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At least 865 records · Page 48Linked to original sources
PubMed1998

Capillaries demonstrate changes in membrane potential in response to pharmacological stimuli.

It has been proposed that capillaries can detect changes in tissue metabolites and generate signals that are communicated upstream to resistance vessels. The mechanism for this communication may involve changes in capillary endothelial cell membrane potentials which are then conducted to upstream arterioles. We have tested the capacity of capillary endothelial cells in vivo to respond to pharmacological stimuli. In a hamster cheek pouch preparation, capillary endothelial cells were labeled with the voltage-sensitive dye di-8-ANEPPS. Fluorescence from capillary segments (75-150 microns long) was excited at 475 nm and recorded at 560 and 620 nm with a dual-wavelength photomultiplier system. KCl was applied using pressure injection, and acetylcholine (ACh) and phenylephrine (PE) were applied iontophoretically to these capillaries. Changes in the ratio of the fluorescence emission at two emission wavelengths were used to estimate changes in the capillary endothelial membrane potential. Application of KCl resulted in depolarization, whereas application of the vehicle did not. Application of ACh and PE resulted in hyperpolarization and depolarization, respectively. The capillary responses could be blocked by including a receptor antagonist (atropine or prazosin, respectively) in the superfusate. We conclude that the capillary membrane potential is capable of responding to pharmacological stimuli. We hypothesize that capillaries can respond to changes in the milieu of surrounding tissue via changes in endothelial membrane potential.

Acetylcholine↗
PubMed1984

Colicin V-treated Escherichia coli does not generate membrane potential.

Colicin V-treated Escherichia coli was inhibited in its capacity to carry out active transport of proline and was unable to generate a membrane potential. Colicin V also prevented membrane potential formation by isolated cytoplasmic membrane vesicles. We conclude that a primary effect of this colicin involves the cytoplasmic membrane as a target.

Biological Transport, Active↗
PubMed1994

Membrane potential changes of skeletomotor neurons in response to random stretches of the triceps surae muscles in decerebrate cats.

The properties of membrane potential changes of skeletomotor neurons (S, FR, and FF) innervating triceps surae muscles during pseudorandom stretching of these muscles were studied in decerebrate cats. Peak amplitudes of pseudorandom muscle stretches ranged from 119 microns to 4.15 mm peak-to-peak. Sequences of ten identical stretching periods were applied for averaging. Shapes of membrane potential changes and probability density distribution of amplitudes of the input and output signals and power spectra suggest that the skeleto-motor neuron membrane has nonlinear properties. First- and second-order Wiener kernels were determined by applying the cross-correlation (Lee-Schetzen) method. The results suggest that the transfer function between muscle stretches and subthreshold membrane potentials is a Wiener-type cascade. This cascade is consistent with a linear, second-order, underdamped transfer function followed by a simple quadratic nonlinearity [linear (L) system followed by nonlinear (N) system, or LN cascade]. Including the nonlinear component calculated from the second-order Wiener kernel improved the model significantly over its linear counterpart, especially in S-type motoneurons. Qualitatively similar results were obtained with all types of motoneurons studied.

Animals↗
PubMed1993

A reevaluation of the critical membrane potential of the effective refractory period in guinea pig ventricular fibres.

The traditional critical membrane potential (CMP), -55(-)-60 mV, which corresponds to effective refractory period (ERP), was anew investigated in guinea pig ventricular muscle fibres. The electrical and contractile responses to the stimulus during repolarization of action potential (AP), particularly from +10 to -60 mV, were observed. One third of 35 tested cells displayed testing action potential (TAP) and local response at > or = -54 mV when they were stimulated by testing pulses in 37 degrees C normal Tyrode's solution. Potential level of TAP which occurred earliest was at -30 mV and that of local response which appeared earliest was at 0 mV during repolarization among 95 systematic tests. Most of the TAPs belonged to the slow response potential type. The ratio of TAP evoked at > or = -54 mV initial membrane potential (IMP) was as high as 86% when the experiment was carried out in 37 degrees C 1.5 mmol KC1/L Tyrode's solution. In view of distribution of IMPs of TAPs, the CMP of ERP in guinea pig ventricular muscle fibres was more positive than traditional CMP measured by Hoffman et al. in dog, sheep Purkinje fibres and had a quite changeable range. The CMP of every cell in ventricular muscle was not all the same, and their CMPs approximated to normal distribution. There was no sharp line separating ERP from relative refractory period in myocardium. Higher temperature and low [K]0 were the important factors elevating CMP of ERP.

Action Potentials↗
PubMed1981

The effects of rubidium ions and membrane potentials on the intracellular sodium activity of sheep Purkinje fibres.

1. Intracellular Na activity, aiNa, was measured in voltage-clamped sheep cardiac Purkinke fibres. 2. Increasing [Rb]0 from 0 to 4 mM in K-free solutions (at a fixed membrane potential) decreased aiNa. Further increases of [Rb]0 (up to 20 mM) had little or no effect. 3. Following exposure to Rb-free, K-free solution, the addition of a test concentration of Rb produced an exponential decrease of aiNa. The rate constant of decay of aiNa increased with increasing [Rb]0 over the measured range (0-20 mM). 4. The accompanying electrogenic Na pump current transient decayed with the same rate constant as aiNa over the range of [Rb]0 examined. During this decay the electrogenic Na pump current was a linear function of aiNa. Increasing [Rb]0 increased the steepness of the dependence of the electrogenic current on aiNa. 5. A constant fraction of the net Na efflux was electrogenic. This fraction was not affected by varying [Rb]0 over the range 0-20 mM. 6. Using a simple model, it is shown that the dependence of steady-state aiNa on [Rb]0 is half-saturated by less than 1 mM-[Rb]0. The rate constant of decay of aiNa and the slope of the relationship between electrogenic Na pump current and aiNa are, however, better fitted with a lower affinity for Rb (K0.5 = 4 mM-[Rb]0). 7. Depolarizing the membrane potential with the voltage clamp decreased aiNa; hyperpolarization increased it. These effects persisted in the presence of 10(-5) M-strophanthidin. An effect of membrane potential on the net passive Na influx can account for the observations. 8. The effects of membrane potential on the net passive Na influx were examined by measuring the maximum rate of rise of aiNa at different holding potentials after inhibiting the Na-K pump in a K-free, Rb-free solution. Depolarization decreased the Na influx. 9. Using the constant field equation, the net passive Na influx was used to estimate the apparent Na permeability coefficient, PNa. This was between 0.8 x 10(-8) and 1.5 x 10(-8) cm sec-1.

Animals↗
PubMed2002

Intracellular distribution of the fluorescent dye nonyl acridine orange responds to the mitochondrial membrane potential: implications for assays of cardiolipin and mitochondrial mass.

Cardiolipin, a polyunsaturated acidic phospholipid, is found exclusively in bacterial and mitochondrial membranes where it is intimately associated with the enzyme complexes of the respiratory chain. Cardiolipin structure and concentration are central to the function of these enzyme complexes and damage to the phospholipid may have consequences for mitochondrial function. The fluorescent dye, 10 nonyl acridine orange (NAO), has been shown to bind cardiolipin in vitro and is frequently used as a stain in living cells to assay cardiolipin content. Additionally, NAO staining has been used to measure the mitochondrial content of cells as dye binding to mitochondria is reportedly independent of the membrane potential. We used confocal microscopy to examine the properties of NAO in cortical astrocytes, neonatal cardiomyocytes and in isolated brain mitochondria. We show that NAO, a lipophilic cation, stained mitochondria selectively. However, the accumulation of the dye was clearly dependent upon the mitochondrial membrane potential and depolarisation of mitochondria induced a redistribution of dye. Moreover, depolarisation of mitochondria prior to NAO staining also resulted in a reduced NAO signal. These observations demonstrate that loading and retention of NAO is dependant upon membrane potential, and that the dye cannot be used as an assay of either cardiolipin or mitochondrial mass in living cells.

Acridine Orange↗
PubMed1991

Intrinsic membrane potential oscillations in hippocampal neurons in vitro.

Membrane potential oscillations (MPOs) of 2-10 Hz and up to 6 mV were found in almost all stable hippocampal CA1 and CA3 neurons in the in vitro slice preparation. MPOs were prominent for pyramidal cells but less pronounced in putative interneurons. MPOs were activated at threshold depolarizations that evoked a spike and the frequency of the MPOs increased with the level of depolarization. MPOs were distinct from and seemed to regulate spiking, with a spike often riding near the top of a depolarizing MPO wave. Analysis of the periodicity of the oscillations indicate that the period of MPOs did not depend on the afterhyperpolarization (AHP) following a single spike. MPOs persisted in low (0-0.1 mM) Ca2+ medium, with or without Cd2+ (0.2 mM), when synaptic transmission was blocked. Choline-substituted low-Na+ (0-26 mM) medium, 3 microM tetrodotoxin (TTX) or intracellular injection of QX-314 reduced or abolished the fast Na(+)-spike and reduced inward anomalous rectification. About 40% of CA1 neurons had no MPOs after Na+ currents were blocked, suggesting that these MPOs were Na(+)-dependent. In about 60% of the cells, a large depolarization activated Ca(2+)-dependent MPOs and slow spikes. MPOs were not critically affected by extracellular Ba2+ or Cs2+, or by 0.2 mM 4-aminopyridine, with or without 2 mM tetraethylammonium (TEA). However, in 5-10 mM TEA medium, MPOs were mostly replaced by 0.2-3 Hz spontaneous bursts of wide-duration spikes followed by large AHPs. Low Ca2+, Cd2+ medium greatly reduced the spike width but not the spike-bursts. In conclusion, each cycle of an MPO in normal medium probably consists of a depolarization phase mediated by Na+ currents, possibly mixed with Ca2+ currents activated at a higher depolarization. The repolarization/hyperpolarization phase may be mediated by Na+/Ca2+ current inactivation and partly by TEA-sensitive, possibly the delayed rectifier, K+ currents. The presence of prominent intrinsic, low-threshold MPOs in all hippocampal pyramidal neurons suggests that MPOs may play an important role in information processing in the hippocampus.

2-Amino-5-phosphonovalerate↗
PubMed1985

Dependence of cytoplasmic calcium transients on the membrane potential in isolated nerve endings of the guinea pig.

The relation of changes in internal, free Ca2+, measured with arsenazo III, to the membrane potential, measured with the cyanine dye di-S-C2(5) or 86Rb+ distribution ratio, was studied in isolated guinea pig cortical nerve endings. Depolarization of the plasma membrane with veratridine or gramicidin as well as addition of ionophore A23187 led to an increase in cytosolic Ca2+. Only the response to veratridine was inhibited by tetrodotoxin. The dependence of the depolarization-induced increase in intraterminal, free Ca2+ on the membrane potential between about -50 to 0 mV was sigmoidal. A maximal increase in cytosolic Ca2+ was reached when the membrane potential was depolarized from the resting level, about -64 mV, to about -40 mV. These results show that in isolated nerve endings the activation of voltage-sensitive Ca2+ channels concomitantly leads to an increase in cytosolic, free Ca2+. Comparison of the results of the present study with the previous electrophysiological observations indicate that Ca2+ channels in synaptosomes, presynaptic nerve terminals of the squid giant synapse and cardiac cells have essentially similar voltage dependency.

Animals↗
PubMed1975

[The protective effect of serotonin against the depolarizing influence of aminazine on the membrane potentials of mouse embryos, in vitro, at the 2-blastomere stage].

The action of chlorpromazine, serotonin and prostaglandin F2-alpha on the cellular membrane potential of 2-cell mouse embryos, as well as a protective effect of serotonin and prostaglandin F2-alpha against the inhibition of the membrane potential by chlorpromazine were studied. Chlorporomazine (1.10-5 g/ml) proved to induce a strong decrease of the membrane potential, but serotonin, prostaglandin F2-alpha were ineffective. Serotonin (1.10-4 g/ml) prevented the action of chlorpormazine (2.10-6 g/ml), whereas prostaglandin F2-alpha (4-8.10-6 g/ml) was ineffective in this respect.

Animals↗
PubMed2004

Effect of fatty acids on the membrane potential of an alkaliphilic bacillus.

Effect of various fatty acids on the membrane potential of an alkaliphilic Bacillus, YN-2000, was examined. Addition of unsaturated fatty acids such as palmitoleic acid, oleic acid, linoleic acid, and linolenic acid at 30 microM caused the instantaneous depolarization of the membrane potential of the bacterium, which appears to result in the drastic decrease of viability. On the other hand, no depolarization was detected by the addition of saturated acids such as palmitic acid, stearic acid, and 12-hydroxystearic acid even at 1 mM.

Bacillus↗
PubMed1983

The relationship between extramitochondrial Ca2+ concentration, respiratory rate, and membrane potential in mitochondria from brown adipose tissue of the rat.

The ability of isolated mitochondria from rat brown-adipose tissue to regulate extramitochondrial Ca2+ (measured by arsenazo) was studied in relation to their ability to produce heat (measured polarographically). The energetic state of the mitochondria was expressed as a membrane potential, delta psi (estimated with safranine), and was varied semi-physiologically by the use of different GDP concentrations. In these mitochondria GDP binds to the 32-kDa polypeptide, thermogenin, which regulates coupling. Ca2+ uptake (at 5 microM extramitochondrial Ca2+) was maximal at delta psi greater than 150 mV. Basal Ca2+ release increased from 1 to 2 nmol x min-1 x mg-1 below 150 mV. Na+ -stimulated rate of Ca2+ release was stable within the investigated delta psi span (100-160 mV). Initial Ca2+ levels were maintained below 0.2 microM for 100 mV less than delta psi less than 160 mV. Ca2+ levels maintained after Ca2+ challenge (20 nmol Ca2+ x mg-1) were below 0.4 microM for delta psi greater than 135 mM. Respiration was unstimulated for delta psi greater than 150 mV and was maximal at delta psi less than or equal to 135 mV. In the presence of well-oxidised substrates, the respiration at maximally activated thermogenin was markedly below fully uncoupled respiration and was probably limited by thermogenin activity--i.e. by a limited H+ reentry (OH- exit) and therefore by a membrane potential maintained at about 135 mV. It is concluded that at membrane potentials of 135 mV and above the mitochondria exhibit full Ca2+ control and are able to regulate thermogenic output up to maximum without interfering with this Ca2+ control. Membrane potential probably does not decrease below 135 mV in vivo. Therefore, Ca2+ homeostasis and thermogenesis are non-interfering and can be hormonally independently regulated, e.g. by alpha-adrenergic and beta-adrenergic stimuli, respectively.

Adipose Tissue, Brown↗
PubMed1980

Effect of Salinity upon Cell Membrane Potential in the Marine Halophyte, Salicornia bigelovii Torr.

The electrophysiology of root cells of the marine halophyte, Salicornia bigelovii Torr., has been investigated. Cellular concentrations of K(+), Cl(-), and Na(+) and resulting cell membrane potentials were determined as functions of time and exposure to dilutions of artificial seawater. Treatment of these data by the Nernst criterion suggests that Cl(-) is actively transported into these root cells, but that active transport need not be invoked to explain the accumulation of Na(+) at all salinities investigated nor for K(+) at moderate to high salinities. In low environmental salinity, the cell electropotential of Salicornia root cells was found to respond to inhibitors in a fashion similar to that observed in glycophytes; in high environmental salinity, root cell membrane potential appears to be insensitive to bathing salinity and m-chlorocarbonylcyanide phenylhydrazone induces membrane hyperpolarization, in contrast to the response of glycophytes to such treatments. The fact that measured membrane potentials exceed diffusion potentials for Na(+), K(+), and Cl(-) and the observation of a rapid depolarization by CO in the dark suggests an electrogenic component in Salicornia root cell membrane potentials.

Journal Article↗
PubMed1994

Isolation and characterization of membrane potential changes associated with release of calcium from intracellular stores in rat thymic lymphocytes.

Membrane potential changes accompanying Ca2+ influx stimulated by release of Ca2+ from intracellular stores (store-regulated Ca2+ uptake) were monitored in BAPTA-loaded rat thymic lymphocytes using the fluorescent indicator bis(1,3-diethylthiobarbituric acid)trimethine oxonol. Depletion of [Ca2+]i stores by the application of thapsigargin, ionomycin or cyclopiazonic acid induced a depolarization which was (i) dependent upon BAPTA-loading, (ii) dependent upon extracellular Ca2+, (iii) independent of extracellular Na+ and (iv) abolished by 5 mM extracellular Ni2+. This depolarization was followed by a charybdotoxin-sensitive repolarization and subsequent hyperpolarization to values approximating the K+ equilibrium potential, consistent with secondary activation of a K+ conductance. These membrane potential changes temporally correlated with Ca2+ influx from the extracellular medium as measured fluorimetrically with indo-1. The divalent cation permeability sequence was investigated by monitoring the magnitude of the depolarization observed following the addition of 4 mM Ca2+, Mn2+, Ba2+ or Sr2+ to cells pretreated with doses of thapsigargin or ionomycin known to activate the store-regulated calcium uptake pathway. On the basis of these experiments, we conclude that the store-regulated Ca2+ uptake pathway has the following permeability sequence: Ca2+ > Mn2+ >> Ba2+, Sr2+ with Mn2+ displaying significant permeability relative to Ca2+. This pathway is distinguishable from other divalent cation uptake pathways reported in other cells types on the basis of its activation by thapsigargin and its high Mn2+ permeability.

Animals↗
PubMed1996

Changes in membrane potential of target cells promotes cytotoxic activity of effector T lymphocytes.

The effector function of CD8+ lymphocytes depends on recognition by the TcR-CD3 complex of an oligopeptide presented by an MHC class I molecule on target cells. Recently it has been shown that MHC class I molecules change their conformation upon depolarization of human B lymphoblastoid JY cells. We studied here the effects of changes in membrane potential of target cells on the function of cytotoxic T lymphocytes (CTL). Selective alterations of plasma membrane potential of JY target cells were achieved by treatments with specific ionophore molecules as well as with Na(+)-K(+)-ATPase inhibitor, while the cytotoxic lymphocytes were not influenced. The plasma membrane was depolarized by gramicidin D and ouabain, while hyperpolarization was induced by valinomycin treatment. Alterations of the resting membrane potential of target cells in both direction resulted in an enhanced cytotoxic activity. The observed changes in cytolytic activities of cytotoxic T effectors may have a more general biological significance, namely apoptotic cells become depolarized after a given time, moreover neoplastic and virus infected cells also frequently show decreased membrane potential. A more efficient recognition of these cells by CTL is supposed to enhance the efficiency of their elimination, as well.

Cytotoxicity, Immunologic↗
PubMed1995

Correlation between membrane potential changes and proliferation of murine peritoneal lymphocytes stimulated by Nocardia water soluble mitogen.

A comparative study of Nocardia water soluble mitogen (NWSM) action on membrane potential and proliferation rate of murine peritoneal lymphocytes was performed at various incubation times. The membrane surface charge was evaluated by laser doppler velocimetry (LDV) through the measurement of the cell electrophoretic mobility at different pH values (from pH 5 to 9). We demonstrated that NWSM treatment decreases the lymphocyte membrane potential. This variation reached a maximal level after 24 hrs. at pH 7 and remained unchanged during the 72 hrs. observation. A significant stimulation of lymphocyte proliferation was noted after a 24 hrs. incubation. However, the highest rate of [3H]-thymidine incorporation was observed at 48 hrs. with a subsequent decrease at 72 hrs. On the basis of these data, it is suggested, that membrane potential changes may represent an early important step in the mechanism of lymphocyte activation by NWSM, as it has been shown for some mitogenic compounds.

Animals↗
PubMed2005

The effect of membrane potential on the development of chemical osmotic pressure in compacted clay.

When clay soils are subjected to salt concentration gradients, various interrelated processes come into play. It is known that chemical osmosis induces a water flow and that a membrane potential difference develops that counteracts diffusive flow of solutes and osmotic flow of water. In this paper, we present the results of experiments on the influence of membrane potential on chemical osmotic flow and diffusion of solutes and we show how we are able to derive the membrane potential value from theory. Moreover, the simultaneous development of water pressure, salt concentration and membrane potential difference are simulated using a model for combined chemico-electroosmosis in clays. A new method for short-circuiting the clay sample is employed to assess the influence of electrical effects on flow of water and transport of solutes.

Journal Article↗
PubMed1992

Effect of nitric oxide on membrane potential and contraction of rat aorta.

Influence of nitric oxide (NO) on the membrane potential of rat aorta was assessed by blocking endothelial NO synthase with N omega-nitro-L-arginine (NOArg). Membrane potential was measured by two different methods: intracellular microelectrodes and [3H]tetraphenylphosphonium bromide ([3H]TPP+) uptake. Blocking of NO synthesis with NOArg (10(-4) M) depolarized the membrane by 4-6 mV. The NOArg-induced depolarization was suppressed by the NO donor SIN-1 (10(-5) M). Incubation with NOArg (10(-4) M) decreased the basal level of cGMP, and increased the basal 45Ca2+ influx as well as the sensitivity of contractile response to KCl. Results indicate that NO released by endothelial cells permanently hyperpolarizes the membrane of rat aorta smooth muscle cells and thereby may control the opening of voltage-dependent Ca2+ channels.

Amino Acid Oxidoreductases↗