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At least 631 records · Page 35Linked to original sources
PubMed1988

Effects of triiodothyronine on resting membrane potential of primary cultured rat submandibular gland cells.

The effect of triiodothyronine (T3) on the resting membrane potential was measured in primary cultured rat submandibular gland cells. The resting membrane potential was 29.5 +/- 0.71 mV. The hormone T3, at concentrations of 10(-9) M or greater, hyperpolarized the cells 5.8 mV (p less than 0.05). Hyperpolarization was complete within 24 hours. Ouabain (1 mM) depolarized the cells 5.9 mV. Cells exposed to T3 and ouabain had the same membrane potential as cells treated with ouabain alone. These data suggest that the hyperpolarization observed can be, in part, attributed to triiodothyronine-induced synthesis of (Na-K)-adenosine triphosphatase.

Animals↗
PubMedDate not supplied

[Effect of acidosis on membrane potential and calcium transport in rat brain synaptosomes].

The influence of acidosis on the transmembrane potential, sodium pump and membranous systems of calcium transport was studied on isolated presynaptic nerve terminals (synaptosomes) from rat brain. It is established that acidic shift causes a decrease of membrane potential, a large inhibition of the sodium pump (by three times at pH 6.0). All the systems controlling both inward- and outward-directed calcium fluxes are partially blocked by low pH. At pH 6.0 the basal influx and calcium pump are reduced two-fold while the voltage-sensitive calcium channels and Na+/Ca2+ exchanger are inhibited by three and four to five times, respectively. We have no found any evidence of acidosis-induced net flux of calcium directed inwards.

Acidosis↗
PubMed1997

Valinomycin induces apoptosis of ascites hepatoma cells (AH-130) in relation to mitochondrial membrane potential.

Valinomycin is a potassium ionophore, and is well known to cause the collapse of the mitochondrial membrane potential. It has been reported that loss of mitochondrial membrane potential is observed in the early stages of apoptosis induced by various agents. Thus, the effects of valinomycin on tumor cells were examined. Valinomycin induced uncoupling of respiration and depolarization of isolated mitochondria. Depolarization of intact mitochondria in AH-130 rat ascites hepatoma cells was also induced by valinomycin. Valinomycin induced apoptosis revealing the typical apoptotic characteristics such as fragmentation and ladder formation of DNA, shrinkage of cells, and formation of pycnotic nucleus. There was a correlation between the depolarization of mitochondria and DNA fragmentation. After depolarization of mitochondria, the activity of caspase-3-like protease but not caspase-1-like protease increased markedly. In contrast, this apoptosis did not involve the release of reactive oxygen species from mitochondria, increase in intracellular calcium concentration, or protein synthesis. In addition, anti-apoptotic members of the Bcl-2 family (Bcl-xL and Bcl-2) were not correlated with apoptosis. These results indicate that valinomycin might induce apoptosis through degradation of the mitochondrial membrane potential. Taken together, these observations suggest that there may be a mechanism that transmits the signal from mitochondrial depolarization to subsequent apoptosis execution steps.

Animals↗
PubMed1983

Alpha and beta-adrenergic mediation of membrane potential changes and metabolism in rat brown adipose tissue.

Membrane potential and flavoprotein redox state have been measured simultaneously and continuously in brown adipose tissue in order to determine how nerve stimulation and adrenergic agonists control its metabolic activity. Both trains of nerve impulses and addition of noradrenaline evoke two temporally distinct cell depolarizations. The first rapid depolarization precedes the increase in flavoprotein reduction. With nerve stimulation, at the time of maximum flavoprotein reduction the cell has repolarized or hyperpolarized. The second slow depolarization follows flavoprotein reduction. Phentolamine, an alpha antagonist, selectively blocks the first depolarization, but not the flavoprotein reduction. However the time of maximum flavoprotein reduction is delayed. Propranolol, a beta antagonist, delays the first repolarization until the end of nerve stimulation and inhibits the transient hyperpolarization, second depolarization and flavoprotein reduction. Isoproterenol, a beta agonist, or the fatty acid octanoate produce only a transient hyperpolarization and subsequent slow depolarization following flavoprotein reduction. Thus brown adipose tissue contains both alpha- and beta-adrenergic receptors. Stimulation of alpha receptors produces an early membrane depolarization. Stimulation of beta receptors leads to an increase in metabolic activity which then appears to produce slow changes in membrane potential.

Adipose Tissue, Brown↗
PubMed1998

Ectopic potassium uptake in trk1 trk2 mutants of Saccharomyces cerevisiae correlates with a highly hyperpolarized membrane potential.

Null trk1 trk2 mutants of Saccharomyces cerevisiae exhibit a low-affinity uptake of K+ and Rb+. We show that this low-affinity Rb+ uptake is mediated by several independent transporters, and that trk1Delta cells and especially trk1Delta trk2Delta cells are highly hyperpolarized. Differences in the membrane potentials were assessed for sensitivity to hygromycin B and by flow cytometric analyses of cellular DiOC6(3) fluorescence. On the basis of the latter analyses, it is proposed that Trk1p and Trk2p are involved in the control of the membrane potential, preventing excessive hyperpolarizations. K+ starvation and nitrogen starvation hyperpolarize both TRK1 TRK2 and trk1Delta trk2Delta cells, thus suggesting that other proteins, in addition to Trk1p and Trk2p, participate in the control of the membrane potential. The HAK1 K+ transporter from Schwanniomyces occidentalis suppresses the K+-defective transport of trk1Delta trk2Delta cells but not the high hyperpolarization, and the HKT1 K+ transporter from wheat suppresses both defects, in the presence of Na+. We discuss the mechanism involved in the control of the membrane potential by Trk1p and Trk2p and the causal relationship between the high membrane potential (negative inside) of trk1Delta trk2Delta cells and its ectopic transport of alkali cations.

Biological Transport↗
PubMed1974

Resting membrane potential and ionic distribution in fast- and slow-twitch mammalian muscle.

The resting membrane potential and intracellular potassium and sodium concentration of three guinea pig hind limb muscles were studied. These properties are related to the gross color, the speed of contraction, and the biochemically defined fiber type composing the muscle. The resting membrane potential and intracellular content were: white vastus (grossly white, fast-twitch glycolytic) -85.3 mV. potassium 171.9 meq/liter; soleus (grossly red, slow-twitch oxidative) -69.7 mV, potassium 137.5 meq/liter; and red vastus lateralis (grossly red, fast-twitch oxidative glycolytic) -71.7 mV, potassium 139.6 meq/liter. In soleus and red vastus lateralis, the relative permeability of sodium to potassium was 0.041 and 0.036, while in white vastus it was 0.015. These results give us the first exception to the hypothesis that fast-twitch fibers have higher intracellular potassium and higher resting membrane potential than slow-twitch fibers.

Animals↗
PubMed1992

Development and properties of spontaneous oscillations of the membrane potential in inferior olivary neurons in the rat.

Previous experiments have shown that the conductances that are thought to underlie the spontaneous oscillations of the membrane potential in inferior olivary (IO) neurons of the mature rat are present at 2 days postnatal (PN). In this study intracellular recordings of transmembrane potentials were made in 209 IO neurons in brainstem slices from rats aged 4-25 days PN. Membrane potential oscillations were not found before 9 days PN but were observed in 41% of neurons examined at 10-15 days PN and in 95% of neurons after 16 days PN. These oscillations exhibited a wide range of frequencies (0.5-9.5 Hz) and amplitudes (2-23 mV). The waveforms of the oscillations in different neurons varied from having 2-3 non-harmonic frequencies of unequal amplitude to being almost sinusoidal. There was a positive relationship between the age of the animal and the frequency (P less than 0.0001) and amplitude (P less than 0.002) of the oscillations. The timecourse of development of the membrane potential oscillations is consistent with ultrastructural data which indicate that neuro-neuronal gap junctions in the rat IO nucleus mature between 10 and 15 days PN. Exposure of the neurons to pharmacological agents that induce oscillations in adult IO neurons failed to induce oscillations in neurons less than 9 days PN. Our findings support the hypothesis that oscillations of the membrane potential in IO neurons depend not only on specific membrane conductances but also on electrotonic coupling between the neurons.

Animals↗
PubMed1990

Ionic regulation of the plasma membrane potential of rainbow trout (Salmo gairdneri) spermatozoa: role in the initiation of sperm motility.

The ionic dependence of the trout sperm plasma membrane potential was analysed by measuring the accumulation of the lipophilic ions 3H-tetraphenylphosphonium (TPP) and 14C-thiocyanate (SCN) following dilution in artificial media isotonic to the seminal fluid. Our data showed that the trout sperm plasma membrane has a mixed conductance: the plasma membrane potential is sensitive upon the transmembrane gradients of K+, Na+, and H+. This potential is negative (less than -40 mV) in a 125 mM choline chloride media (ChM) at pH 8.5. Replacement of choline by sodium has a small depolarizing effect. The membrane potential is about -15 mV in a 125 mM potassium chloride and falls near zero mV only if valinomycin is added. In ChM changing the external pH (pHe) greatly affects the membrane potential: its value rises from less than -40 mV at pHe 9.0 to -17 mV at pHe 5.0. This pH effect is observed also in presence of sodium or potassium. A decrease in the transmembrane proton gradient produced by increasing internal pH without changing pHe induces also a depolarisation of the plasma membrane. In the different media in which trout sperm remain immotile after dilution (media with [K+] greater than 20-40 mM or a pH less than 7.5) the plasma membrane is more depolarized than in media allowing motility, suggesting a relationship between the state of membrane polarization and the intracellular effectors of the axonemal movement.

Animals↗
PubMed1998

Effects of sympathetic nerve stimulation on membrane potential in the circular muscle layer of mouse distal colon.

Little is known about the effects of sympathetic nerve stimulation on the membrane potential of colonic smooth muscle. In the distal colon of the mouse, intracellular microelectrodes were used to record the effects of lumbar colonic (LCN) and intermesenteric nerve (IMN) stimulation on circular muscle membrane potential in vitro. A two-compartment organ bath was used to selectively perfuse the colon and inferior mesenteric ganglion (IMG). In the presence of nifedipine (1-2 microM) (to the colonic compartment only), spontaneous depolarizations (myoelectric complexes, MCs) were recorded about every 4 min. MCs consisted of a prolonged burst of rapid oscillations in membrane potential (approximately 2 Hz) that were superimposed on a slow depolarization (mean amplitude 12 mV). Single electrical stimuli (600 microseconds duration) delivered to the LCN or IMN did not elicit a detectable change in the membrane potential. However, trains of stimuli (e.g., 60 pulses at 10-20 Hz) to the LCN or IMN during the intervals between MCs evoked a depolarization (with superimposed action potentials in the absence of nifedipine). Trains of stimuli delivered during the plateau phase of the MC reduced or abolished the rapid oscillations, without a further membrane depolarization. The MC period was unaffected by stimulation of the IMN or LCN. Responses were abolished by the selective perfusion of guanethidine (1 microM) to the colon, or by severing the LCN. Hexamethonium (500 microM) (to the colon) abolished MCs, induced sustained depolarization and attenuated the amplitude of the sympathetic depolarizations by 74%. In hexamethonium, sympathetic responses remained attenuated when the membrane of the circular muscle was repolarised by sodium nitroprusside (1 microM). Immunohistochemical studies of the colon revealed intense immunoreactivity for tyrosine hydroxylase in the myenteric plexus but not in the circular muscle layer. It is suggested that responses to sympathetic nerve stimulation in the circular muscle layer of the mouse colon are secondary to actions on the enteric nervous system.

Animals↗
PubMed2004

Correlation between membrane potential responses and tentacle movement in the dinoflagellate Noctiluca miliaris.

Membrane potential responses and tentacle movement of the marine dinoflagellate Noctiluca miliaris were recorded simultaneously and their time relationships were examined. The food-gathering tentacle of Noctiluca exhibited slow extension-flexion movements in association with the spontaneously recurring membrane potential responses termed the tentacle regulating potentials (TRPs). The flexion of the tentacle began during the slow depolarization of the TRPs. The rate of the flexion increased after the hyperpolarizing (negative) spike following the slow depolarization. The tentacle then extended slowly during the hyperpolarized level of the TRPs. A TRPs-associated flexion did not occur when the external Ca(2+) ions were removed. On the contrary, the tentacle showed conspicuous flexion (coiling) when the external Ca(2+) concentration was raised. In association with the stimulus-evoked action potential, which triggers bioluminescent flash (flash-triggering action potential; FTP), the tentacle coiled quickly. The FTP-associated coiling took place even in the Ca(2+)-deprived condition. The coupling mechanisms of the TRPs-associated and FTP-associated tentacle movements were compared, and their biological significance was discussed.

Animals↗
PubMed1985

No correlation between membrane potential and increased cytosolic free Ca2+ concentration, 86Rb+ influx or subsequent [3H]-thymidine incorporation in neoplastic human B cells stimulated with antibodies to surface immunoglobulin.

We have followed the changes in the membrane potential of neoplastic B cells after addition of antibodies to cell specific surface immunoglobulin heavy chains (anti-Ig). Two methods were used, both based on the distribution of lipophilic fluorescent indicators: the anionic bis(1,3-diethylthiobarbiturate)-trimethine oxonol (fluorescence measurement made on whole cell suspensions) and the cationic 3,3-dihexyloxacarbocyanine iodide (diOC6-(3] (using flow cytofluorimetric analysis). By the latter method, the resting membrane potential was calculated to range from -40 to -63 mV. The stimulatory effect of anti-Ig was investigated on two B cell populations. In one, which may be stimulated in this way to [3H]-thymidine incorporation, the membrane potential was apparently unchanged, at least during the first hour of stimulation. In the other population, anti-Ig induced a rapid depolarization (oxonol method), but these cells did not, on the other hand, respond with [3H]-thymidine incorporation. The nature of this depolarization was further investigated. Both Na+ and K+ permeabilities appeared increased, while Ca2+ influx did not contribute to the change in membrane potential. Nor did depolarization itself change free cytosolic Ca+ concentration, [Ca2+]i, as estimated by the quin-2 method. Furthermore, anti-Ig stimulation increased [Ca2+]i in these cells, even when depolarization was abolished by lowering the extracellular Na+ concentration. Thus, in cells where depolarization could be demonstrated, it was linked neither to early changes in [Ca2+]i nor to late [3H]-thymidine incorporation. In contrast, such effects of anti-Ig stimulation were observed in other cells without any significant early change in the membrane potential.

Antibodies↗
PubMed1994

Lidocaine hydrochloride and acetylsalicylate kill bacteria by disrupting the bacterial membrane potential in different ways.

Lidocaine hydrochloride (LH), a local anesthetic, and acetylsalicylate (AcSAL), show antibacterial activity for both gram-negative and gram-positive bacteria. Kinetic studies indicated that antibacterial activity of LH was different from that of AcSAL. A subinhibitory concentration of LH and AcSAL enhanced the sensitivity of Escherichia coli, Salmonella typhimurium, and Pseudomonas aeruginosa to novobiocin and nalidixic acid. The synergistic effect of AcSAL with novobiocin and nalidixic acid was higher than that of LH. The effect of both drugs on the membrane potential of inner membrane was also studied using inverted membrane vesicles of bacteria. Both LH and AcSAL depolarized the membrane potential after the vesicles were energized with nicotinamide adenine dinucleotide. However, unlike AcSAL, pre-treatment of vesicles with LH had no effect on the generation of membrane potential. These results suggest that depolarization of the cytoplasmic membrane, preceded by the permeabilization of the outer membrane for gram-negative bacteria, is associated with antibacterial activity of LH and AcSAL. The difference in actions of LH and AcSAL was discussed.

Anti-Bacterial Agents↗
PubMed1988

Polarized thyroid cells in monolayers cultured on collagen gel: their cytoskeleton organization, iodine uptake, and resting membrane potentials.

Porcine thyroid cells were cultured on collagen gel-coated cover glasses. They were reorganized into polarized monolayer cells; the basal cell membranes were in contact with the collagen gel, and the apical ones faced the culture medium. We studied cytoskeleton organization, resting membrane potentials, and iodine uptake of these cells. The quick-freezing and deep-etching replica method provided three-dimensional images of the cytoskeleton organization. Networks of microfilaments were observed under the apical cell membrane. In the deep cytoplasm and near the basal cell membranes, intermediate filaments predominated and were interlinked with the microfilaments. When the cells were cultured in the presence of TSH, TSH induced the formation of microvilli at the apical cell membranes and the accumulation of microfilaments under these membranes; in the deep cytoplasm, the intermediate filaments were more closely interlinked with the microfilaments. The microfilaments were immunostained with antiactin antibody. Thus, collagen is a factor in determining the cell polarity, and TSH further augments polarization through reorganizing the cytoskeletons. Electrophysiological study revealed that the resting membrane potential of cells cultured in the absence of TSH was -46 mV, and that of cells cultured in the presence of TSH was -58 mV. TSH hyperpolarized resting membrane potentials. These cells took up iodine. TSH in the medium augmented this uptake. TSH augments thyroid cell polarization through reorganizing the cytoskeletons and hyperpolarizing the resting membrane potentials and enhances iodine uptake by the cells.

Animals↗
PubMed2002

Artificial cell based on lipid hollow polyelectrolyte microcapsules: channel reconstruction and membrane potential measurement.

A new model system as an artificial cell based on hollow polyelectrolyte microcapsules (HPM), fabricated by step-wise adsorption of polyelectrolytes and phospholipids, was proposed. To demonstrate the feasibility of the functioning of HPM coated with lipid layers as a model biosystem, the membrane permeability for ions and the channel reconstruction were examined by measuring the membrane potential as one of the most important cell parameters. The membrane potential was measured by confocal microscopy using the potentiometric fluorescent dye tetramethylrhodamine ethyl ester perchlorate (TMRE). The influence of the lipid composition (phosphatidylcholine--DPPC-HPM, phosphatidylcholine/phosphatidic acid 9/1-(DPPC/DPPA)-HPM) and metal cations (Na+, K+, Ca2+) on the membrane potential was shown. Addition of DPPA was found to lead to an increase of the negative membrane potential value. To investigate the ion-transport activity of the lipid-HPM, the ion channel-forming peptides valinomycin and gramicidin were used. The selectivity of the valinomycin and gramicidin channels for K+ and for K+, and Na+ ions, respectively, and the tolerance for Ca2+ ions is evidence that lipid-HPM functions as an artificial cell.

Biomimetic Materials↗
PubMed1991

Membrane potential fluctuations and transient inward currents induced by reactive oxygen intermediates in isolated rabbit ventricular cells.

The cellular basis of reactive oxygen intermediate-induced arrhythmias was investigated in isolated rabbit ventricular cells using the whole-cell voltage- and current-clamp techniques. Singlet oxygen and superoxide were generated by the photoactivation of rose bengal. Single ventricular cells exposed to rose bengal (10-100 nM) exhibited spontaneous membrane potential fluctuations at plateau potentials and at the level of the resting membrane potential. The voltage fluctuations induced in the resting potential occasionally triggered repetitive action potential discharges. At the resting membrane potential, the magnitude and dominant frequency of the voltage fluctuations were 1-3 mV and 1.5 Hz, respectively. At plateau potentials, the amplitude of the voltage fluctuations was about 2-5 mV, and the dominant oscillatory frequency was 2.6 Hz. In voltage-clamp experiments, transient inward currents were induced on repolarization after a depolarizing clamp step. Oscillatory currents also occurred occasionally during clamp steps to positive potentials. The peak frequencies of transient inward currents recorded at -20 and -70 mV were approximately 3.7 and 2.3 Hz, respectively, indicating that these currents may underlie the arrhythmogenic membrane potential fluctuations observed in current-clamp experiments. The rose bengal-induced transient inward currents were shown to be dependent on the magnitude and duration of the preceding voltage step. Studies of the voltage dependence of transient inward currents showed that these currents remained inward even at positive potentials (+30 mV), and replacement of extracellular sodium with lithium decreased transient inward current to approximately 10% of its initial value. Thus, the major component of oxidant stress-induced inward current appears to be electrogenic Na-Ca exchange. This oscillatory transient inward current may be responsible for the arrhythmias induced in isolated hearts exposed to reactive oxygen intermediates, and since oxidant stress has been implicated in reperfusion injury, it is possible that similar oscillatory currents may underlie reperfusion-induced arrhythmias.

Animals↗
PubMedDate not supplied

The effect of papaverine on synaptosomal membrane potential.

The authors studied the effect of graded concentrations of papaverine on membrane potential in isolated synaptosomes from pig brain by fluorescence. The indicator dye for membrane potential is rhodamine 6G (Rh6G). The membrane voltage is determined at both high (127.2) and low (30 mM) final sodium (Na+) concentrations. The results demonstrate a hyperpolarizing action of papaverine directly proportional to papaverine concentration.

Animals↗
PubMed2001

Chemical hypoxia in hippocampal pyramidal cells affects membrane potential differentially depending on resting potential.

The aim of the present study was to analyze the effect of chemical hypoxia (cyanide) on the membrane potential of hippocampal CA1 neurons and to elucidate the reason for previously found differences in the reaction to hypoxia in these cells. Recordings were performed in brain slices from 8-19-day-old rats with whole-cell patch clamp on cells identified with near-infrared video microscopy. Cyanide (0.1-2.0 mM) caused different responses depending on the resting potential of the cells: hyperpolarization (or an initial depolarization followed by hyperpolarization) was generally seen in cells with less negative resting potential (-56+/-6.1 mV), and depolarization in cells with more negative resting potential (-62+/-3.4 mV). After 10 min in cyanide the membrane potential in all cells had reached approximately the same level (-62+/-5.8 mV), the direction and size of the voltage response having an inverse linear relation to the resting potential (k=-0.98, r=0.71). The direction of the cyanide response was not reversed by current injection (depolarization by 12 mV) in cells with more negative resting potential (-60+/-2.8 mV). Wash out of cyanide caused hyperpolarization in 70% of the cells. Presence of ouabain (2 microM) resulted in pronounced depolarization during cyanide perfusion, and potentiated the hyperpolarization during wash out indicating that this part of the effect is not dependent on a reactivation of the Na/K pump. In conclusion, chemical hypoxia with cyanide changes the membrane potential in CA1 cells in size and direction depending on the original resting potential of the cells. The present findings suggested that cyanide activated not only K+ channels but in addition increased a Na+ current which has a more positive equilibrium potential.

Animals↗
PubMedDate not supplied

Measurement of intracellular calcium concentration and plasma membrane potential in human spermatozoa using flow cytometry.

We report 2 novel approaches using flow cytometry to measure intracellular calcium concentration and plasma membrane potential in human spermatozoa. Both approaches have the potential to measure different responses in subpopulations of cells, which is particularly useful when studying heterogeneous populations such as human spermatozoa. Intracellular calcium concentration ([Ca2+]i) was measured using the probe indo-1/AM. This allowed measurements to be made that were independent of variation in cell size and dye loading. It also enabled dead cells to be directly identified and excluded from the analyses without the need for counterstaining. Mean basal [Ca2+]i was determined as 50 nM (25-75 nM range) and, in response to the agonist progesterone (20 microM), this increased transiently to 195 nM (125-285 nM range) before declining to approximately half the maximal level within 2 minutes (values in parentheses correspond to the range of values typically found within a sperm population from 1 sample). These results are comparable with previously published data on whole sperm populations. Sperm membrane potential (VM) was assayed using the probe DiOC6(3). In carefully controlled experiments, a marked depolarization of the plasma membrane potential of capacitated spermatozoa was observed in response to progesterone (20 microM). Following in vitro capacitation, the sperm plasma membrane potential became hyperpolarized compared with the noncapacitated state. Therefore, this technique may be used to assay for sperm capacitation in vitro.

Calcium↗