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PubMedDate not supplied

[The role of ATP and membrane potential in the penetration of phage T17 DNA into the cell during infection].

The role of ATP and membrane potential in phage T7 DNA injection into E. coli during infection has been studied. Entrance of phage T7 genes of class II and III was shown to be prevented by arsenate, indicating the requirement for phosphorylated macroergs in the phage DNA injection. The injection process was also inhibited by exposition of the cells to the uncoupler of oxidative phosphorylation. Dependence of the injection efficiency on the membrane-potential value has been shown to be sigmoidal, which suggests a regulatory role of the membrane potential in phage T7 DNA injection from the virion into the host cell.

Adenosine Triphosphate↗
PubMed1992

Voltage-sensitive dyes: measurement of membrane potentials induced by DC and AC electric fields.

Dye indicators of membrane potential have been available for the past 15 years and have been employed in numerous studies of cell physiology. Since the cell membrane is a likely primary site for the cascade of events resulting in a biological response to electromagnetic fields, methodologies for monitoring the membrane voltage will be critical. This laboratory has developed a series of dyes by using theoretical molecular orbital calculations to predict electrochromic structures. The spectra of electrochromic dyes are altered via a direct coupling of the molecular electronic states with an electric field. This mechanism has the advantage of providing both high temporal and high spatial resolution because the effect is instantaneous and is localized to the level of individual indicator molecules. It therefore can have significant advantages over traditional microelectrode techniques because fast changes in potential can be monitored simultaneously over many different regions of a biological preparation. We have used these dyes to monitor membrane potentials induced by both DC and AC electric fields. In a series of studies with a model membrane system, a spherical lipid bilayer, we showed that the potential develops on the membrane in good agreement with a time-dependent solution to Laplace's equation. Cell membranes can also be stained with voltage sensitive dyes. In experiments with dc fields, we are able to map the variation of the induced membrane potential along the surface of the cell by employing digital video fluorescence microscopy. We can also use the fluorescence microscope to detect membrane potential induced by ac fields by using a phase-sensitive detection scheme to extract the corresponding change in the light intensity from the fluorescent indicator. The technology can be extended to more complex biological preparations and can be used in conjunction with other optical techniques such as those which monitor intracellular ion concentrations. It may, therefore, prove highly valuable for the elucidation of biological responses to electromagnetic fields.

Animals↗
PubMed1988

Sustained excitatory synaptic input to motor cortex neurons in awake animals revealed by intracellular recording of membrane potentials.

1. Most of the intracellular electrophysiological data on cortical neurons has been obtained in anesthetized or reduced preparations, and differs from observations in awake, intact animals. To determine whether these differences are due to experimental techniques or physiological factors, we recorded membrane potentials intracellularly from motor cortex neurons in chronically prepared cats and monkeys under Nembutal-anesthetized, Halothane-anesthetized, and unanesthetized conditions, or during transitions between anesthetized and awake conditions. 2. Resting membrane potentials were found to depend on the anesthetic state of the animal. Membrane potentials of neurons recorded in awake animals were more depolarized than those recorded in the anesthetized state. In the awake state membrane potentials were all less than -65 mV. 3. The input resistance of neurons recorded in awake animals were significantly smaller than those measured in the anesthetized state. Action potentials recorded in awake animals typically showed an undershoot (i.e. negative values at peak), implying that voltage-dependent conductances may be altered. Undershoot of the action potential was more prominent in pyramidal tract neurons (PTNs) than non-PTNs. 4. These data suggested that in awake animals motor cortex neurons, especially PTNs, receive sustained excitatory synaptic input or neuro-modulatory activities.

Action Potentials↗
PubMed1993

Membrane potential regulates Ca2+ uptake and inositol phosphate generation in rat sublingual mucous acini.

In salivary acinar cells, muscarinic-induced fluid secretion is associated with a 1,4,5-IP3 induced increase in the cytosolic free Ca2+ concentration ([Ca2+]i), which in turn activates Ca(2+)-dependent K+ and Cl- channels that modulate the membrane potential. In the present study the influence of the membrane potential on [Ca2+]i and inositol phosphates was monitored in rat sublingual mucous acini. Depolarization induced by switching from 5.8 mM extracellular K+ ([K+]e) to 116 mM [K+]e resulted in a transient increase in the [Ca2+]i measured using the Ca2+ sensitive fluorescent indicator Fura-2. This initial rapid (t1/2 approximately 5 s) increase (approximately 3-fold) in [Ca2+]i was dependent on extracellular Ca2+, insensitive to nifedipine, and followed by establishment of a 'new' resting [Ca2+]i, approximately 35% higher than the level in physiological [K+]e. Depolarization also induced a significant rise in the resting cellular inositol trisphosphate (IP3) and inositol tetrakisphosphate (IP4) contents, but not 1,4,5-IP3 content. Stimulation with 10 microM carbachol (CCh, a muscarinic agonist) produced a biphasic increase in [Ca2+]i, the initial transient phase due to mobilization of Ca2+ from an intracellular pool, and a sustained phase mediated by an influx of Ca2+. Membrane depolarization had no effect on the initial phase, while, the sustained increase in [Ca2+]i was eliminated. The CCh-enhanced quench of the Fura-2 signal by Mn2+ (an index for divalent cation entry) was reversibly inhibited by depolarization. The enhanced Mn2+ uptake induced by inhibiting microsomal Ca(2+)-ATPase with thapsigargin was similarly inhibited by membrane depolarization, consistent with the effect of depolarization primarily acting on the Ca2+ entry pathway and not on receptor coupling. Depolarization did not alter the initial CCh-induced increases in IP3, IP4 or 1,4,5-IP3 content, or the sustained increase in 1,4,5-IP3, whereas, depolarization significantly blunted (> 70%) the sustained, CCh-induced generation of IP3 and IP4. The membrane potential, therefore, appears to modulate Ca2+ activated fluid secretion by controlling the driving force for Ca2+ entry via a depletion-activated Ca2+ entry pathway. Inositol phosphate metabolism is also influenced by the membrane potential, but this effect apparently plays a minor role in regulating [Ca2+]i since 1,4,5-IP3 levels were unchanged by depolarization.

Animals↗
PubMed1983

Role of pH gradient and membrane potential in dipeptide transport in intestinal and renal brush-border membrane vesicles from the rabbit. Studies with L-carnosine and glycyl-L-proline.

We examined the role of pH gradient and membrane potential in dipeptide transport in purified intestinal and renal brush-border membrane vesicles which were predominantly oriented right-side out. With an intravesicular pH of 7.5, changes in extravesicular pH significantly affected the transport of glycyl-L-proline and L-carnosine, and optimal dipeptide transport occurred at an extravesicular pH of 5.5-6.0 in both intestine and kidney. When the extravesicular pH was 5.5, glycyl-L-proline transport was accelerated 2-fold by the presence of an inward proton gradient. A valinomycin-induced K+ diffusion potential (interior-negative) stimulated glycyl-L-proline transport, and the stimulation was observed in the presence and absence of Na+. A carbonyl cyanide p-trifluoromethoxyphenylhydrazone-induced H+ diffusion potential (interior-positive) reduced dipeptide transport. It is suggested that glycyl-L-proline and proton(s) are cotransported in intestinal and renal brush-border membrane vesicles, and that the process results in a net transfer of positive charge.

Animals↗
PubMed1987

Oxygen radicals alter the cell membrane potential in a renal cell line (LLC-PK1) with differentiated characteristics of proximal tubular cells.

We employed a carbocyanine dye (1,1',3,3,3',3'-hexamethylindocarbocyanine iodide) to measure the plasma membrane potential of LLC-PK1 renal epithelial cells exposed to either xanthine oxidase-generated oxygen radicals or to hydrogen peroxide. Measurements were performed using a fluorescent-activated cell sorter to record fluorescence on a cell by cell basis. Initial exposure of cells to low concentrations of either H2O2 or xanthine oxidase resulted in a transient increase in membrane potential relative to control cells (P less than 0.001), followed by an exponential decline in potential (P less than 0.001). The addition of extracellular catalase diminished the H2O2-related decline in potential, consistent with a role for hydrogen peroxide in producing this effect. Pretreatment of cells with inhibitors of intracellular catalase and superoxide dismutase prior to exposure to xanthine oxidase caused an even larger decline in potential (P less than 0.001). Cells could be partially protected from the radical-mediated loss of potential by incubating them in a hypertonic (400 mosmolal) environment during radical exposure. Similarly, the loss of membrane potential was increased after incubation of cells in a hypotonic (200 mosmolal) environment during radical exposure. These observations are consistent with a reduction in membrane potential effected by exposure to oxygen radicals (including superoxide anion and hydrogen peroxide). This reduction may be prevented, in part, by radical scavenging enzymes and by reducing the degree of cellular swelling in response to oxygen radical exposure.

Carbocyanines↗
PubMed1986

Amplitude reduction of motor unit twitches during repetitive activation is accompanied by relative increase of hyperpolarizing membrane potential trajectories in homonymous alpha-motoneurons.

In anaesthetized cats, medial gastrocnemius motor units (MUs) were electrically stimulated via their ventral-root axons with independent random patterns. Isometric muscle tension and homonymous alpha-motoneuron (MN) membrane-potential fluctuations in response to these stimuli were recorded simultaneously, usually for periods of about 2 min. The tension and membrane potential were averaged with respect to a stimulus train over two disjoint time intervals, one stretching 20-40 s at record beginning, and the other a similar duration at the end of recording. Whereas average MU twitch amplitudes usually decreased between these periods, average membrane potential trajectories did not do so, such that, when normalized to the change in twitch amplitude, the membrane potential trajectories usually increased in size. This suggests that the decline in the mechanical effect of MU activation was accompanied by an increase in the gain of the afferent pathway to homonymous MNs, which was confirmed by gain computations in the frequency domain. This compensation could be a mechanism to maintain the high quality of information about MU contractions transmitted to MNs in the course of MU fatigue.

Animals↗
PubMed1994

Membrane potential oscillations underlying firing patterns in neocortical neurons.

Membrane potential oscillations were studied in slices of rat somatosensory cortex maintained in vitro, using intracellular recordings from cells in layers 2/3 and 5. The cells were classified according to their firing patterns during long (0.8-1 s) depolarizing current steps. Subthreshold voltage oscillations were revealed by depolarizing the membrane to voltages around threshold for action potentials; however, these were obvious mainly in cells showing marked spike adaptation. When neurons of all firing patterns were stimulated to fire at 40-60 Hz for tens of seconds, spikes abruptly indicated. Hyperpolarizing the cells by 5-10 mV precipitated pronounced oscillations in 24 out of 35 cells. These oscillations existed in a narrow voltage range, and their frequency varied between 7 and 40 Hz, in a voltage-dependent manner. Spiking frequency was faster than the oscillation frequency for the same membrane potential in a given cell. The Na+ channel blocker tetrodotoxin abolished both the spikes and the oscillations, and blockade of K+ channels by tetraethylammonium converted the oscillations into prolonged and irregular plateaus. Blocking Ca2+ conductance with Co2+ reduced the oscillations amplitude and frequency in two out of three cells. The oscillations that followed spike inactivation varied in amplitude, frequency and persistence among different cells. Layer 5 nonadapting cells possessed the most periodic oscillations, as judged by autocorrelation analysis. Oscillations were also most persistent in this group, maintaining a stable steady-state. In other cell types, the oscillations were less regular and decayed with time. There was no difference among cell groups in the maximal peak to peak amplitude of the oscillations, or their frequency range. It is suggested that the oscillations are generated by ionic conductances that operate within the voltage range just above and below spike threshold, and thus can shape the cells' firing pattern. The prominence of the oscillations in a specific subset of layer 5 cells may indicate the mechanism that underlies the rhythmic firing pattern of those cells.

Animals↗
PubMed1995

Simultaneous measurement of pH and membrane potential in rat dorsal vagal motoneurons during normoxia and hypoxia: a comparison in bicarbonate and HEPES buffers.

1. The effects of oxygenated and hypoxic bicarbonate/CO2, 10 and 25 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered artificial cerebrospinal fluid (ACSF) have been studied in a rat brain slice preparation. Double-barreled pH-selective microelectrodes were used to measure intracellular pH (pHi) and membrane potential in dorsal vagal motoneurons (DVMs) and to measure extracellular pH (pHe) in the dorsal vagal motonucleus. 2. In bicarbonate ACSF, pHi averaged 7.24 +/- 0.05 (mean +/- SE, n = 21) and ranged from 6.86 to 7.79 pH units. pHe averaged 7.13 +/- 0.08 (n = 10). 3. On changing from oxygenated bicarbonate ACSF to either 10 or 25 mM HEPES ACSF, pHi decreased by 0.13-0.15 units, and the membrane depolarized by 10-11 mV. pHe also decreased in 10 mM HEPES ACSF (pHe 6.89 +/- 0.02, n = 8) but not in 25 mM HEPES ACSF (pHe 7.15 +/- 0.06, n = 3). In most neurons changes in pHi preceded changes in membrane potential. 4. In bicarbonate ACSF and in 25 mM HEPES ACSF, there was a significant linear relationship between prehypoxic pHi and the direction and amplitude of the hypoxia-induced membrane potential change (either an hyperpolarization or a depolarization). 5. In 10 mM HEPES ACSF, hypoxia always induced a depolarization; there was no correlation between prehypoxic pHi and the membrane potential response. 6. In bicarbonate ACSF and in 10 and 25 mM HEPES ACSF, hypoxia resulted in intracellular and extracellular acidification. However, the extracellular acidification in hypoxic 10 mM HEPES buffer was most pronounced (pH 6.40 +/- 0.11, n = 8), reflecting a preexisting extracellular acidification in oxygenated 10 mM HEPES buffer. 7. Various hypotheses that could give rise to a relationship between changes in membrane potential and pH are discussed; arguments are presented in favor of the concept that modulation of ion channels by either pHi or pHe, or both, is responsible for the observed correlations.

Animals↗
PubMed1983

Studies on energy supply for genetic processes. Requirement for membrane potential in Escherichia coli infection by phage T4.

In this study the hypothesis considering the requirement for an electrochemical proton gradient in the injection of phage T4 DNA into Escherichia coli cell has been verified experimentally. The phage caused a reversible depolarization of cell membrane, while phage 'ghosts' induced an irreversible depolarization. The phage infection was strictly dependent on E. coli membrane potential value when phage/cell ratio was 5 and higher. When the ratio was close to 1, the decrease in the membrane potential up to -100 mV caused practically no effect on the phage infection. The infection inhibition was observed when the membrane potential was lowered below this 'threshold' value. On the other hand, the decrease in the membrane potential caused no effect on the phage infection under conditions promoting a concomitant increase in the value of the transmembranous pH gradient. The phage DNA transfer through the membrane of ATPase-deficient cells was reversibly inhibited by switching off the respiratory chain - the sole generator of a protonmotive force in these mutant cells. The membrane should be kept in the energized state during the phage DNA entrance into the cell. Adsorption of the phage on E. coli was followed by the reversible release of the respiratory control. Thus the results presented here indicate the requirement of the electrochemical proton gradient across the plasma membrane for injection of phage T4 DNA into E. coli. They support the concept postulating an expenditure of host cell metabolic energy for phage T4 DNA transfer through the membrane.

Biological Transport, Active↗
PubMed1998

ATP-inhibited K+ channels and membrane potential of identified leech neurons.

The effect of the ATP-inhibited K+ channel on the membrane potential of leech Retzius neurons was analyzed using electrolyte-filled single-barrelled microelectrodes. The membrane potential was independent of the external nutrient supply during a period of 11 h, probably because the internal energy reserves were sufficient. The K+ channel activator HOE 234 ((3S,4R)-3-hydroxy-2, 2-dimethyl-4-(2-oxo-1-pyrrolidinyl)-6-phenylsulfonylchromane hemihydrate, 500 microM) induced a membrane hyperpolarization. In the presence of HOE 234, action potentials occurred with a reduced after-hyperpolarization and were discharged in bursts, possibly because of an inhibition of Ca2+ channels. The blocker of ATP-inhibited K+ channels tolbutamide did not significantly alter the membrane potential. In the absence of tolbutamide, the metabolic inhibitors iodoacetate, azide and cyanide (10 mM) evoked membrane hyperpolarizations, but in the presence of 1 mM tolbutamide their hyperpolarizing actions were reduced or abolished while membrane depolarizations were intensified. We conclude that ATP-inhibited K+ channels in the soma membrane of leech Retzius neurons provide coupling of cellular metabolism to electrical activity and ionic fluxes.

ATP-Binding Cassette Transporters↗
PubMed1980

Cyanine dye measurement of a light-induced transient membrane potential associated with the metarhodopsin II intermediate in rod-outer-segment membranes.

The fluorescent dye 3,3'-dipropylthiodicarbocyanin iodide [diS-C3-(5)] is used as a probe of fast membrane potential variations in the study of rod-outer-segment membranes. The formation of metarhodopsin II is found to be associated with the generation of a transmembrane potential, which is dissipitated by ionic movements across the membrane; its risetime is very similar to that of the protonation of the protein, which is also associated with the formation of metarhodopsin II.

Animals↗
PubMed1992

Membrane-potential-dependent uptake of tryptamine by rat intestinal brush-border membrane vesicles.

The effect of membrane potential on the uptake of tryptamine, an organic cation, by rat intestinal brush-border membrane vesicles was studied. In the presence of an outwardly directed H(+)-gradient, the initial uptake of tryptamine was stimulated remarkably and the overshoot phenomenon was observed. In contrast, the uptake was depressed by an inwardly-directed H(+)-gradient. The effect of H(+)-gradient on the uptake of tryptamine was maintained in the presence of FCCP, whereas it vanished when voltage-clamped vesicles were used. Moreover, the uptake of tryptamine was linearly augmented with increase of the valinomycin-induced inside-negative K+ diffusion potential. These results suggest that tryptamine is taken up into intestinal brush-border membrane vesicles depends upon the ionic diffusion potential. The effect of several indole derivatives and amine compounds on the uptake of tryptamine was also examined. The uptake of tryptamine was inhibited by all amine compounds used, but anionic and zwitterionic compounds had no effect, suggesting that these amines interact on brush-border membrane and cause an inhibitory effect.

Amines↗
PubMed1984

Dissipation of membrane potential of Escherichia coli cells induced by macromolecular polylysine.

Macromolecular polylysine caused a rapid and drastic decrease in the membrane potential of Escherichia coli cells, monitored with the uptake of the lipophilic cation, tetraphenylphosphonium cation (TPP+). Respiration of cells was not affected to a significant extent by polylysine. Polylysine treatment induced the efflux of K+ from cells, suggesting that an increase in permeability of cytoplasmic membrane may be responsible for the decrease in the membrane potential. The action of polylysine is discussed in comparison with that of colicin E1 which is known to dissipate the membrane potential of E. coli cells.

Cell Membrane Permeability↗
PubMed1990

[Effect of the membrane potential on the Mg2+,ATP-dependent transport of Ca2+ across smooth muscle sarcolemma].

The effect of the membrane potential (K(+)-valinomycin system) on the Mg2+, ATP-dependent transport of Ca2+ in inside-out vesicles of myometrium sarcolemma has been studied. The membrane potential was identified by using a cyanine potential-sensitive probe, diS-C3-(5). In the presence of valinomycin (5.10(-8) M) the inside-out directed K+ gradient (delta psi = -86 mV, with a negative charge inside) stimulated the initial rate of the energy-dependent accumulation of Ca2+ transfer whereas the oppositely directed K+ gradient (delta psi = +72 mV, with a positive charge inside) had no effect on this process. The K+ gradient was formed by isotonic substitution of K+ in intra- or extravesicular space for choline +. At the same time, in the absence of K+ gradient the Mg2+, ATP-dependent accumulation of Ca2+ in membrane vesicles did not depend on the chemical nature of the cations (K+ or choline+) used for isotonicity. The decrease of delta psi from 0 to -86 mV affects the initial rate of Ca2+ accumulation but not the maximal content of the accumulated cation. Preliminary dissipation of the membrane potential (delta psi = -86 mV) in Mg2(+)-free isotonic (with respect of K+ and choline+) media containing ATP and Ca2+ resulted in the inhibition of Mg2+, ATP-dependent Ca2+ transport induced by subsequent addition of Mg2+. These results indicate that the negative (intravesicular) electrical potential activates the Ca-pump of smooth muscle sarcolemma. This activation is based on the increase in the turnover number of the Ca2+ transporting system but not on its affinity for the transfer substrate. The use of the absolute reaction rates theory made it possible to establish that the Ca-pump effectuates the transport of a single positive charge in inside-out vesicles of smooth muscle plasma membranes, i.e., the energy-dependent transport of Ca2+ occurs either as a symport (with an anion (Cl-) or an antiport with a monovalent cation (K+) or a proton. It is assumed that the potential dependence of the Ca-pump in the smooth muscle plasma membrane plays a role in the realization of effects of mediators and physiologically active substances that are manifested as stimulation of the contractile response and depolarization of the sarcolemma. In is quite probable that the delta psi-dependent Ca-pump is also responsible for the maintenance of intracellular homeostasis of monovalent cations (K+, H+, Cl-) in smooth muscle tissues.

Adenosine Triphosphate↗
PubMed1994

[Effects of nilvadipine on membrane potential in cultured neuroblastoma-glioma hybrid NG108-15 cells].

Examination was made of the effects of nilvadipine on membrane potential in cultured neuroblastoma-glioma hybrid NG108-15 cells using the current clamp method. The NG108-15 cells line differentiates into neuronal cells following the addition of 1mM dibutyryl cAMP to the culture medium. This agent (nilvadipine) was found to inhibit both sodium and calcium current on the cell membranes of differentiated NG108-15 cells. The inhibitory effect was reversible in a dose-dependent manner between 10 and 100 microM. A substantial washing-time with normal saline, over 20 minutes, was needed for complete recovery from inhibition. The higher the concentration of nilvadipine, the more suppressive was the action on the membrane potential. A higher dose of nilvadipine, 100 microM, caused the disappearance of the peak membrane potential. This effect appeared irreversible, when cells were incubated in the presence of 100 microM nilvadipine for a longer time. Nilvadipine may thus exert inhibitory effect on the electrophysiological activity of neuronal cells, especially the calcium current of the membrane.

Animals↗
PubMed1990

Voltage-gated potassium channels and the control of membrane potential in human platelets.

1. Human platelets were studied using a combination of patch-clamp and fluorescent indicators of membrane potential and [Ca2+]i. 2. Whole-cell and cell-attached patch recordings showed voltage-gated channels selective for K+ (IK(V]. These channels were activated by depolarization at a threshold close to the platelet resting potential and were blocked by the venom charybdotoxin (CTX; 10-20 nM). Several different conductance states were observed, ranging from 5 to 34 pS, with isotonic KCl in the patch pipette and bath. 3. Measurements with the potential-sensitive dye 3,3'-dipropylthia-dicarbocyanine, diS-C3-(5), in platelet suspensions showed that CTX depolarized the resting potential by approximately 25 mV. Thus, CTX-sensitive, voltage-gated K+ channels appear to play a major part in setting the resting potential. 4. ADP-evoked Ca2+ influx, monitored with Fura-2, was reduced by 10 nM-CTX. Restoration of a large negative membrane potential with valinomycin reversed this effect of CTX. These results suggest that the Ca2+ influx depends on the negative membrane potential and that K+ channels may be important in maintaining this potential during activation.

Blood Platelets↗