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PubMed1985

Membrane potential and catecholamine secretion by bovine adrenal chromaffin cells: use of tetraphenylphosphonium distribution and carbocyanine dye fluorescence.

Changes in plasma membrane potential of isolated bovine adrenal chromaffin cells were measured independently by two chemical probe methods and related to corresponding effects on catecholamine secretion. The lipophilic cation tetraphenylphosphonium (TPP+) and the carbocyanine dye 3,3'-dipropylthiadicarbocyanine [DiS-C3-(5)] were used. The necessity of evaluating the subcellular distribution of TPP+ among cytoplasmic, mitochondrial, secretory granule, and bound compartments was demonstrated and the resting plasma membrane potential determined to be -55 mV. The relationship between membrane potential and catecholamine secretion was determined in response to variations in extracellular K+ and to the presence of several secretagogues including cholinergic receptor ligands, veratridine, and ionophores for Na+ and K+. The dependence of potential on K+ concentration fit the Goldman constant field equation with a Na/K permeability ratio of 0.1. The dependence of both K+- and veratridine-evoked catecholamine secretion on membrane potential exhibited a potential threshold of about -40 mV before a significant rise in secretion occurred. This is likely related to the threshold for opening of voltage-sensitive Ca2+ channels. Acetylcholine and nicotine evoked a large secretory response without a sufficiently sustained depolarization to be detectable by the relatively slow potential sensitive chemical probes. Decamethonium induced a detectable depolarization of the chromaffin cells. Veratridine and gramicidin evoked both membrane depolarization and catecholamine release. By contrast the K ionophore valinomycin evoked significant levels of secretion without any depolarization. This is consistent with its utilization of an intracellular source of Ca2+ and the independence of its measured secretory response on extracellular Ca2+.

Acetylcholine↗
PubMedDate not supplied

Effect of cadmium on membrane potential in isolated rat hepatocytes.

The effect of cadmium (Cd) on rat hepatocytes upon short term exposure was studied by focusing on the integrity of mitochondria and on the possible consequences of its disturbance, such as alterations in plasma membrane potential and loss of cell viability. Changes in the potential of mitochondrion and plasma membranes were monitored using [3H]triphenylmethylphosphonium (TPMP+) and [14C]SCN- probes, respectively. Isolated rat hepatocytes were exposed to increasing CdCl2 concentrations for short time periods (30-120 min). Cd measurement by atomic absorption showed that the cells efficiently accumulated Cd, as did mitochondria in situ. In CdCl2-treated cultures, it was observed that the release of TPMP+, which revealed a drop in the mitochondrial membrane potential, was time- and concentration-dependent, and that the first significant efflux was caused by a 30-min exposure to 89 microM CdCl2. No significant change in plasma membrane potential, as judged from the increase in the uptake of SCN-, was detected after 30 min, suggesting the greater precocity of the mitochondrial attack. Finally, the release of lactate dehydrogenase (LDH) occurred only after 2 h of exposure, reflecting ultimate stages of cell injury induced by Cd. These results suggest that Cd induces an alteration in mitochondrial function in hepatocytes which may lead to the loss of plasma membrane potential and cell viability. The study therefore adds further evidence of the role of mitochondria as primary targets in Cd-induced cytotoxicity.

Animals↗
PubMed1992

The effects of Na(+)-K(+)-Cl- co-transport and Cl(-)-HCO3-exchange blockade on the membrane potential and intracellular chloride levels of rat arterial smooth muscle, in vitro.

Membrane potential and intracellular chloride levels have been measured simultaneously in vascular smooth muscle from the femoral artery of the rat, in vitro, using double-barrelled chloride-sensitive microelectrodes. These values are compared in the presence and absence of bicarbonate, and inhibitors of Cl(-)-HCO3- exchange and Na(+)-K(+)-Cl- co-transport. Both DIDS and bumetanide caused a hyperpolarization of membrane potential (Em) and a fall in [Cl-]i, in the presence of extracellular HCO3-. The effects of bumetanide were reversible, but those of DIDS were not. The effect of both agents were additive. The results demonstrate that both Cl(-)-HCO3- exchange and Na(+)-K(+)-Cl- co-transport accumulate intracellular chloride in this preparation, and it is suggested that this may allow the modulation of membrane potential (and hence excitability) of smooth muscle.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1980

Membrane potential measurements in cultured intestinal villi.

Fragmented epithelia of newborn rat small intestine were successfully cultured for periods of up to 4 weeks. Stable intracellular recordings of membrane potential were obtained from these cultured cells. Membrane resting potential varied according to cell location along a villus. The potentials rangged from -70 to - 15 mV, being highest at the tip of the villus. The mean resting potential and membrane resistance were -72.4 mV and 8.6 M omega, respectively. The membrane potential was markedly dependent on the extracellular K+ concentration ([K] 0), but not significantly on [Na] 0 and [Cl] 0. Deprivation of Ca2+ from the surrounding medium depolarized the membrane by 20 mV. When the cells were cooled down to 6 degrees C, membrane potential was reduced by 40 mV. Based on these data, basic mechanisms underlying the resting potential are discussed in connection with cell differentiation or maturation.

Animals↗
PubMed1988

Effects of membrane potential on electrical slow waves of canine proximal colon.

The effects of membrane potential on the waveforms and propagation of slow waves were tested using circular muscles of the canine colon. Studies were conducted with intracellular recording techniques on cross-sectional strips of canine proximal colon. Circular muscle cells near the submucosa generated slow waves that decayed in amplitude as they spread through the circular layer. The membrane potentials of cells were less negative as a function of distance from the submucosal border. Cells near the submucosa were depolarized with elevated external K+ and electrical pulses using the partitioned chamber technique. The waveforms of depolarized submucosal cells were compared with events recorded from cells in the bulk of the circular layer. The waveform changes caused by experimental depolarization were different from the changes in waveform that occur during propagation, suggesting the latter are due to a different mechanism than depolarization. The effects of the membrane potential on syncytial input resistance and length constant were also evaluated. The results of these studies are consistent with the hypothesis that slow-wave propagation across the circular layer in canine proximal colon occurs passively.

Animals↗
PubMed1982

Interference of electron donors in the measurement of the proton gradient and membrane potential by flow dialysis.

The three most commonly used electron donors for flow dialysis measurements of membrane potential lead to the development of an apparent but artifactual membrane potential with the interior negative in the presence or absence of membrane vesicles. The same three electron donors used in flow dialysis determinations of delta pH in the presence or absence of membrane vesicles lead to the development of an apparent but artifactual delta pH with the interior acidic. These artifacts have been evaluated using two probes for membrane potential, namely, TPP+ and rubidium in the presence of valinomycin and for two probes of delta pH, namely, acetate and DMO. Measurements were made over a range of ionic strengths.

Dialysis↗
PubMed1990

Selective actions of anesthetic agents on membrane potential trajectory in bulbar respiratory neurons of cats.

The effects of two anesthetic agents, halothane and thiopental, on the membrane potential trajectory of respiratory-related neurons in the ventral respiratory group were investigated in decerebrate cats, of which the carotid sinus and vagal afferents were denervated. Infusion of halothane (2% for 90 s) depolarized the membrane in nearly half of the inspiratory (12/21), post-inspiratory (10/26) and expiratory (4/6) neurons and caused hyperpolarization in the rest of the population. Thiopental (2.5 mg/kg i.v.) produced depolarization in 11 inspiratory and 10 post-inspiratory neurons and hyperpolarization in 1 expiratory, 4 inspiratory and 7 post-inspiratory neurons. In both hyperpolarized and depolarized neurons, reduction of the respiratory membrane potential fluctuations and an increase of input resistance were commonly observed. Both drugs depressed spontaneous firing in most of the neurons studied. An increase of firing was observed in 9 out of 47 depolarized cells. These two contrasting effects on the membrane potential trajectory occurred similarly in the known groups of respiratory neurons, but the response of a given cell was consistent for the two anesthetic agents. The present results demonstrate that the anesthetic drugs exert various influences on the ventral respiratory group neuron population in maintaining the membrane potential trajectory and discharge activity. This may reflect a functional heterogeneity in the bulbar respiratory network of neurons.

Action Potentials↗
PubMed1997

Membrane potential and human erythrocyte shape.

Altered external pH transforms human erythrocytes from discocytes to stomatocytes (low pH) or echinocytes (high pH). The process is fast and reversible at room temperature, so it seems to involve shifts in weak inter- or intramolecular bonds. This shape change has been reported to depend on changes in membrane potential, but control experiments excluding roles for other simultaneously varying cell properties (cell pH, cell water, and cell chloride concentration) were not reported. The present study examined the effect of independent variation of membrane potential on red cell shape. Red cells were equilibrated in a set of solutions with graduated chloride concentrations, producing in them a wide range of membrane potentials at normal cell pH and cell water. By using assays that were rapid and accurate, cell pH, cell water, cell chloride, and membrane potential were measured in each sample. Cells remained discoid over the entire range of membrane potentials examined (-45 to +45 mV). It was concluded that membrane potential has no independent effect on red cell shape and does not mediate the membrane curvature changes known to occur in red cells equilibrated at altered pH.

2,3-Diphosphoglycerate↗
PubMed2004

Methylprednisolone-induced expression of mitochondrial heat shock protein 60 protects mitochondrial membrane potential in the hypoxic rat liver.

This study investigated the contribution made by mitochondrial heat shock protein (hsp) 60 to methylprednisolone-mediated protection against mitochondrial membrane depolarization under hypoxic conditions. A low-flow hypoxia model was generated in isolated male, fasted, pathogen-free Sprague-Dawley rat livers by reducing perfusate inflow pressure from 10 to 2.5 cm H2O for 2 h. The effects of methylprednisolone on mitochondrial membrane potential and expression of mitochondrial hsp 60 protein and mRNA were determined. We measured mitochondrial membrane potential by imaging rhodamine 123 fluorescence. Induction of mitochondrial hsp 60 was detected using two different anti-hsp 60 antibodies: one against the N-terminal signal sequence, which reacted exclusively with cytoplasmic hsp 60, and one against a different epitope, which reacted with cytoplasmic and mitochondrial hsp 60. In addition, the distribution of hsp 60 mRNA was examined using in situ hybridization. We found that under hypoxic conditions, there was a significant decline in mitochondrial membrane potential that was accompanied by a mild decline in the level of mitochondrial hsp 60, and that cytosolic hsp 60 was translocated into mitochondria. Pretreatment with methylprednisolone inhibited the declines in mitochondrial membrane potential and hsp 60 protein, as well as the translocation of cytosolic hsp 60. This raises the possibility that one way in which methylprednisolone protects the mitochondrial membrane potential under hypoxic conditions is to induce expression of mitochondrial hsp 60.

Animals↗
PubMed1988

Electromobile surface charge alters membrane potential changes induced by applied electric fields.

The relation between extracellular electric fields and changes in membrane potential that such fields directly induce has previously been described both theoretically and experimentally. It is clearly established that extracellular electric-field-induced membrane potential changes are well described by Poisson's equation of electrostatics. A modification of this simple theory to include effects of the electric-field-induced redistribution of charged cell surface components is introduced and is shown to produce major alterations in calculated membrane potential changes over times of the order of minutes to hours. Implications for biological systems which respond to extracellular electric fields are discussed.

Electric Conductivity↗
PubMed2004

Membrane potential responses of paramecium caudatum to external Na+.

The membrane potential responses of Paramecium caudatum to Na+ ions were examined to understand the mechanisms underlying the sensation of external inorganic ions in the ciliate by comparing the responses of the wild type and the behavioral mutant. Wild-type cells exhibited initial continuous backward swimming followed by repeated transient backward swimming in the Na+-containing test solution. A wild-type cell impaled by a microelectrode produced initial action potentials and a sustained depolarization to an application of the test solution. The prolonged depolarization, the depolarizing afterpotential, took place subsequently after stimulation. The ciliary reversal of the cell was closely associated with the depolarizing responses. When the application of the test solution was prolonged, the wild-type cell produced sustained depolarization overlapped by repeated transient depolarization. A behavioral mutant defective in the Ca2+ channel, CNR (caudatum non reversal), produced a sustained depolarization but no action potential or depolarizing afterpotential. The mutant cell responded to prolonged stimulation with sustained depolarization overlapped by transient depolarization, although it did not show backward swimming. The results suggest that Paramecium shows at least two kinds of membrane potential responses to Na+ ions: a depolarizing afterpotential mediating initial backward swimming and repeated transient depolarization responsible for the repeated transient backward swimming.

Action Potentials↗
PubMed1983

Resting membrane potential, extracellular potassium activity, and intracellular sodium activity during acute global ischemia in isolated perfused guinea pig hearts.

Transmembrane potentials, extracellular potassium activity, and intracellular sodium activity were determined during acute global ischemia in Langendorff perfused guinea pig ventricles by microelectrode techniques. Resting membrane potential decreased with a sigmoidal time course from -82 mV to -49.5 +/- 2.7 mV (SD, n = 6) and extracellular potassium activity increased from 4 to 5 mM to 14.7 +/- 1.3 mM (n = 8) during 15 minutes of ischemia. The estimated potassium equilibrium potential was 7 mV more negative than resting membrane potential prior to occlusion, but approached resting membrane potential during ischemia. An increase in extracellular potassium accumulation occurred when heart rate was increased abruptly from 60 to 170 beats/min. After rapid stimulation, a transient decrease of extracellular potassium activity occurred which was abolished in the presence of 10(-6) M strophanthidin. If the preparations were paced before and after aortic occlusion at a constant rate, potassium accumulation was independent of heart rate within a range of 50-170 beats/min. Intracellular sodium activity was 8.8 +/- 2.8 mM (n = 8) prior to occlusion and decreased slightly to values between 4.7 and 7.6 mM after 10-15 minutes of ischemia. The results suggest that relative potassium permeability largely predominates over relative sodium permeability during the decrease of resting membrane potential after interruption of aortic flow. Furthermore, active sodium-potassium exchange compensates for the rate-dependent fraction of potassium efflux and maintains a low intracellular sodium activity. For reasons of electroneutrality, the potassium efflux underlying extracellular potassium accumulation must be balanced by an equivalent charge movement which is not carried by sodium. The most probable hypothesis regarding the charge carriers is that net potassium efflux occurs secondary to efflux of phosphate and lactate generated during ischemia.

Animals↗
PubMed1981

Morphine and opioid peptides reduce inhibitory synaptic potentials in hippocampal pyramidal cells in vitro without alteration of membrane potential.

We used intracellular recording in the hippocampal slice in vitro to characterize further the mechanisms behind the unusual excitatory action of opiates and opioid peptides on hippocampal pyramidal cells in vivo. No significant effect on resting membrane potential, input resistance, or action potential size in cortical area 1 (CA1) pyramidal cells was observed with morphine sulfate, beta-endorphin, [Met5]enkephalin, or [D-Ala2, D-Leu5]enkephalin at 1-50 microM. However, in all cells studied, these agents markedly reduced the size of inhibitory postsynaptic potentials generated by stimulation of the stratum radiatum or alveus. Excitatory postsynaptic potentials were also diminished in many of these cells. The effects of the opioids were antagonized by naloxone. These results are consistent with excitation of pyramidal neurons by a disinhibitory mechanism.

Animals↗
PubMed1981

Relationship between membrane potential and calcium ion fluxes in the fragmented sarcoplasmic reticulum.

The relation between membrane potential and Ca2+ fluxes in the skeletal fragmented sarcoplasmic reticulum (FSR) was investigated using cyanine dye (diS-C3-(5) as a potential probe. Change of membrane potential and Ca2+ release from FSR were induced by changing the ionic composition of the medium. When the medium was changed from K-gluconate to Tris-gluconate, a large fluorescence intensity change was observed, while no Ca2+ release occurred. On the other hand, when the medium was changed from K-gluconate to KCl, Ca2+ release occurred notwithstanding a relatively small fluorescence intensity change. This KCl-induced Ca2+ release from FSR was inhibited by the addition of sucrose. Also, the presence of both permeable anion and cation was required for induction of Ca2+ release. These results suggest that there is no correlation between "depolarization" and Ca2+ release. Ca2+ uptake by FSR created the positive-inside potential which was reversed by the application of Ca2+ ionophore A23187. The addition of valinomycin or nigericin, and the replacement of Cl- with gluconate-affected potential formation. These facts suggest that Ca2+ uptake is accompanied by K+ efflux and/or Cl- influx for partial compensation of the change.

Animals↗
PubMed1981

Chemotaxis of Spirochaeta aurantia: involvement of membrane potential in chemosensory signal transduction.

The effects of valinomycin and nigericin on sugar chemotaxis in Spirochaeta aurantia were investigated by using a quantitative capillary assay, and the fluorescent cation, 3,3'-dipropyl-2,2'-thiodicarbocyanine iodide was used as a probe to study effects of chemoattractants on membrane potential. Addition of a chemoattractant, D-xylose, to cells in either potassium or sodium phosphate buffer resulted in a transient membrane depolarization. In the presence of valinomycin, the membrane potential of cells in potassium phosphate buffer was reduced, and the transient membrane depolarization that resulted from the addition of D-xylose was eliminated. Although there was no detectable effect of valinomycin on motility, D-xylose taxis of cells in potassium phosphate buffer was completely inhibited by valinomycin. In sodium phosphate buffer, valinomycin had little effect on membrane potential or D-xylose taxis. Nigericin is known to dissipate the transmembrane pH gradient of S. aurantia in potassium phosphate buffer. This compound did not dissipate the membrane potential or the transient membrane depolarization observed upon addition of D-xylose to cells in either potassium or sodium phosphate buffer. Nigericin did not inhibit D-xylose taxis in either potassium or sodium phosphate buffer. This study indicates that the membrane potential but not the transmembrane pH gradient of S. aurantia is somehow involved in chemosensory signal transduction.

Chemotaxis↗
PubMed1996

Infrared nonlinear optical measurements of membrane potential in photoreceptor cells.

In the past it has not been possible to measure optically the membrane potential of cells and collections of cells that are either naturally photosensitive or that can be activated by photolyzable caged transmitter molecules. This paper reports on a unique application of nonlinear optics that can monitor the potential of cellular membranes with a near-infrared source. Among many other singular advantages, this nonlinear optical approach to measuring membrane potential does not activate light sensitive cells or cell suspensions and cellular networks surrounded with photolyzable molecules. To demonstrate this capability we show that the technique can be applied to living photoreceptor cells that are very sensitive to visible light. These cells are ideal for characterizing such a new technique, not only because of their unmatched sensitivity to light, but also because their electrical responses have been extensively characterized (Minks and Selinger, 1992).

Animals↗
PubMed1992

Flow Cytometric Analysis of Rhodamine 123 Fluorescence during Modulation of the Membrane Potential in Plant Mitochondria.

The fluorescent dye rhodamine 123, which selectively accumulates in mitochondria based on the membrane potential, was used with flow cytometry to evaluate variations in activity of mitochondria isolated from plant tissues. In the presence of succinate and ATP, potato (Solanum tuberosum L.) tuber mitochondrial activity was affected by metabolic inhibitors and compounds that modify the membrane potential. The more uniform the mitochondrial population, the higher the observed membrane potential. The reactive population corresponds to the proportion of intact mitochondria (94-97%) defined by classic methods. Changes in the light-scattering properties are more related to internal modifications affecting the inner membrane-matrix system of the mitochondria during metabolic modulation than to specific volume change or outer membrane surface modifications. We tested our approach using an Arum maculatum preparation that contains three different types of mitochondria and demonstrated the validity of the light-scatter measurements to distinguish the alpha, beta, and [ill] mitochondria and to measure their ability to built up a membrane potential in the presence of succinate. These results demonstrate clearly that flow cytometric techniques using rhodamine 123 can be employed to study the activity in isolated plant mitochondria.

Journal Article↗
PubMedDate not supplied

Alterations of membrane potential and Ca2+ flux of sarcoplasmic reticulum vesicles in ischemic myocardium.

The sequence of contraction-relaxation for myocardial cells is believed to be linked to Ca2+ flux across the sarcoplasmic reticulum. Alterations of sarcoplasmic reticulum function during ischemia may result in depressing the myocardial contraction-relaxation sequence. This study examines the relationship between the membrane potential and Ca2+ flux across sarcoplasmic reticulum vesicles isolated from non-ischemic and ischemic myocardium. Ischemic myocardium was produced by ligating the coronary artery of swine hearts for 15 and 30 minutes. Membrane potential was determined by use of the fluorescence-sensitive dye, 3,3'-diethylthiadicarbocyanine, and Ca2+ uptake was studied spectrophotometrically with the use of murexide. Results are as follows: (1) membrane potential and Ca2+ uptake by sarcoplasmic reticulum from ischemic myocardium progressively decreased with the length of ischemia; and (2) preincubation of sarcoplasmic reticulum from non-ischemic myocardium with deoxycholate (0.01 approximately 0.09 percent) resulted in progressively decreasing membrane potential and Ca2+ uptake. Apparently a correlation exists between membrane potential and the rate of Ca2+ uptake. These results suggest that membrane characteristics of sarcoplasmic reticulum are altered within as early as 15 minutes of the onset of ischemia. Alteration of membrane permeability in sarcoplasmic reticulum from ischemic myocardium may be responsible for the observed decrease in membrane potential and Ca2+ uptake.

Animals↗