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PubMed1980

Measurement of membrane potentials (psi) of erythrocytes and white adipocytes by the accumulation of triphenylmethylphosphonium cation.

The accumulation of the lipophilic cation, triphenylmethylphosphonium, has been employed to determine the resting membrane potential in human erythrocytes, turkey erythrocytes, and rat white adipocytes. The triphenylmethylphosphonium cation equilibrates rapidly in human erythrocytes in the presence of low concentrations of the hydrophobic anion, tetraphenylborate. Tetraphenylborate does not accelerate the uptake of triphenylmethylphosphonium ion by adipocytes. The cell associated vs. extracellular distribution of the triphenylmethylphosphonium ion is proportional to changes in membrane potential. The distribution of this ion reflects the membrane potential determining concentration of the ion with dominant permeability in a "Nernst" fashion. The resting membrane potentials for the human erythrocyte, turkey erythrocyte, and rat white adipocyte were found to be -8.4 +/- 1.3, -16.8 +/- 1.1, and -58.3 +/- 5.0 mV, respectively, values which compare favorably with values obtained by other methods. In addition, changes in membrane potential can be assessed by following triphenylmethylphosphonium uptake without determining the intracellular water space. The method has been successfully applied to a study of hormonally induced changes in membrane potential of rat white adipocytes.

Adipose Tissue↗
PubMed1999

Dopamine-selective response in membrane potential by homooxacalix[3]arene triether host incorporated in PVC liquid membrane.

Selectivities of membrane potential changes for catecholamines and inorganic cations were investigated with lipophilic derivatives of calix[6]arene and related hosts incorporated in poly(vinyl chloride) (PVC) matrix liquid membranes. Homooxacalix[3]arene triether displayed an excellent selectivity for dopamine against other catecholamines (adrenaline, noradrenaline) and also against inorganic cations (K+, Na+).

Dopamine↗
PubMed1990

Plasma membrane potential of the alga dunaliella, and its relation to osmoregulation.

A fluorescent dye sensitive to membrane potential was used to follow the plasma-membrane potential in the unicellular halo-tolerant alga Dunaliella salina. The signal observed during dissipation of the plasma membrane potential by the addition of excess K(+) and valinomycin, or a protonophore, was taken as a measure of the preexisting potential. A resting potential of -85 to -100 millivolts (negative inside) was calculated. Following a hypertonic shock, the plasma membrane was rapidly hyperpolarized. This hyperpolarization was transient, and the algae resumed their resting potential about 30 minutes after the shock. The resting plasma membrane potential was decreased by vanadate and is concluded to be generated mostly by the plasma membrane ATPase of Dunaliella. The transient hyperpolarization following a hypertonic shock indicates, therefore, a transient activation of the ATPase. This is further corroborated by a rapid transient decrease in the intracellular ATP following a hypertonic shock and its inhibition by vanadate. It is suggested that activation of the plasma membrane ATPase may be the trigger for osmoregulation in Dunaliella.

Journal Article↗
PubMed1991

Digitonin permeabilization does not affect mitochondrial function and allows the determination of the mitochondrial membrane potential of Trypanosoma cruzi in situ.

Digitonin can be used to permeabilize selectively the plasma membrane of Trypanosoma cruzi epimastigotes without significantly affecting the functional integrity of mitochondria. Addition of digitonin at concentrations close to 64 microM caused decrease in the rate of basal respiration of epimastigotes similar to that caused by oligomycin. A further addition of carbonyl cyanide p-trifluorophenylhydrazone (FCCP) brought respiration to the same rate observed prior to the inclusion of digitonin or oligomycin. This suggests that like oligomycin, digitonin is shifting respiration to a nonphosphorylating state probably by depleting the cells from adenine nucleotides due to permeabilization of the plasma membrane. The use of low concentrations of digitonin allowed the quantitative determination of the mitochondrial membrane potential of these cells in situ using safranine O. The response of epimastigotes mitochondrial membrane potential to phosphate, FCCP, valinomycin, nigericin, ADP, and Ca2+ indicates that these mitochondria behave similarly to vertebrate mitochondria regarding the properties of their electrochemical proton gradient. In addition, T. cruzi mitochondria are able to build up and retain a membrane potential of a value comparable to that of mammalian mitochondria. The trypanocidal drug crystal violet, as well as other cationic drugs such as dequalinium, induced a rapid dose-related collapse of the inner mitochondrial membrane potential.

Adenosine Diphosphate↗
PubMed1981

Membrane potential depolarization and increased intracellular pH accompany the acrosome reaction of sea urchin sperm.

The intracellular pH and membrane potential in sperm of the sea urchin Strongylocentrotus purpuratus were investigated by using fluorescent and radiolabeled probes. The weak bases [14C]methylamine, [14C]diethylamine, and 9-aminoacridine were concentrated within sperm 5-fold or greater. The weak acid [14C]dimethyloxazolidine-2,4-dione (DMO) was excluded from sperm. These data suggested that the apparent intracellular pH is acidic with respect to seawater (pH 8.0). Induction of the acrosome reaction caused efflux of the amines and uptake of DMO, consistent with an increase in apparent intracellular pH of 0.1-0.2 pH unit. The presence of an internally negative membrane potential was indicated by estimating the distribution of [3H]tetraphenylphosphonium (Ph4P+) and [14C]SCN-. From SCN- exclusion we estimated a value of about -30 mV for the nonmitochondrial membrane potential, whereas from Ph4P+ accumulation an apparent potential of -90 to -150 mV was demonstrated. The membrane potentials obtained with Ph4P+ and SCN- were dependent upon the external K+ concentration, with increasing K+ leading to depolarization. Induction of the acrosome reaction led to efflux of Ph4P+ and uptake of SCN- for an approximate depolarization of about 30 mV, primarily due to the collapse of the plasma membrane potential.

Acrosome↗
PubMed1979

Characteristics of fast excitatory postsynaptic current in bullfrog sympathetic ganglion cells. Effects of membrane potential, temperature and Ca ions.

The membrane current underlying the fast excitatory postsynaptic potential (EPSC) of bullfrog sympathetic ganglion cells was studied. The relationship between the EPSC amplitude and membrane potential was linear at negative levels of membrane potential, but deviated from the linearity toward a smaller amplitude at positive levels. The falling phase of EPSC almost followed a single exponential decay. The half-decay time (HDT) of EPSC's increased exponentially with an increase in the negativity of membrane potential. The rise time (RT) was also prolonged slightly with membrane hyperpolarization. Lowering of temperature decreased the EPSC amplitude, lengthened markedly the HDT and increased the slope relating the logarithm of the HDT to membrane potential. Neostigmine (1 x 10(-5) M) prolonged both the RT and HDT. A decrease in Ca2+ concentration caused a marked reduction in the EPSC amplitude, and a slight shortening in the RT and HDT. An increase in Ca2+ concentration significantly prolonged the RT and HDT without altering the slope of the relationship between the HDT and membrane potential, while the amplitude of EPSC was increased slightly. The HDT was independent of EPSC amplitude. It is suggested that the mechanism responsible for closing the ion channels of the nicotinic receptor at the subsynaptic membrane is regulated by membrane potential. The possible mechanisms of the action of Ca2+ on the decay phase of EPSC were discussed.

Animals↗
PubMed1984

Phosphate transport, membrane potential, and movements of calcium in rat liver mitochondria.

The membrane potential and calcium accumulation of mitochondria were followed by ion-specific electrodes in the presence of the proton-donor anions phosphate, acetate, glutamate, and beta-hydroxybutyrate. Phosphate was the only anion which allowed rapid and complete restoration of both the membrane potential and the steady-state extramitochondrial calcium concentration after the uptake of 100-200 nmol calcium per mg protein. If there was no influx of any proton-donor anion, the extent of calcium uptake depended on the intramitochondrial phosphate content. Both the fall of the membrane potential and the increase of the external calcium concentration brought about by a given amount of uncoupler were counteracted by phosphate transported into the mitochondria.

Animals↗
PubMed2007

Role of membrane potential in calcium signaling during rhythmic bursting in tritonia swim interneurons.

Rhythmic bursting in neurons is accompanied by dynamic changes in intracellular Ca(2+) concentration. These Ca(2+) signals may be caused by membrane potential changes during bursting and/or by synaptic inputs. We determined that membrane potential is responsible for most, if not all, of the cytoplasmic Ca(2+) signal recorded during rhythmic bursting in two neurons of the escape swim central pattern generator (CPG) of the mollusk, Tritonia diomedea: ventral swim interneuron B (VSI) and cerebral neuron 2 (C2). Ca(2+) signals were imaged with a confocal laser scanning microscope while the membrane potential was recorded at the soma. During the swim motor pattern (SMP), Ca(2+) signals in both neurons transiently increased during each burst of action potentials with a more rapid decay in secondary than in primary neurites. VSI and C2 were then voltage-clamped at the soma, and each neuron's own membrane potential waveform recorded during the SMP was played back as the voltage command. In all regions of VSI, this completely reproduced the amplitude and time course of Ca(2+) signals observed during the SMP, but in C2, the amplitude was lower in the playback experiments than during the SMP, possibly due to space clamp problems. Therefore in VSI, the cytoplasmic Ca(2+) signal during the SMP can be accounted for by its membrane potential excursions, whereas in C2 the membrane potential excursions can account for most of the SMP Ca(2+) signal.

Animals↗
PubMed2000

Use of a lipophilic cation to monitor electrical membrane potential in the intact rat lens.

PURPOSE: Tetraphenylphosphonium (TPP+) is a permeant lipophilic cation that accumulates in cultured cells and tissues as a function of the electrical membrane potential across the plasma membrane. This study was undertaken to determine whether TPP+ can be used for assessing membrane potential in intact lenses in organ culture. METHODS: Rat lenses were cultured in media containing 10 microM TPP+ and a tracer level of 3H-TPP+ for various times. 3H-TPP+ levels in whole lenses or dissected portions of lenses were determined by liquid scintillation counting. Ionophores, transport inhibitors, and neurotransmitters were also added to investigate their effects on TPP+ uptake. RESULTS. Incubation of lenses in low-K+ balanced salt solution and TC-199 medium, containing physiological concentrations of Na+ and K+, led to a biphasic accumulation of TPP+ in the lens that approached equilibrium by 12 to 16 hours of culture. The TPP+ equilibrated within 1 hour in the epithelium but penetrated more slowly into the fiber mass. The steady state level of TPP+ accumulation in the lens was depressed by 90% when the lenses were cultured in a medium containing high K+. The calculated membrane potential for the normal rat lens in TC-199 was -75 +/- 3 mV. Monensin (1 microM) and nigericin (1 microM), Na+H+ and K+H+ exchangers respectively, as well as the protonophore carbonylcyanide-m-chlorophenylhydrazone (CCCP, 10 microM) and the calcium ionophore A23187 (10 microM), abolished TPP+ accumulation and caused cloudiness of the lenses. The neurotransmitter acetylcholine at 50 microM decreased TPP+ accumulation in the lens, but this effect could be prevented by simultaneous application of 1 mM atropine. CONCLUSIONS: TPP+ accumulation can be used as an indicator of changes in membrane potential in intact lenses, but because of the long time required to reach steady state, its utility is limited. The slow accumulation of TPP+ and its slow efflux from the lens under conditions known to depolarize membranes are consistent with a diffusion barrier in the deep cortex and nucleus of the lens.

Animals↗
PubMed1984

Monitoring of mitochondrial membrane potential in isolated perfused rat heart.

Optical methods were tested for measuring the membrane potential changes of mitochondria in isolated perfused rat hearts. Safranin was found to be rapidly taken up by the Langendorff-perfused heart, and after loading with the dye there was practically no washout of the stain during perfusion with Krebs-Ringer bicarbonate solution. Staining with safranin induced the appearance of an intense absorption band in the reflectance spectrum of the heart, but the absorbance spectrum changes were not useful for monitoring the mitochondrial membrane potential changes because of interference by endogenous hemoproteins. The fluorescence intensity, however, responded in a manner which indicated that its changes originated from dye attached to the mitochondria. A decrease of the fluorescence was found on energizing the mitochondria by decreasing the cellular energy consumption by arrest induced by 18 mM K+ or by decreasing the beating rate of an electrically paced heart from 5 Hz to the endogenous ventricular frequency of 1.5 Hz. In hearts arrested by Ca2+ depletion, 18 mM K+ did not affect the safranin fluorescence. This was taken to indicate that under these conditions the safranin fluorescence was not sensitive to the plasma membrane potential. The uncoupler carbonyl cyanide m-chlorophenylhydrazone induced an intense enhancement of safranin fluorescence in the perfused heart, demonstrating that the probe is sensitive to mitochondrial membrane potential.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Assessment of mitochondrial membrane potential as an indicator of cytotoxicity.

Mechanistically based short-term in vitro tests to evaluate the relative cytotoxicity of of chemicals will complement in vitro genotoxicity testing during the initial phases of toxicity evaluation as well as provide information on the cellular site of action for chemicals found to be toxic in animals. The objective of this study was to characterize a procedure for evaluating mitochondrial membrane potential, an integral component of cellular energy homeostasis and normal cellular function, as an in vitro indicator of chemically induced cytotoxicity. Rhodamine 123, a cationic fluorescent dye whose mitochondrial fluorescence intensity decreases quantitatively in response to dissipation of mitochondrial transmembrane potential, was used to evaluate disturbances in mitochondrial membrane potential. Cultured rat liver epithelial cells (WB cell line) or human skin fibroblasts (MSU-2 cell line) treated with the oxidative phosphorylation uncoupler 2,4-dinitrophenol (DNP) or the cytochrome oxidase inhibitor sodium azide were used to characterize the system. In addition, acetaldehyde, which has been reported to damage the plasma membrane, but not the mitochondrial membrane, was used to demonstrate the specificity of this assay system. Mitochondrial membrane potential was not significantly affected by the cell culture density, as long as the cells were in the logarithmic phase of growth. The stage of the cell cycle influenced the mitochondrial membrane potential in human skin fibroblasts (highest in late G1-early S) but not in rat liver cells. DNP and sodium azide significantly (p less than 0.01) reduced the mitochondrial membrane potential in both cell lines compared to untreated cells, while acetaldehyde did not reduce the mitochondrial membrane potential in either cell line. This assay provides a tool for evaluating the effect of chemical treatments on mitochondrial membrane potential, as well as an indicator of cytotoxicity which does not require the use of animals.

Animals↗
PubMedDate not supplied

[L-type calcium channels involvement in aortic smooth muscle contraction as revealed by membrane potential and active force dynamics].

Membrane potential (MP) is essential in smooth muscle (SM) contractile activity, mainly by its effect upon L-type Ca2+ channels. We simultaneously recorded SM isometric tension and MP in de-endothelised rat aorta rings and examined their submaximal activation by K+, norepinephrine (NE) or phenylephrine (PHE) and the influence of methoxyverapamil (D600). K+ -induced contraction strictly correlated with depolarization, while faster contractions induced by NE or PHE started and peaked with a less depolarized membrane. D600 completely relaxed K+ or NE contracted rings, time-correlated with full repolarization, but partially relaxed PHE-contracted rings, with partial repolarization, which did not precede relaxation. The observed MP and force dynamics support known mechanisms of action of the drugs used. L-type channels participate in the depolarizing and contractile effect of NE, as opposite to their minor involvement in the effects of PHE.

Adrenergic alpha-Agonists↗
PubMed1991

Depolarization of synaptosomal membranes: a study of mechanism by which rhodamine 6G measures membrane potential.

The fluorescence intensity of Rhodamine 6G in synaptosomal suspensions has been measured to monitor the membrane potential changes in pre-synaptic nerve terminals. The fluorescence response of the dye was seen to be a function of potential-dependent partitioning of dye molecules between the synaptosomes and the extracellular medium. Binding of dye molecules to the hydrophobic regions of membranes results in the quenching of fluorescence. Upon depolarization of the synaptosomal membrane, the dye molecules are released from the cells. The effect of changing extracellular ionic composition was also studied. The membrane potential increased linearly with log of [K]0. The resting membrane potential in buffer containing 5 mM K+ was calculated to be -60 mV. Raising the extracellular Ca2+ and Mg2+ from 1.2 mM to 10 mM did not change the membrane potential. Ca2+ ionophore A23187, in the presence of Ca2+ was found to depolarize the membranes.

Animals↗
PubMed1967

Steroid production and membrane potential measurement in cells of the adrenal cortex.

1. The relation between corticosteroid production and the cellular membrane potential of adrenocortical cells has been investigated using a flow system for the incubation in vitro of adrenal glands from neonatal rabbits. Corticosteroid production by the adrenal cells was determined by a fluorescence method; membrane potentials were measured with glass micro-electrodes.2. Adrenocorticotrophic hormone (ACTH) increased corticosteroid production without altering the membrane potential of the adrenocortical cells. Conversely, a 5-fold increase in [K](o) did not increase corticosteroid production but decreased the cellular membrane potential. The increase in [K](o) did not impair the stimulation of corticosteroid production by ACTH.3. The log dose-response relation between the concentration of ACTH in the incubation medium and the amount of corticosteroid produced by the adrenal tissue was linear.4. No evidence was found of a direct relation between the production of corticosteroid by adrenocortical cells and the cellular membrane potential. Indeed, the output of steroid appeared to be relatively independent of the polarization of the cell membrane.

Journal Article↗
PubMed1971

Effects of batrachotoxin on membrane potential and conductance of squid giant axons.

The effects of batrachotoxin (BTX) on the membrane potential and conductances of squid giant axons have been studied by means of intracellular microelectrode recording, internal perfusion, and voltage clamp techniques. BTX (550-1100 nM) caused a marked and irreversible depolarization of the nerve membrane, the membrane potential being eventually reversed in polarity by as much as 15 mv. The depolarization progressed more rapidly with internal application than with external application of BTX to the axon. External application of tetrodotoxin (1000 nM) completely restored the BTX depolarization. Removal or drastic reduction of external sodium caused a hyperpolarization of the BTX-poisoned membrane. However, no change in the resting membrane potential occurred when BTX was applied in the absence of sodium ions in both external and internal phases. These observations demonstrate that BTX specifically increases the resting sodium permeability of the squid axon membrane. Despite such an increase in resting sodium permeability, the BTX-poisoned membrane was still capable of undergoing a large sodium permeability increase of normal magnitude upon depolarizing stimulation provided that the membrane potential was brought back to the original or higher level. The possibility that a single sodium channel is operative for both the resting sodium, permeability and the sodium permeability increase upon stimulation is discussed.

Action Potentials↗
PubMed2000

Changes in mitochondrial membrane potential during staurosporine-induced apoptosis in Jurkat cells.

Cytochrome c release from mitochondria is central to apoptosis, but the events leading up to it are disputed. The mitochondrial membrane potential has been reported to decrease, increase or remain unchanged during cytochrome c release. We measured mitochondrial membrane potential in Jurkat cells undergoing apoptosis by the uptake of the radiolabelled lipophilic cation TPMP, enabling small changes in potential to be determined. The ATP/ADP ratio, mitochondrial and cell volumes, plasma membrane potential and the mitochondrial membrane potential in permeabilised cells were also measured. Before cytochrome c release the mitochondrial membrane potential increased, followed by a decrease in potential associated with mitochondrial swelling and the release of cytochrome c and DDP-1, an intermembrane space house keeping protein. Mitochondrial swelling and cytochrome c release were both blocked by bongkrekic acid, an inhibitor of the permeability transition. We conclude that during apoptosis mitochondria undergo an initial priming phase associated with hyperpolarisation which leads to an effector phase, during which mitochondria swell and release cytochrome c.

Apoptosis↗
PubMed1994

A BASIC program for teaching membrane potential.

A qualitative discourse on membrane potential, albeit simple, may be equivocal at crucial points while a purely mathematical treatise on the subject, for all its exactitude, may be incomprehensible to a student of Physiology. A quasi-quantitative approach has therefore been attempted as a compromise between clarity and exactness. A BASIC program is utilised to compute the stereotype calculations and to give instant displays of the results through figures and graphic animations.

Animals↗
PubMed2004

Mitochondrial membrane potential and aging.

The mitochondrial membrane potential (or protonmotive force) is the central bioenergetic parameter that controls respiratory rate, ATP synthesis and the generation of reactive oxygen species, and is itself controlled by electron transport and proton leaks. As a consequence of extensive research, there has emerged a consensus as to how these parameters integrate. Despite this consensus, the literature contains contradictory reports on the extent to which these parameters are modified in animal models of aging. This article critically examines the basis for a number of these reports.

Adenosine Triphosphate↗