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PubMed1975

Pancreatic islet cells: electrogenic and electrodiffusional control of membrane potential.

1. Responses of the membrane electrical characteristics of mouse pancreatic islet cells to ionic environmental changes have been used to assess the role of [Na]0 and [K]0 in the control of membrane potential, i.e. by electrodiffusion or via an electrogenic sodium pump. Islet cell electrical properties were measured in vitro with intracellular glass micro-electrodes. 2. Substitution of LiCl for extracellular NaCl did not change the islet cell membrane potential significantly in low (2.8 mM) glucose solutions, but readmission of NaCl caused a transient hyperpolarization (membrane potential maximum: -70 mV) in high glucose; when choline chloride was substituted for NaCl no hyperpolarization was observed on NaCl re-admission. 3. Superfusion with K-free solution gave no marked change in membrane potential during 30 min incubation in either low (2-8 mM) or high (28 mM) glucose concentrations but longer periods of exposure to K-free solutions caused progressive depolarization. 4. Readmission of K+ induced a transient hyperpolarization of up to 30 mV magnitude and 10 min duration in the presence of high (28 mM) but not low glucose (2-8 mM) concentrations. At the level of maximum hyperpolarization the membrane potential reached -60 mV, the electrical activity induced by the high glucose concentration being concurrently completely blocked. Replacement of [Cl]0 by isethionate accentuated these effects. 5. Ouabain, 10(-3) M, or a decrease in temperature from 37 to 7 degrees C depolarized the islet cells and blocked the transient hyperpolarization induced by readmission of K+. 6. Diphenylhydantoin, 1-5 times 10(-4) M, caused a significant hyperpolarization of the islet cells in low glucose (2-8 mM) and inhibited the electrical activity induced by high glucose (28 mM) or tolbutamide (0-7 mM). 7. It is concluded from these results that both an electrogenic and ionic component contribute to the membrane potential of the mouse pancreatic islet cell although electrodiffusional control normally predominates; acceleration of the Na-K exchange pump by diphenylhydantoin inhibits glucose-induced electrical activity. These findings are discussed in relation to the permeability characteristics of the islet cell membrane and the mechanism of insulin release.

Animals↗
PubMed1989

Changes in the membrane surface charge density and/or membrane potential of the porcine intestinal brush-border membrane vesicles induced by treatment with neuraminidase.

The effects of neuraminidase treatment on the membrane surface charge density and/or membrane potential of the porcine intestinal brush-border membrane vesicles were studied by using three fluorescent dyes, 1,6-diphenyl-1,3,5-hexatriene (DPH), 1-anilino-8-naphthalene sulfonate (ANS), and 3,3'-dipropyl-2,2'-thiadicarbocyanine iodide (DiS-C3(5]. The results of quenching studies of DPH-labeled membranes using cationic (T1+) and anionic (I-) quenchers suggested an increase of negative charge on the membrane surface by desialylation upon neuraminidase treatment. This interpretation was further supported by a decrease of ANS-binding affinity of the membranes after treatment with the enzyme. In addition, the degree of valinomycin-induced fluorescence change of DiS-C3(5)-probed membranes in the presence of various concentrations of KCl was reduced by treatment of the membranes with neuraminidase. This suggests that penetration of the dye molecules into the vesicle interior is facilitated by the treatment. The membrane potentials estimated from the null point of valinomycin-induced changes in the DiS-C3(5) fluorescence of the control and neuraminidase-treated membranes were -25 to -29.7 and -40 to -48.8 mV, respectively. From these results, it is suggested that the membrane surface charge density and/or membrane potential of the intestinal brush-border membranes are susceptible to modification of carbohydrate moieties on the membrane surface by neuraminidase treatment.

Animals↗
PubMed1986

Depolymerization of microtubules alters membrane potential and affects the motional freedom of membrane proteins.

Two independent lines of evidence were obtained indicating that microtubule depolymerization affects the functions and the physical state of membranes in intact Chinese hamster ovary cells. The first type of evidence was obtained by using the dye dihexyloxacarbocyanine iodide to measure membrane potential before and after treatment with several microtubule active agents. Microtubule depolymerization resulted in a decrease in cell fluorescence, whereas stabilization of microtubules with taxol resulted in an increase in cell fluorescence. These effects of the drugs were due to their interactions with microtubules and not to direct effects of the drugs on the plasma membranes for the following reasons: effects were time dependent and required entry into the cells as indicated by the lack of fluorescence change in a multi-drug-resistant mutant that does not accumulate antimicrotubule drugs and a colcemid-resistant tubulin mutant did not show these effects on cell fluorescence. Evidence for altered motional freedom of membrane proteins in the plasma membrane was obtained by using electron spin resonance analysis of maleimide spin probe labeled cells. This study showed that depolymerization of microtubules results in increased motional freedom of maleimide-labeled sulfhydryl group containing proteins. Taken together, these data argue that microtubules function in mammalian cells to regulate the physical state of membranes and modulate membrane potential generated across cell membranes.

Animals↗
PubMed1983

Recovery of Ca currents from inactivation: the roles of Ca influx, membrane potential, and cellular metabolism.

Ca currents were examined with regard to their recovery from inactivation. The experiments were done on isolated nerve cell bodies of Helix aspersa using a combined suction pipet , microelectrode method for voltage clamp, and internal perfusion. Ca currents were separated by suppressing K and Na currents. The time course of recovery was determined by applying a test pulse at intervals ranging from 1 msec to 20 sec after prepulses varying from 20 to 3000 msec in duration. Each pair of pulses was preceded by a control pulse to ensure that the Ca currents had recovered before the next test pair was applied. Ba and Ca currents were compared and the effects of intracellular perfusion with EGTA, ATP, and vanadate were examined. Ba currents recovered in two stages and this time course was well fit by a sum of two exponentials with amplitudes and time constants given by A1 and tau 1 for the fast component and A2 and tau 2 for the slow component. In Ba the time constants were unchanged when prepulse durations were prolonged from 70 to 700 msec, although the initial amplitudes A1 and A2, particularly A2, were increased. Comparable influxes of Ca during the prepulse caused much more inactivation, but interestingly the recovery occurred at the same rate. The time course of Ca current recovery was also fit by a sum of two exponentials, the time constants of which were both smaller than the time constants of Ba current recovery. However, the time constants of Ca current recovery were increased markedly when prepulse durations were prolonged. Increasing the extracellular Ca concentration had a similar effect. Increasing the Ba influx had no effect on the recovery time constants, and the Ba results are consistent with reversible inactivation gating of potential-dependent membrane Ca channels. The Ca results show that Ca influx enhances inactivation. Intracellular perfusion with EGTA resulted in less inactivation in the cast of Ca but it had no effect on Ba currents. Intracellular ATP increased the rate of recovery of Ca currents, and intracellular vanadate inhibited recovery. It is concluded that recovery of Ca channels depends upon both Ca influx and membrane potential and is modulated by agents which affect Ca metabolism.

Adenosine Triphosphate↗
PubMed1971

The membrane potential and permeabilities of the L cell membrane to Na, K and chloride.

1. The chloride content and fluxes, and the membrane potential of L cells have been measured.2. L cells contain chloride, 70 m-mole/l. intracellular water and have a flux of 5.5 p-mole/cm(2) sec.3. The membrane potential is -15 mV.K-free Krebs causes an increase in E(m) and replacing chloride with sulphate causes a temporary reduction in E(m).4. These values for E(m) and chloride, and previously obtained values for Na and K fluxes and contents were used to calculate the permeabilities of the various ions using the Goldman constant field theory. This gave permeabilities of 6.3, 4.2 and 51 x 10(-9) cm/sec for K, Na and chloride respectively, a ratio of 1:0.67:8.10.5. It is concluded that these cells have a low membrane potential because the P(K) is some 100 times lower than in skeletal muscle, therefore leading to a P(K) of the same order as P(Na).

Animals↗
PubMed1997

Membrane potential manipulation in synaptic plasma membrane vesicles for studying neurotransmitter uptake and release.

Synaptic plasma membrane (SPM) vesicles represent a membrane fraction very useful in studying non-vesicular neurotransmitter release. The procedure described here to isolate SPM vesicles from a crude synaptosomal fraction of sheep brain cortex is quick, simple (ultracentrifugation in a discontinuous density gradient of dextran T110), and combines a high yield (130 micrograms/g brain) with a satisfactory grade of purification. The preparation of SPM vesicles consists of vesicles (approximately 0.54 +/- 0.8 micron diameter) delimited by a single membrane with the native orientation. We are able to ascertain these characteristics on the basis of morphology studies (electron microscopy observations), enzyme activities (Na+/K(+)-ATPase, Ca2+/Mg(2+)-ATPase, acetylcholinesterase and glucose-6-phosphatase), biochemical composition (lipid and protein analysis) and the tetrodotoxin sensitivity of the veratridine-induced gamma-aminobutyric acid (GABA) release. Isolating the SPM vesicles by the proposed procedure permits manipulating the ionic gradients across the membrane by changing the ion concentrations on either side or by utilizing specific ionophores. The vesicles retain their various activities, including their capacity for neurotransmitter uptake and release assays for at least 3 months, when preserved at -70 degrees C. Furthermore, the vesicles permit depicting the electrochemical gradients across the membranes into chemical and electrical components. We describe the use of the tetraphenylphosphonium cation (TPP+) to dissipate the membrane potential (delta psi) of the vesicles, while preserving ionic gradients. The characteristics of the lipid-soluble cation TPP+ allows a massive inflow of this cation into vesicular compartments and a consequent depolarization.

Animals↗
PubMedDate not supplied

Biological significance of enhanced mitochondrial membrane potential in regenerating liver.

Liver mitochondrial membrane potential was assessed during regeneration following partial hepatectomy in rabbits. Absorbance change of safranine O per milligram of mitochondrial protein was used to evaluate mitochondrial membrane potential. Absorbance change was calibrated to the membrane potential in millivolts produced by valinomycin-induced potassium diffusion potential. At 24 hr after hepatectomy, absorbance change of safranine O per milligram of mitochondrial protein increased from 15.0 +/- 2.2 X 10(-3) to 37.4 +/- 3.3 X 10(-3) per mg (p less than 0.005). This represents a mitochondrial membrane potential increase from 77.0 +/- 4.6 to 124.4 +/- 6.7 mV. Phosphorylative activity increased from 59.9 +/- 5.0 to 106.1 +/- 7.4 nmoles ATP synthesized per mg per min (p less than 0.005). The enhancement of phosphorylative activity was closely linked to the elevation in liver mitochondrial membrane potential (r = 0.77, p less than 0.005). We suggest that elevation of mitochondrial membrane potential, coupled with enhanced oxidative and phosphorylative activities, plays an important role in the regeneration process following hepatectomy.

Adenosine Triphosphate↗
PubMedDate not supplied

Significant differences between procyclic and bloodstream forms of Trypanosoma brucei in the maintenance of their plasma membrane potential.

The plasma membrane potential (deltapsi) of procyclic and bloodstream trypomastigotes of Trypanosoma brucei was studied using the potentiometric fluorescent dye bisoxonol. Our results suggest that a proton pump plays a significant role in the regulation of deltapsi in procyclic and bloodstream forms, as evidenced by depolarization of the plasma membrane by H(+)-ATPase inhibitors (e.g. dicyclohexylcarbo-diimide, N-ethylmaleimide, diethylstilbestrol, and bafilomycin A1). In bloodstream stages the plasma membrane was significantly depolarized by ouabain only when the cells were incubated in sodium-rich buffers indicating that a sodium pump was being inhibited. In contrast, ouabain had no effect on the deltapsi of the procyclic stages in a sodium-rich buffer. However, it induced an additional significant depolarization in these stages when their plasma membrane was already partially depolarized by the H(+)-ATPase inhibitor dicyclohexylcarbo-diimide, indicating the presence of an ouabain-sensitive sodium pump whose activity is masked by the H(+)-ATPase. Unlike procyclic forms, the deltapsi of bloodstream-stage trypomastigotes was markedly sensitive to extracellular Na+ and K+ concentrations. Thus, there are significant differences between procyclic and bloodstream forms in the maintenance of the deltapsi and in their permeability to cations.

Animals↗
PubMed1989

Two stage carcinogenesis by membrane potential changes.

The membrane potential theory is modified and extended. It is shown to be applicable to carcinogenesis by prolonged treatment of target tissues with an initiating external carcinogen or by a single sub-threshold exposure to the initiating external carcinogen followed by subsequent treatment with a phorbol ester internal promoter.

Animals↗
PubMed1997

Assessment of the effects of gramicidin, formaldehyde, and surfactants on Escherichia coli by flow cytometry using nucleic acid and membrane potential dyes.

Two membrane potential sensitive dyes (Rhodamine 123 and bis-oxonol) and three nucleic acid dyes (propidium iodide, SYTO-13, and SYTO-17) were used to assess the effect of surfactants on Escherichia coli. The ability of E. coli to be stained by these probes was validated at different physiological states. Propidium iodide was used to assess the integrity of cell envelopes. Two double staining methods based on propidium iodide with SYTO-13 and bis-oxonol with SYTO-17 were used to improve the discrimination between bacteria and micelles or aggregated particles generated by the presence of surfactants. A rapid (1 h contact time between cells and surfactants, and less than 5 min for staining and obtaining data) Rhodamine 123 flow cytometric assay was developed to assess the bactericidal effect of surfactants.

Anti-Infective Agents, Local↗
PubMed1985

[Cooperative phenomena in the membrane potential of parathyroid cells induced by divalent cations].

Membrane potentials of mouse parathyroid cells were measured by means of the intracellular microelectrode method. The membrane potential in external Krebs solution containing 2.5 mM of Ca++ was -23.6 +/- 0.4 mV (mean +/- standard error of mean). The low concentration of Ca++ (1.0 mM) caused hyperpolarization of the membrane potential to -61.7 +/- 0.8 mV. The membrane potential was proportional to the logarithm of the concentration of K ion in the solution of low Ca ion. The concentration of external Na+, C1- and HPO4-- had no effect on the membrane potential. The sigmoidal transition of membrane potentials was induced by the change of Ca ion concentration in the range from 2.5 to 1.0 mM. The change of the membrane potentials in low Ca ion is originated from increase in potassium permeability of the cell membrane. The similar sigmoidal changes of the membrane potentials were observed in the solution containing 4 to 3 mM of Sr ion. The Mg and Ba ion showed smaller effect on the membrane potential. The Goldman equation was extended to divalent ions. Appling the extended membrane potential equation, ratios of the permeability coefficients were obtained as follows: PK/PCa = 0.067 for 2.5 mM Ca++, 0.33 for 1.0 mM Ca++; PK/PSr = 0.08 for 4 mM Sr++ and 0.4 for 3 mM Sr++; PK/PMg = 0.5; PK/PBa = 0.67 for all range of concentration. The Hill constants of Sr ion and Ca ion were 20; the relationship between Sr ion and Ca ion was competitive. The Hill constants of Mg and Ba ion were 1 each. The Hill constant of Ca ion was depend of the temperature; nmax = 20 at 36 degrees C, n = 9 at 27 degrees C, n = 2 at 22 degrees C. The enthalpy of Ca-binding reaction was obtained from the Van't Hoff plot as 0.58 kcal. The activation energies of the K+ permeability increase were obtained from the Arrhenius plots as 3.3 kcal and 4 kcal. The difference, 0.7 kcal, corresponds to the enthalpy change of this reaction, of which value is close to that of the Ca-binding reaction.

Animals↗
PubMed1983

[The effects of low temperature and extracellular ions on the membrane potential of newt red cells].

The membrane potential of the newt red cell was measured with a microelectrode to investigate the relation to its respiratory function. The membrane potential hyperpolarized with increasing oxygen density of the medium (pO2 0%; -13.4 +/- 0.4 mV, 21%; -16.2 +/- 0.4 mV, 100%; -18.9 +/- 0.7 mV) (mean +/- standard deviation of mean). As the temperature was reduced, the red cell membrane potential increased linearly, either in the completely oxygenated or in the deoxygenated medium. These two regression lines were almost parallel to that in the control medium (pO2 21%). At 0 degrees C, a) the membrane potential changed linearly to the Cl- concentration of the external medium, similarly in the case of that at room temperature. But its gradient was 0.3mV/10 mM, whereas 1.2mV/10 mM at 18 degrees C. b) The changes in the concentration of the external Na+ and Ca++ were not so remarkable on the membrane potential. c) Increase of the external K+ had a tendency to reduce the membrane potential.

Animals↗
PubMed2003

Ratiometric fluorescence measurements of membrane potential generated by yeast plasma membrane H(+)-ATPase reconstituted into vesicles.

Potential-sensitive fluorescent probes oxonol V and oxonol VI were employed for monitoring membrane potential (Delta(psi)) generated by the Schizosaccharomyces pombe plasma membrane H(+)-ATPase reconstituted into vesicles. Oxonol VI was used for quantitative measurements of the Delta(psi) because its response to membrane potential changes can be easily calibrated, which is not possible with oxonol V. However, oxonol V has a superior sensitivity to Delta(psi) at very low concentration of reconstituted vesicles, and thus it is useful for testing quality of the reconstitution. Oxonol VI was found to be a good emission-ratiometric probe. We have shown that the reconstituted H(+)-ATPase generates Delta(psi) of about 160 mV on the vesicle membrane. The generated Delta(psi) was stable at least over tens of minutes. An influence of the H(+) membrane permeability on the Delta(psi) buildup was demonstrated by manipulating the H(+) permeability with the protonophore CCCP. Ratiometric measurements with oxonol VI thus offer a promising tool for studying processes accompanying the yeast plasma membrane H(+)-ATPase-mediated Delta(psi) buildup.

Cell Membrane↗
PubMed1987

L-glutamine: an amino acid required for maintenance of the tegumental membrane potential of Schistosoma mansoni.

The tegumental membrane potential (-63 +/- 2.9 mV) of adult male Schistosoma mansoni in RPMI-1640 is significantly depolarized (-26 +/- 7.3 mV) when the parasite is incubated in inorganic media (Hank's Balanced Saline or RPMI-1640 without organic constituents). Of 9 amino acids (L-glutamine, D-glutamine, L-arginine, L-proline, L-aspartate, L-glutamate, L-asparagine, L-isoleucine and L-methionine) L-glutamine alone is sufficient to repolarize the membrane potential to a value (-56 +/- 4.5 mV) not significantly different from that found in RPMI-1640. Repolarization by glutamine is dose-dependent, with significant effects obtained as low as 0.10 mM. The concentration of phosphate in the medium also significantly alters the membrane potential. Physiological levels of phosphate (5.6 mM) are necessary in conjunction with L-glutamine to obtain the full repolarization of the membrane potential. In the absence of organic constituents, the membrane potential is strongly dependent on the external medium pH. When L-glutamine is present in the medium, the membrane potential becomes virtually independent of the external pH.

Amino Acids↗
PubMed1983

Exclusive potassium dependence of the membrane potential in cultured mouse oligodendrocytes.

Membrane potential, conductance, and intracellular potassium concentration were measured in oligodendrocytes in 3- to 10-week-old cultures of embryonic mouse spinal cord. After intracellular recording the cells were first injected with Lucifer Yellow and then stained by immunofluorescence using rhodamine-labeled monoclonal antibody 01 specific for oligodendrocyte cell surfaces. The membrane potential of these identified oligodendrocytes was in mV -66 +/- 4.3 SD; it could be reversibly reduced almost to zero by the addition of ouabain. Changes in external K+ but not Na+, Ca++, or Cl- changed the membrane potential. A 10-fold increase in extracellular potassium concentration ([K+]0) depolarized the cell by about 52 mV. This is less than the 61 mV predicted by the Nernst equation for a K+ electrode assuming a constant intracellular potassium concentration ([K+]i). However, when [K+]i was measured with an ion-selective electrode during the increase in [K+]0 it was found to rise. The Nernst equation for K+ accurately predicts the oligodendrocyte membrane potential when the increase in [K+]i is taken into account. Oligodendrocytes may be described as accurate K+ electrodes with a variable reference solution.

Animals↗
PubMed2005

The human platelet membrane proteome reveals several new potential membrane proteins.

We present the first focused proteome study on human platelet membranes. Due to the removal of highly abundant cytoskeletal proteins a wide spectrum of known platelet membrane proteins and several new and hypothetical proteins were accessible. In contrast to other proteome studies we focused on prefractionation and purification of membranes from human platelets according to published protocols to reduce sample complexity and enrich interesting membrane proteins. Subsequently protein separation by common one-dimensional SDS-PAGE as well as the combined benzyldimethyl-n-hexadecylammonium chloride/SDS separation technique was performed prior to mass spectrometry analysis by nano-LC-ESI-MS/MS. We demonstrate that the application of both separation systems in parallel is required for maximization of protein tagging out of a complex sample. Furthermore the identification of several potential membrane proteins in human platelets yields new potential targets in functional platelet research.

Amino Acid Sequence↗
PubMed1984

Membrane potential generation and calcium transport in plasma membrane enriched fractions from fetal human brain.

Plasma membrane fractions isolated from fetal human brain of 14-19 weeks of gestation are capable of generating a membrane potential of 30-50 mV as a response to a gradient of K+ ions. Valinomycin, a K+ conducting ionophore, does not affect the membrane potential whereas it is markedly reduced by veratridine which opens Na+ channels in excitable membranes. The membrane fractions concentrate Ca2+ by an ATP-dependent mechanism. The uptake has a high affinity for Ca2+, it is enhanced by oxalate and abolished by the 2H+/Ca2+ exchanger A 23187. Trifluoroperazine (40 microM), a calmodulin antagonist, inhibits Ca2+ uptake by 80%. Addition of Na+ causes efflux of part of the Ca2+ taken up in the presence of ATP, suggesting that a Na+-linked Ca2+ transport is also present in the membranes. The results show that the neuronal membranes of the fetal human brain already in the early second trimester of gestation have properties similar to those of the adult animal brain.

Acetylcholinesterase↗