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PubMed1978

Erythrocyte membrane potentials determined by hydrogen ion distribution.

If the extracellular fluid is left unbuffered, dynamic membrane potential changes in the red blood cell may be determined from external pH readings. For some types of experiments it is necessary to accelerate H+ equilibration by adding minute amounts of hydrogen carriers. The method is independent of hematocrit over a wide range of membrane potential changes. Membrane potential jumps produced by permeability changes or by changes in ionic composition may be measured. The method provides a convenient means of measuring parameters of both the conductive and non-conductive anion pathways in the red cell.

Carbonyl Cyanide m-Chlorophenyl Hydrazone↗
PubMed1982

The role of platelet membrane potential in the initiation of platelet aggregation.

The membrane potential of human platelets, and the role of this potential in platelet aggregation, was assessed using the noncovalent, fluorescent probe DiS-C3-5. High K+ and Gramicidin depolarised the cells, whereas valinomycin in standard (4 mMK+) solution produced a hyperpolarisation. Very small changes in potential were observed when choline Cl replaced NaCl. These findings indicate that platelets possess a relatively K+-perm-selective membrane. The resting potential calculated from the "valinomycin null point" (the K+ concentration gradient at which valinomycin did not change the potential) was approximately -60 mV. Other factors that contribute to the platelet membrane potential include a significant Cl- permeability, demonstrated by replacing Cl- with methylsulphate, and an electrogenic Na+ pump, demonstrated using strophanthidin. Little or no change in potential was observed upon addition of ADP, collagen, U44069 or thrombin. Neither strong depolarisation with high K+ or gramicidin nor hyperpolarisation with valinomycin induced platelet aggregation or altered platelet responses to agonists. It is concluded that the information transduction mechanisms involved in platelet activation do not include changes in platelet membrane potential.

Benzothiazoles↗
PubMed1999

Inward and outward rectifying potassium currents set membrane potentials in activated rat microglia.

Activation of cultured rat microglial cells with lipopolysaccharide (LPS), induced outward rectifying K+ (K(V)) current in addition to already existing inward rectifying K+ current (K(IR)). By measuring zero-current membrane-potentials using whole-cell patch-clamp method, we showed that K(V) current plays a direct role in setting membrane potential to near -45 mV. Since the membrane potentials of microglia show two prominent peaks at -45 and -70 mV, we hypothesize that K(IR) current might set the membrane potential to near -70 mV. We observed that cells with larger K(IR) current had a zero-current membrane-potential at around -70 mV, and that blocking of K(IR) current with Ba2+ depolarized membrane potentials to near -45 mV. These results indicate that the amounts of K(IR), and K(V) current determine the zero-current membrane-potentials in LPS-activated microglia.

Animals↗
PubMed1986

Cyclosporin A depolarizes cytoplasmic membrane potential and interacts with Ca2+ ionophores.

Cytoplasmic membrane potential of mouse lymphocytes was determined with flow cytometry and fluorescence spectroscopy using 3,3'-dihexylcarbocyanine iodide (DiOC6(3)). The amount of this lipophilic cation incorporated into the cytoplasmic membrane is dependent upon the transmembrane potential, so the dye is suitable for continuous monitoring of this parameter, under controlled conditions. Membrane potential of the cells was decreased in the presence of cyclosporin A and cyclosporin G in a dose-dependent manner. However, the depolarization caused by Ca2+ ionophores, ionomycin and A23187, was reduced in the presence of cyclosporin A. Electron spin resonance spectroscopy with 5-doxylstearic acid as a probe indicated that cyclosporin A decreased the apparent motional freedom of membrane lipids. These data suggest incorporation of cyclosporin A into the cytoplasmic membrane, causing changes in ion fluxes. The membrane potential change induced by cyclosporin A may have selective biological consequences in certain subpopulations of lymphocytes.

Animals↗
PubMed1977

The effects of gastrin and gastrin analogues on pancreatic acinar cell membrane potential and resistance.

1 Intracellular recordings of membrane potentials and input resistance have been made from the exocrine acinar cells of mouse and rat pancreas placed in a tissue bath perfused with Krebs-Henseleit solution.2 The resting acinar cell membrane potential was about -38 mV. The acinar cells were stimulated by cholecystokinin-pancreozymin (CCK-PZ), gastrin and the gastrin-related polypeptides, caerulein and desulphated caerulein. The immediate effect of stimulation with these secretagogues was always a depolarization and a concomitant reduction in input resistance and time constant. Depolarization of the acinar cell membrane by these secretagogues was not abolished in the presence of atropine (1.4 muM).3 These peptide secretagogues were divided into the gastrin group and the CCK-PZ group according to the time course of the depolarizations and the shape of the dose-response curve. The depolarization evoked by the gastrin group returned quickly to the resting level but that evoked by the CCK-PZ group was long lasting. The time course and the dose-response curve for desulphated caerulein was identical with that of gastrin.4 It was confirmed electrophysiologically that the activity of gastrin is exerted by the C-terminal tetrapeptide; but the activity of caerulein depends on the C-terminal heptapeptide, especially the presence in the molecule of the sulphated tyrosyl residue at position 7 (numbering from the C-terminus). The equivalent sulphated tyrosyl residue in CCK-PZ is probably necessary for optimal activity of this polypeptide.5 The dose-response curves obtained by electrophysiological methods indicated that the relative potencies of the peptides on mouse pancreatic acinar cells were caerulein > CCK-PZ > gastrin. Synthetic human gastrin I was found to have a higher potency than either tetra- or pentagastrin.

Acetylcholine↗
PubMed2002

Ciguatoxin-induced oscillations in membrane potential and action potential firing in rat parasympathetic neurons.

The actions of ciguatoxins from the Pacific (P-CTX-1) and Caribbean (C-CTX-1) regions were investigated in isolated parasympathetic neurons from rat intracardiac ganglia using patch-clamp recording techniques. Under current-clamp conditions, bath application of P-CTX-1 (1-10 nm) or C-CTX-1 (10-30 nm) caused a gradual depolarization that was accompanied by oscillation of the membrane potential leading to tonic action potential firing. Membrane potential oscillations were observed between -45 and -60 mV and had an amplitude of 10-20 mV and a mean frequency of 10 Hz. Oscillation frequency was temperature-dependent with a Q10 of 2.0. Membrane oscillations were temporarily inhibited by hyperpolarizing current pulses and potentiated by weak depolarizing current pulses. The amplitude of oscillations was reduced upon lowering the external Na+ concentration and inhibited by tetrodotoxin (TTX), tetracaine or Zn2+. Tetraethylammonium, 4-aminopyridine, Cs+, Cd2+, Ba2+, 1,4,4'-diothiocyanato-2,2'-stilbenedisulphonic acid (DIDS) and ouabain had no effect on the CTX-1-induced membrane depolarization and oscillations. Brevetoxin (PbTx-3, 100 nm), in contrast to CTX-1, caused a membrane depolarization that was not associated with oscillation of the membrane potential. Under voltage-clamp conditions, P-CTX-1 inhibited the peak amplitude of the voltage-dependent Na+ current and shifted the activation curve to more negative potentials, but membrane oscillations were not seen in this configuration. These results suggest that ciguatoxins cause oscillation of the membrane potential in mammalian autonomic neurons by modifying the activation and inactivation properties of a population of TTX-sensitive Na+ channels.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1997

Role of the Na+/K+-ATPase in regulating the membrane potential in rat peritoneal mast cells.

1. The aim of this study was to investigate the effect of the Na+/K+-ATPase on the membrane potential of peritoneal mast cells isolated from male Sprague-Dawley SPF-rats. 2. Experiments were performed at 22-26 degrees C in the tight-seal whole-cell configuration of the patch-clamp technique by use of Sylgard-coated patch pipettes (3-6 M[omega]). High-resolution membrane currents were recorded with an EPC-9 patch-clamp amplifier controlled by the 'E9SCREEN' software. In addition, a charting programme on another computer synchronously recorded at low resolution (2 Hz) membrane potential and holding current (low-pass filtered at 500 Hz). 3. Na+/K+-ATPase activity was measured as the ouabain-sensitive change in the zero-current potential. The zero-current potential in rat peritoneal mast cells measured 2 min after obtaining whole-cell configuration amounted to 1.7 +/- 2.5 mV (n = 21). Ouabain (5 mM), a Na+/K+-ATPase-inhibitor, had only a very minor effect upon the membrane potential under resting conditions (n = 3). 4. When mast cells were superfused with nominal calcium-free external solution, the cells hyperpolarized (delta mV: 20.2 +/- 3.8 mV (n = 5)). In addition, when the mast cells were preincubated in nominal calcium-free external solution for 12 +/- 1.6 min before whole-cell configuration, the membrane potential amounted to -53.7 +/- 9.8 mV (n = 8). A subsequent superfusion with ouabain (5 mM) depolarized the membrane potential (ouabain-sensitive hyperpolarization (delta mV): 23.0 +/- 8.4 mV (n = 8)). 5. A high intracellular concentration of Na+ ([Na+]i) (26.6 mM) also resulted in hyperpolarization (delta mV: 20.2 +/- 9.1 mV (n = 7)), but only when ATP was present. A subsequent superfusion with ouabain (5 mM) repolarized these cells to -1.2 +/- 14 mV (ouabain-sensitive hyperpolarization (delta mV): 19.7 +/- 7.7 mV (n = 7)). 6. The size of the [Na+]i-dependent hyperpolarization was dose-dependent. Low [Na+]i (1 mM) had no effect on membrane potential and these cells were unaffected by superfusion with calcium-free external solution. 7. These data thus directly confirm that the stimulant effect of calcium-free external solutions on the ouabain-sensitive changes in the zero-current potential, and hence the Na+/K+-ATPase, is mediated through [Na+]i and that the activity of the Na+/K+-ATPase can have an important influence on the resting membrane potential in rat peritoneal mast cells.

Animals↗
PubMed2000

[Effect of ion channel modulators on the membrane potential of human chondrocytes].

As all living cell systems, human chondrocytes are provided with a membrane potential. For its origin the existence of ion channels at the cell membrane is an essential prerequisite. In non-human chondrocytes, different ion channels could already be identified. A connection between the potassium channel activity and the proliferation has been detected in different human cell systems. Whereas, the proof of a connection between ion channel activity of human chondrocytes and the proliferation has yet to be established. In this study the concentration-dependent influence of the ion channel modulators tetraethylammonium (TEA), 4-amino-pyridin (4-AP), 4',4'diisothiocyanatostilbene-2,2'disulfonic acid (DIDS), 4-acetamido-4'isothiocyano-2,2'disulfonic acid stilbene (SITS) and verapamil on the membrane potential and the proliferation of human chondrocytes was investigated using flow cytometry. The results show an effect of the used ion channel modulators causing a change of the membrane potential of human chondrocytes. The decrease of the membrane potential by 18% was measured with 0.25 mmol/l verapamil meaning the maximal measurable effect compared with a control group. When measuring DNA distribution, it became apparent that the human chondrocytes are diploid cells with a very low proliferation tendency. These results allow the conclusion of an influence of ion channel modulators on chondrocyte proliferation.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1989

Characterization of resting membrane potential and its electrogenic pump component in cultured chick myotubes.

The role of the electrogenic Na+-K+ pump in the determination of the level of the resting membrane potential in cultured chick limb muscle was investigated. Transmembrane resting potential and ouabain-sensitive 86Rb-uptake were measured in myotubes at different ages in culture from 2 to 10 days in vitro. Inhibition of the Na+-K+ pump with ouabain prevented the developmental increase in membrane potential which normally follows fusion of myotubes (day 2-3). In mature myotubes, ouabain caused a dose-related decrease in both membrane potential and 86Rb-uptake, with values for EC50 and maximal effect being nearly the same on both variables. The decrease in membrane potential by ouabain, up to 20 mV maximum, occurred within 2-5 sec and was not accompanied by detectable changes in input resistance. Membrane potential was also reduced by a decrease in temperature of the recording medium and removal of extracellular K+, both of which reduce Na+-K+ pump activity. We also found that the relation between membrane potential and extracellular K+ concentration was completely attenuated by ouabain in the physiological range (2-10 mM). We conclude that the electrogenic Na+-K+ pump plays an important role in the determination of the resting membrane potential of chick myotubes and that regulation of its level is not entirely explained by the diffusion potential hypothesis.

Action Potentials↗
PubMed1980

Effect of membrane potential on Na+-dependent sugar transport by ATP-depleted intestinal cells.

The role of the membrane potential as a component of the thermodynamic driving force and as a determinant of kinetic parameters of Na+-dependent sugar transport was investigated using ATP-depleted isolated chicken intestinal cells. Inside-negative membrane potentials were established by incubating K+-loaded rotenone-inhibited cells with valinomycin in a low K+ medium. Overshoots of 3-O-methylglucose (3-OMG) accumulation as high as 10-fold were observed in the presence of valinomycin even in the absence of a Na+ chemical gradient. The magnitude of overshoot was diminished by decreasing the magnitude of the imposed K+ gradient and abolished altogether when nigericin was also included. An Eadie-Hofstee plot of initial flux data showed that the imposed membrane potential increases the Vmax of transport in the absence of a chemical gradient for Na+ from 3 to 12 nmol 3-OMG . mg protein-1 . min-1. The KT is not significantly altered. Similar kinetic results were obtained when a membrane potential as well as a Na+ gradient were imposed. These results suggest that the membrane potential is a more important contributor to alterations in the kinetics of transport than the Na+ chemical potential.

Adenosine Triphosphate↗
PubMed1985

Relationship between membrane potential changes and superoxide-releasing capacity in resident and activated mouse peritoneal macrophages.

In an attempt to understand better the molecular basis for the enhanced respiratory burst of activated macrophages (M phi), we investigated the relationship between stimulus-induced changes in membrane potential and release of superoxide anion (O2-) in mouse peritoneal M phi. Resident M phi and M phi elicited by injection of lipopolysaccharide (LPS-M phi) or obtained from animals infected with bacille Calmette-Guérin (BCG-M phi) were used. LPS-M phi and BCG-M phi showed more pronounced changes in membrane potential (depolarization) and greater release of O2- on contact with phorbol myristate acetate (PMA) than did resident macrophages. The lag time between addition of stimulus and onset of release of O2- was reduced in activated compared with resident cells. Membrane potential changes began 60 to 90 sec before release of O2- could be detected in each cell type. The dose-response curves for triggering of membrane potential changes and O2- release by PMA were identical. The magnitude of membrane potential changes and of O2- release in LPS-M phi and BCG-M phi declined progressively during in vitro culture, and values on day 3 approached those in resident macrophages ("deactivation"). Extracellular glucose was required for effective stimulated change in membrane potential and O2- release. These findings indicate that membrane potential changes are closely associated with O2- -releasing capacity in macrophages, and that the systems that mediate membrane potential changes and production of O2- develop or decline concomitantly during activation or deactivation of the cells. Although the plasma membrane was highly depolarized by high extracellular K+ or by the sodium ionophore gramicidin, O2- release was not induced by these maneuvers, indicating that changes in membrane potential by themselves are not sufficient to trigger the respiratory burst in macrophages. Release of O2- was not impaired in buffers in which Na+ was completely replaced with equimolar concentrations of K+ or choline+; thus, induction or maintenance of the respiratory burst in M phi does not require an influx of Na+.

Animals↗
PubMed1991

Resting membrane potential in 41A3 mouse neuroblastoma cells. Effect of increased glucose and galactose concentrations.

Neuroblastoma cells were used to examine the effect of high concentrations of glucose or galactose and accumulation of polyols on the resting membrane potential. Polyol levels are increased and myo-inositol content decreased when neuroblastoma cells are chronically exposed to media containing 30 mM glucose or 30 mM galactose compared to cells grown in media containing 30 mM fructose. Furthermore, the 6 h accumulation and incorporation into phospholipid of extracellular myo-inositol is decreased in cells exposed to media containing 30 mM glucose or 30 mM galactose compared to cells grown in media containing 30 mM fructose. The resting membrane potential was determined by examining the steady-state accumulation of the lipophilic cation tetra[3H]phenylphosphonium bromide (TPP+). The resting membrane potential of cells grown in media containing 30 mM fructose is about -70 mV which is very similar to the resting membrane potential of cells grown in unsupplemented media. The resting membrane potential is significantly decreased in cells grown in media containing 30 mM glucose or 30 mM galactose. myo-Inositol metabolism and content and polyol levels are maintained at near normal values and the resting membrane potential is improved when media containing 30 mM glucose or 30 mM galactose are supplemented with 0.4 mM sorbinil. Acute exposure of neuroblastoma cells to 2 mM ouabain had no significant effect on [3H]TPP+ accumulation. This suggests that acute inhibition of Na+/K+ pump activity does not decrease the resting membrane potential of neuroblastoma cells. The decrease in resting membrane potential may be induced by the metabolic abnormalities and/or chronic decrease in Na+/K+ pump activity which occur when neuroblastoma cells are chronically exposed to increased glucose or galactose concentrations.

Animals↗
PubMed1992

A negative resistance region underlies the triggering property of membrane potential in human T-lymphocytes.

Steady-state current-voltage relationships (SSCVRs) of the plasma membrane of human T-lymphocytes were studied at the physiological temperature of 37 degrees C by using the whole-cell patch-clamp technique. SSCVRs displayed a characteristic N-like shape with a negative resistance region (NRR) in a voltage range of -45 to -35 mV. The majority of cells assayed revealed SSCVR patterns crossing the V-axis at three points (in mV): V1 = -55 to -45, V2 = -40 to -35, V3 = -30 to -10. SSCVRs of T-cells activated by phytohaemagglutinin (48-96 h) also displayed NRR, but crossed the V-axis at one point only (V1 = -55 to -60 mV). It implies the possibility of two stable levels of membrane potential (V1 and V3) for the resting T-cells, but only one (V1) for activated T-cells. These data thus account for the triggering property of T-cell membrane potential previously reported. The NRR can be explained on the basis of the Hodgkin-Huxley type n4j model of K+ channel kinetics. According to the model the possibility for a membrane to have one or two stable levels of membrane potential depends on the ratio of selective K+ conductance to non-selective leaky conductance (Gk/G(leak)). The steady-state level of K+ conductance in resting T-lymphocytes proved to be sensitive to Ca2+. Buffering Ca2+ ions from either external or internal solution resulted in an appreciable increase in K+ conductance. The possibility for membrane potential to have two stable levels of membrane potential in connection with the Ca2+ dependence of K+ conductance was supposed to be important for Ca(2+)-signalling during T-cell activation.

Calcium↗
PubMed1997

Carbachol induces oscillations in membrane potential and intracellular calcium in a colonic tumor cell line, HT-29.

The patch-clamp technique was used to study the effects of carbachol (CCh) on HT-29 cells. During CCh exposure, the cells (n = 23) depolarized close to the equilibrium potential for Cl- (E(Cl-); -48 mV) and the membrane potential then started to oscillate (16/23 cells). In voltage-clamp experiments, similar oscillations in whole cell currents could be demonstrated. The whole cell conductance increased from 225 +/- 25 pS in control solution to 6,728 +/- 1,165 pS (means +/- SE, n = 17). In substitution experiments (22 mM Cl- in bath solution, E(Cl-) = 0 mV), the reversal potential changed from -41.6 +/- 2.2 mV (means +/- SE, n = 9) to -3.2 +/- 2.0 mV (means +/- SE, n = 7). When the cells were loaded with the calcium-sensitive fluorescent dye, fluo 3, and simultaneously patch clamped, CCh caused a synchronous oscillating pattern of fluorescence and membrane potential. In cell-attached patches, the CCh-activated currents reversed at a relative membrane potential of 1.9 +/- 3.7 mV (means +/- SE, n = 11) with control solution in the pipette and at 46.2 +/- 5.3 mV (means +/- SE, n = 10) with a 15 mM Cl- solution in the pipette. High K+ (144 mM) did not change the reversal potential significantly (P < or = 0.05, n = 8). In inside-out patches, calcium-dependent Cl- channels could be demonstrated with a conductance of 19 pS (n = 7). It is concluded that CCh causes oscillations in membrane potential that involve calcium-dependent Cl- channels and a K+ permeability.

Calcium↗
PubMed1985

Transient and sustained effects of hormones and calcium on membrane potential in a bone cell clone.

Measurements were made of the electrophysiological and cAMP response to changes in extracellular [Ca2+] and to hormone application in a bone cell clone. Both transient and long-term electrophysiological responses were studied. An increase in extracellular [Ca2+] usually resulted in a transient hyperpolarization of about 60-sec duration. In addition, increases in extracellular [Ca2+] from 0.9 to 1.8 mM and from 1.8 to 3.6 mM resulted in long-term hyperpolarization and increased potential fluctuations. Increasing bathing [Ca2+] until the membrane potential reached the K+ equilibrium level resulted in a significant decrease in fluctuations. Addition to the bathing medium of quinine, a putative blocker of the Ca2+-dependent K+ channel, resulted in long-term depolarization of the mean membrane potential, and a long-term decrease in potential fluctuations. Addition of Mg2+, a mild antagonist of Ca2+ entry into the cell, produced transient depolarization and reduction of potential fluctuations. These effects suggest that the potential fluctuations reflect cytoplasmic [Ca2+] fluctuations via Ca2+-dependent K+ membrane channels. Under an extracellular [Ca2+] of 1.8 mM, the application of prostaglandin E2 (PGE2), isoproterenol, and parathyroid hormone produced no significant effect on mean membrane potential or on the sustained potential fluctuations, but PGE2 did significantly raise intracellular cAMP. Under an increased bathing [Ca2+], significant changes in mean potential and fluctuations did occur in response to PGE2, but not in response to the other hormones, while the PGE2 effect on cAMP was not greatly changed. Hyperpolarizing transients of about 30-sec duration occurred in response to all of the hormones, particularly at an extracellular [Ca2+] of 3.6 mM. Thus, there are both transient and long-term electrophysiological responses to hormone application, with only the long-term response correlated with the production of cAMP. These electrophysiological responses may represent separate transient and long-term calcium transport responses to hormone application.

Animals↗
PubMed1986

Effect of extracellular potassium on amino acid transport and membrane potential in fetal human fibroblasts.

The distribution ratio of the lipophilic cation tetraphenylphosphonium (TPP+) has been used to estimate the electrical potential difference across the plasma membrane in cultured human fibroblasts. These cells exhibit a membrane potential markedly influenced by the diffusion potential of K+. High extracellular potassium concentrations depolarize human fibroblasts and depress the activity of transport systems A, ASC (both serving for zwitterionic amino acids), X-AG (for anionic amino acids), and y+ (for cationic amino acids). High doses (100 microM) of the K+-ionophore valinomycin hyperpolarize the cells. This condition enhances the activity of systems A, ASC and y+. Transport systems L (for neutral amino acids) and x-C (for anionic amino acids) are insensitive to changes in extracellular K+ or to valinomycin. System X-AG is inhibited by the addition of 100 microM valinomycin, but the effect of the ionophore appears to be potential-independent. These results indicate that: (a) the activity of systems L and x-C is potential-independent and (b) the activity of systems A, ASC, X-AG and y+ is sensitive to alterations of external [K+] associated to changes in membrane potential.

Amino Acids↗