring changes in the fluorescence intensity of 3,3'-dipropylthiocarbocyanine iodide [disS-C3(5)]. Ten odorants examined increased the fluorescence intensity of the liposome-dye suspensions in a dose-dependent manner, which indicates that odorants depolarize the liposomes. Concentrations of odorants that depolarized the liposomes greatly varied among the odorants. There existed a good correlation between the minimum concentrations of odorants to depolarize the liposomes and the thresholds of respective odorants in the frog or porcine olfactory responses. (2) Addition of sphingomyelin (SM) to azolectin led to a large enhancement of depolarizations by nonanol, citral, and n-amyl acetate. The results indicate that lipid composition of liposomes is one of the factors that control the sensitivity to odorants. (3) Odorants changed the membrane fluidity of the liposomes, which was monitored by changes in the fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene (DPH). The membrane fluidity was changed in concentration ranges of odorants similar to those where the membrane potential changes occurred, which suggests that changes in the membrane fluidity are related to generation of the membrane potential changes. (4) Changes in the membrane potential in response to odorants were electrically measured with the planar lipid bilayer made of an azolectin-SM (2:1 w/w) mixture. It was shown that odorants (nonanol, citral, and n-amyl acetate) depolarized the planar lipid bilayer.(ABSTRACT TRUNCATED AT 250 WORDS)

Liposomes↗
PubMed1994

The role of the membrane potential of endothelial and smooth muscle cells in the regulation of coronary blood flow.

In the mammalian heart the supply of oxygen and energy-rich substrates through the coronary arterioles is continuously adapted to the variations of cardiac work. The coronary resistance arteries and the surrounding myocardium form a functional unit with multiple interactions between coronary endothelial cells, smooth muscle cells, perivascular nerves, and cardiac muscle cells. We describe the mechanisms underlying the electrical and chemical communication between the different cell types, the ionic channels contributing to the resting potential of endothelial and smooth muscle cells, and the mechanisms responsible for modulation of the resting potential. The main conclusion of our analysis is that the membrane potential of coronary endothelial and smooth muscle cells is one of the major determinants of coronary blood flow, and that modulation of the membrane potential provides a way to dilate or constrict coronary resistance arteries. It is proposed that the membrane potential of the myo-endothelial regulatory unit, i.e., of the endothelial cells and the underlying smooth muscle cells in the terminal arterioles, may function as an integrator of the numerous local and global vasodilator and constrictor signals that provide for the adaptation of coronary blood flow to the metabolic demands of the heart.

Animals↗
PubMed2003

Rhodamine 123 as a probe of mitochondrial membrane potential: evaluation of proton flux through F(0) during ATP synthesis.

Rhodamine 123 (RH-123) was used to monitor the membrane potential of mitochondria isolated from rat liver. Mitochondrial energization induces quenching of RH-123 fluorescence and the rate of fluorescence decay is proportional to the mitochondrial membrane potential. Exploiting the kinetics of RH-123 fluorescence quenching in the presence of succinate and ADP, when protons are both pumped out of the matrix driven by the respiratory chain complexes and allowed to diffuse back into the matrix through ATP synthase during ATP synthesis, we could obtain an overall quenching rate proportional to the steady-state membrane potential under state 3 condition. We measured the kinetics of fluorescence quenching by adding succinate and ADP in the absence and presence of oligomycin, which abolishes the ADP-driven potential decrease due to the back-flow of protons through the ATP synthase channel, F(0). As expected, the initial rate of quenching was significantly increased in the presence of oligomycin, and conversely preincubation with subsaturating concentrations of the uncoupler carbonyl cyanide p-trifluoro-metoxyphenilhydrazone (FCCP) induced a decreased rate of quenching. N,N'-dicyclohexylcarbodiimide (DCCD) behaved similarly to oligomycin in increasing the rate of quenching. These findings indicate that RH-123 fluorescence quenching kinetics give reliable and sensitive evaluation of mitochondrial membrane potential, complementing steady-state fluorescence measurements, and provide a mean to study proton flow from the mitochondrial intermembrane space to the matrix through the F(0) channel.

Animals↗
PubMed1984

Astrocytes in primary cultures: membrane potential characteristics reveal exclusive potassium conductance and potassium accumulator properties.

Mouse astrocytes in homogenous primary cultures were used to study the membrane potential response, measured with intracellular microelectrodes, to alterations of external ion composition and to certain drugs, and the observations were correlated with radiotracer measurements of equilibrated K+ content. The membrane potential was--92 mV at 3 mM K+, and reduction of external Na+ and Cl-concentration, as well as addition of furosemide, which acts on Cl- and Na+ fluxes, had no effect, showing that there is no other ion than K+ which significantly contributes to membrane conductance. Addition of ouabain showed that there is no electrogenic component of the membrane potential at either 'resting' conditions or during stimulation. Nevertheless, the behavior of the membrane potential was found to deviate from a Nernst potential for K+ when extracellular K+ was changed (the slope was linear from 1.5 to 100 mM K+ with 51 mV/10-fold change compared with 61 mV for a Nernstian behavior at 37 degrees C). The radioisotope measurements at different external K+ showed that this was due to accumulation of intracellular K+. We conclude that these astrocytes have spatial buffer and active accumulator properties towards the K+ ion.

Animals↗
PubMed1991

Low doses of ethanol have Ca2+ ionophore-like effects on apical membrane potential of in vitro Necturus antrum.

The effects of low doses of luminal ethanol on the amiloride-sensitive apical membrane potential of Necturus antral mucosa were studied using conventional microelectrode techniques. Luminal ethanol (0.250-4.0% vol/vol) caused a dose-dependent hyperpolarization of the apical membrane potential (Vmc), an increase in transepithelial resistance (Rt) and resistance ratio (Ra/Rb), and a decrease in transepithelial potential (Vms). Luminal amiloride (100 microM) to 4% ethanol-treated antra did not cause any additional hyperpolarization of Vmc. Compared with luminal 2% ethanol-Ringer, an equivalent osmotic mannitol solution depolarized Vmc and basolateral potential (Vcs), decreased Rt and Ra/Rb, and increased Vms. A single dose of 0.50% ethanol attenuated the effects of a second 2% ethanol exposure on Vmc. No change in periodic acid-Schiff (PAS)-positive mucous granule content could be found between control and 2% ethanol-treated antra. The Ca2+ ionophores A23187 or ionomycin (0.25-5.0 microM) dose dependently hyperpolarized the Vmc and Vcs, increased Rt and Ra/Rb, and decreased Vms. Luminal Ca(2+)-free Ringer had no effect on luminal 2.00% ethanol-induced changes in membrane potentials or resistances. Pretreatment with BAPTA blocked by approximately 70 and 55% the Vmc hyperpolarization of 2 and 4% ethanol, respectively. Pretreatment with ruthenium red (10-50 microM) also dose dependently reduced the 2% ethanol-induced changes in Vmc. The data indicate that 1) low doses of luminal ethanol and Ca2+ ionophores have similar effects on Necturus gastric antral membrane potentials and resistances, 2) ethanol-induced hyperpolarizations of the Vmc are partially mediated through an alteration in intracellular Ca2+, and 3) low doses of luminal ethanol do not cause the release of antral epithelial mucous granules at the time when significant changes are occurring in the Vmc.

Animals↗
PubMed1995

Regulation of membrane potential and diameter by voltage-dependent K+ channels in rabbit myogenic cerebral arteries.

The hypothesis that voltage-dependent K+ channels are involved in the regulation of arterial smooth muscle membrane potential and blood vessel diameter was tested by examining the effects of inhibitors [4-aminopyridine (4-AP) and 3,4-diaminopyridine (3,4-DAP)] of voltage-dependent K+ channels on the membrane potential and diameter of pressurized small (100- to 300-microns diam) cerebral arteries from rabbit. In response to graded elevations in transmural pressure (20-100 mmHg), the membrane potential of smooth muscle cells in these arteries depolarized and the arteries constricted. 4-AP (1 mM) and 3,4-DAP (1 mM) depolarized cerebral arteries by 19 and 21 mV, respectively, when they were subjected to a transmural pressure of 80 mmHg. 3-Aminopyridine (3-AP, 1 mM), which is a relatively poor inhibitor of voltage-dependent K+ channels, depolarized smooth muscle cells in the arteries by 1 mV. 4-AP and 3,4-DAP constricted pressurized (to 80 mmHg) cerebral arteries. 3-AP had little effect on arterial diameter. 4-AP increased the arterial constriction to transmural pressure over a wide range of pressures (40-90 mmHg). The effects of 4-AP and 3,4-DAP on membrane potential and diameter were not prevented by inhibitors of calcium channels, calcium-activated K+ channels, ATP-sensitive K+ channels, inward rectifier K+ channels, blockers of adrenergic, serotonergic, muscarinic, and histaminergic receptors, or removal of the endothelium. These results suggest that voltage-dependent K+ channels are involved in the regulation of membrane potential and response of small cerebral arteries to changes in intravascular pressure.

4-Aminopyridine↗
PubMed1990

Effects of membrane potential on electrically silent transport. Potential-independent translocation and asymmetric potential-dependent substrate binding to the red blood cell anion exchange protein.

Tracer anion exchange flux measurements have been carried out in human red blood cells with the membrane potential clamped at various values with gramicidin. The goal of the study was to determine the effect of membrane potential on the anion translocation and binding events in the catalytic cycle for exchange. The conditions were arranged such that most of the transporters were recruited into the same configuration (inward-facing or outward-facing, depending on the direction of the Cl- gradient). We found that the membrane potential has no detectable effect on the anion translocation event, measured as 36Cl(-)-Cl- or 36Cl(-)-HCO3- exchange. The lack of effect of potential is in agreement with previous studies on red cells and is different from the behavior of the mouse erythroid band 3 gene expressed in frog oocytes (Grygorczyk, R., W. Schwarz, and H. Passow. 1987. J. Membr. Biol. 99:127-136). A negative potential decreases the potency of extracellular SO4= as an inhibitor of either Cl- or HCO3- influx. Because of the potential-dependent inhibition by SO4=, conditions could be found in which a negative intracellular potential actually accelerates 36Cl- influx. This effect is observed only in media containing multivalent anions. The simplest interpretation of the effect is that the negative potential lowers the inhibitory potency of the multivalent anion by lowering its local concentration near the transport site. The magnitude of the effect is consistent with the idea that the anions move through 10-15% of the transmembrane potential between the extracellular medium and the outward-facing transport site. In contrast to its effect on extracellular substrate binding, there is no detectable effect of membrane potential on the competition between intracellular Cl- and SO4= for transport sites. The lack of effect of potential on intracellular substrate binding suggests that the access pathway leading to the inward-facing transport site is of lower electrical resistance than that leading to the extracellular substrate site.

Anion Transport Proteins↗
PubMed1998

Subthreshold membrane potential oscillations in neurons of deep layers of the entorhinal cortex.

Neuronal oscillations are important for information processing. The entorhinal cortex is one of the structures which is involved in generation of theta rhythm. The major role of the entorhinal cortex is to feed diverse sources of information both to and from the hippocampus. Far from simply being a funnel for this information it becomes clear that the entorhinal cortex has its own active properties that contribute to signal processing. Interestingly, stellate cells in layer II of the entorhinal cortex can intrinsically generate subthreshold, Na+-dependent membrane potential oscillations. Here, using intracellular and patch-clamp recordings, we report a similar phenomenon from neurons of the deep layers of the entorhinal cortex. In our in vitro slice preparation about two-thirds of recorded neurons were able to generate voltage-sensitive subthreshold membrane potential oscillations. At a membrane potential of about 50 mV the mean frequency of the voltage-oscillations was 8.1 Hz, whereby at slightly more positive potentials (-44 mV) the frequency of the membrane potential oscillations was 20 Hz and the oscillations became interrupted by clusters of non-adapting trains of spikes. Pharmacological experiments revealed that the oscillations were not affected by Cs+, but could be blocked by the fast Na+-channel blocker tetrodotoxin. We therefore conclude that voltage- and Na+-dependent subthreshold membrane potential oscillations are not only present in stellate cells of entorhinal cortex-layer II, but are also typical for neurons of the deep layers of the entorhinal cortex.

Animals↗
PubMed1975

Membrane potential and conductance during pinocytosis induced in Amoeba proteus with alkali metal ions.

An investigation of the relationship between the polarized state of the membrane and the onset and the intensity of pinocytosis was made in Amoeba proteus. Membrane potential and input resistance was in all instances found to decrease in approximate proportion to the number of channels when pinocytosis was induced by a variety of alkali metal ions at varying pH. Channels began to appear when the membrane was depolarized to -30 mV by the inducer of pinocytosis. With all inducers the maximum pinocytosis was encountered at membrane potentials close to zero. No positive potentials were recorded when the chloride salts of the inducing cations were used. At high concentrations of alkali ions a transient increase of the chloride permeability caused short-lasting hyperolarizations of the membrane. Inhibition of pinocytosis by Ca++ was accompanied by an increase of input resistance and membrane potential. The selectivity of the membrane to different alkali metal ions observed as changes in pinocytosis intensity, membrane potential and input resistance was found to vary with the concentration of the inducer and with the Ca++ concentration of the extracellular solution. Displacement of membrane bound Ca++ appeared to decrease the field strength of charged groups in the membrane altering its selectivity among alkali cations. The formation of pinocytotic channels is suggested to require translocation of Ca++ from the membrane into the cell and would therefore be closely related to the electrical properties of the amoeba.

Alkalies↗
PubMed1993

Control of intracellular calcium by membrane potential in human melanoma cells.

The modulation of intracellular calcium ([Ca2+]i) by the membrane potential was investigated in human melanoma cells by combining the nystatin-perforated patch-clamp technique with Ca2+ measurements. Voltage steps to -100 mV induced a rise in [Ca2+]i and a creeping inward current. These effects were absent in Ca(2+)-free solution and could be blocked by Ni2+ or La3+. Voltage ramps revealed a close correlation between [Ca2+]i and voltage, with the strongest voltage dependence around the resting potential. Long-lasting tail currents, closely correlated with the rise in [Ca2+]i and a reversal potential close to the K+ equilibrium potential, occurred if the membrane potential was clamped back to 0 mV. They were absent if intracellular K+ was replaced by Cs+ and blocked by extracellular tetraethylammonium (5 mM), Ba2+ (1 mM), or a membrane-permeable adenosine 3',5'-cyclic monophosphate analogue. These observations are discussed in relation to cell proliferation. The enhanced expression of K+ channels during cell proliferation provides a positive-feedback mechanism resulting in long-term changes in [Ca2+]i required for the G1-S transition in the cell cycle.

Barium↗
PubMed1981

Membrane potential changes during the first steps of coliphage infection.

Immediately after adsorption, phages T4 and T5 induce a partial depolarization of the host cytoplasmic membrane. Infected bacteria respond to this phage-induced effect by a repolarization that leads to a new steady state of reduced membrane potential. The rate and extent of repolarization are adjusted to the intensity of depolarization, which depends on the number of adsorbed phages. Consequently, the new steady state membrane potential is attained in the same interval of time regardless of the maximum depolarization. These membrane potential changes appear to be independent of phage-specific properties (type of phage, presence of DNA and internal proteins, injection process) and of several membrane-related parameters (temperature, external pH, preinfectious level of membrane potential). We propose that phage adsorption to the outer membrane triggers the emission of a signal that is transmitted to the cytoplasmic membrane. Additivity of independent signals is possible when stimuli (phages) are added at the same time. Additional adsorption of phages has no further depolarizing effect as soon as the repolarization begins. We propose that this refractoriness to secondary depolarization nd the shut-off of the first depolarization are induced by the same chemical modification also initiated by adsorption of the first phage.

Cell Membrane↗
PubMed2003

Membrane potential fluorescence: a rapid and highly sensitive assay for nicotinic receptor channel function.

Seven cell lines expressing native and transfected nicotinic receptor subtypes were evaluated functionally by using fluorescent assays based on membrane potential and calcium dynamics with "no-wash" dye systems. Both assays provided the same rank orders of potency for (+/-)-epibatidine, 2S-(-)-nicotine, 7R,9S-(-)-cytisine, and 1,1-dimethyl-4-phenylpiperazinium in a cell line expressing rat alpha 3 beta 4 receptors. Nicotinic antagonists mecamylamine and dihydro-beta-erythroidine inhibited responses in both assays. Both agonist and antagonist activity were assessed within the same experiment. Agonists seemed more potent in the membrane potential assay than in the calcium assay, whereas the converse was true for antagonists. The membrane potential assay afforded robust responses in K-177 cells expressing human alpha 4 beta 2 receptors, in IMR-32 and SH-SY5Y cells expressing human ganglionic receptors, and in TE-671 cells expressing human neuromuscular receptors. These lines gave weak to modest calcium responses. Moreover, membrane potential responses were obtained in cell lines expressing rat alpha 4 beta 2 and alpha 4 beta 4 receptors, which were devoid of calcium responses. Thus, membrane potential serves as a sensitive measure of nicotinic activity, and the resulting depolarization may be as important as calcium in cell signaling.

Animals↗
PubMed1993

Intraluminal flow-initiated hyperpolarization and depolarization shift the membrane potential of arterial smooth muscle toward an intermediate level.

We examined the effect of intraluminal flow of physiological saline on the membrane potential of vascular smooth muscle cells in isolated rabbit cerebral arteries. Intraluminal flow (20 microL/min) caused a depolarization of 4.8 +/- 0.7 mV in muscle cells with a resting membrane potential of -62.5 +/- 1.2 mV (n = 19). However, when cells were depolarized to -48.7 +/- 1.8 mV using histamine and serotonin, the response to intraluminal flow was the opposite, a hyperpolarization of 5.6 +/- 1.0 mV (n = 9). These opposing effects of flow on membrane potential appear to balance at -57.8 +/- 1.1 mV (n = 31). Our results suggest that intraluminal flow may affect the level of basal tone present in arteries in vivo through modulating the membrane potential of vascular smooth muscle cells by concurrently activated depolarization and hyperpolarization.

Animals↗
PubMed1988

[Effect of NH4+ on synaptosomal membrane potential in the rat brain].

The effect of NH4+ on synaptosomal membrane potential was examined using rat brains. The membrane potential was measured by the rhodamine 6G fluorescence method. Both NH4+ diffusion potential (NH4+-potential) and K+ diffusion potential (K+-potential) were observed in the synaptosomes. Upon replacement of medium Cl- with SCN-, both K+- and NH4+-potentials depolarized. On the other hand, replacement of medium Cl- with gluconate resulted in the hyperpolarization of K+-potential, but not of NH4+-potential. Ethacrynic acid (0.3 mM), a Cl- -ATPase inhibitor, depolarized both K+(Cl-)- and NH4+ (Cl-)-potentials. In the presence of ethacrynic acid, both of the potentials were further depolarized by replacement of medium Cl- with SCN-, but not with gluconate-. Picrotoxin (5 mM), a Cl- channel inhibitor, did not significantly affect either K+- or NH4+-potential. In the presence of picrotoxin, replacement of medium Cl- with SCN- depolarized both K+- and NH4+-potentials with or without ethacrynic acid. Gluconate depolarized the K+-potential with ethacrynic acid and the NH4+-potential with or without ethacrynic acid. These findings suggest that NH4+ forms a diffusion potential in nerve endings, and inhibits the anion-mediated hyperpolarization through mechanisms other than anion channels.

Ammonia↗
PubMed1986

Microelectrode studies of D-glucose- and K+-induced changes in membrane potential of electrofused insulin-producing cells.

In the present study electrical field-induced fusion has been applied to both normal pancreatic islet cells isolated from obese hyperglycemic mice and clonal insulin-producing cells (RINm5F) derived from a transplantable rat insulinoma. The fused cells were then punctured with microelectrodes to measure changes in membrane potential after exposure to stimulatory concentrations of D-glucose or K+. Fused cells of normal islet cellular origin revealed a resting membrane potential of -60 mV and were depolarized by 24 or 27 mV after exposure to 11 mM D-glucose or 30 mM K+. Although D-glucose induced depolarization, it was not possible to establish the existence of an oscillating burst pattern superimposed by action potentials. The resting membrane potential of the fused RINm5F cells was also -60 mV and decreased to -30 mV after exposure to 30 mM K+. As judged from the membrane potential measurements, the reconstitution of the plasma membrane subsequent to electrical breakdown is essentially the same whether the giant cells originated from normal islet cells or RINm5F cells.

Animals↗
PubMed1991

A study of membrane potential across isolated fruit cuticles for NaCl and CaCl2 solutions.

Fixed charge density and ionic diffusion ratio in an isolated tomato fruit cuticular membrane have been estimated from membrane potential measurements for NaCl and CaCl2 electrolyte solutions. The values of the parameters studied show marked differences in the electrical behaviour of the electrolytes, and evidence the asymmetric character of the cuticular membrane. While the membrane potential values for NaCl solutions can be explained in terms of a Donnan potential plus diffusion potentials, for CaCl2 solutions the membrane potential values agree very well with the diffusion potential. These facts could be explained by taking into account some structural features of the cuticular membrane.

Calcium Chloride↗