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At least 685 records · Page 38Linked to original sources
PubMed2001

FCCP depolarizes plasma membrane potential by activating proton and Na+ currents in bovine aortic endothelial cells.

We investigated the effects of carbonylcyanide p-trifluoromethoxyphenylhydrazone (FCCP), a protonophore and uncoupler of mitochondrial oxidative phosphorylation in mitochondria, on plasma membrane potential and ionic currents in bovine aortic endothelial cells (BAECs). The membrane potential and ionic currents of BAECs were recorded using the patch-clamp technique in current-clamp and voltage-clamp modes, respectively. FCCP activated ionic currents and depolarized the plasma membrane potential in a dose-dependent manner. Neither the removal of extracellular Ca2+ nor pretreatment with BAPTA/AM affected the FCCP-induced currents, implying that the currents are not associated with the FCCP-induced intracellular [Ca2+]i increase. FCCP-induced currents were significantly influenced by the changes in extracellular or intracellular pH; the increased proton gradient produced by lowering the extracellular pH or intracellular alkalinization augmented the changes in membrane potential and ionic currents caused by FCCP. FCCP-induced currents were significantly reduced under extracellular Na+-free conditions. The reversal potentials of FCCP-induced currents under Na+-free conditions were well fitted to the calculated equilibrium potential for protons. Interestingly, FCCP-induced Na+ transport (subtracted currents, I(control)- I(Na+-free) was closely dependent on extracellular pH, whereas FCCP-induced H+transport was not significantly affected by the absence of Na+. These results suggest that the FCCP-induced ionic currents and depolarization, which are strongly dependent on the plasmalemmal proton gradient, are likely to be mediated by both H+ and Na+ currents across the plasma membrane. The relationship between H+ and Na+ transport still needs to be determined.

Animals↗
PubMed1993

Deoxygenation-induced cation fluxes in sickle cells. III. Cation selectivity and response to pH and membrane potential.

Deoxygenation of sickle cells increases membrane permeability to Na, K, and Ca and contributes to cellular cation depletion. This study examines the physiological nature of the pathway that mediates deoxygenation-induced movements of monovalent cations. Deoxygenation-induced Rb influx was a linear function of external Rb concentration, with no evidence of saturation. Activation of the deoxygenation-induced pathway was fostered by alkaline pH (7.5), whereas ion movements via the activated pathway were optimal between pH 6.9 and 7.0 in cells incubated in media in which NO3 replaced Cl to eliminate KCl cotransport. The deoxygenation-induced pathway exhibited no selectivity among the alkali metal cations Li, Na, K, Rb, or Cs, but the monovalent organic cations tetramethylammonium, tetraethylammonium, and N-methylglucamine were excluded. Sickle cells incubated in low-Cl media (external Cl, 40 mM) to depolarize the membrane exhibited increased deoxygenation-induced K efflux and reduced Na influx. Cells treated with valinomycin to hyperpolarize the membrane showed increased deoxygenation-induced Na influx. These characteristics of the deoxygenation-induced transport pathway, linear concentration dependence, lack of cation selectivity, and response to membrane potential, argue against a carrier-mediated mechanism in favor of a diffusional process. The exclusion of small organic cations, however, suggests that factors other than ion size influence deoxygenation-induced permeability.

Anemia, Sickle Cell↗
PubMed1994

Nitric oxide-mediated inhibitory response of rat proximal colon: independence from changes in membrane potential.

1. We studied the relation of nitric oxide-mediated relaxation of smooth muscle to changes in membrane potential of cells in the proximal colon of rats. 2. The resting membrane potential and electrical field stimulation (EFS)-induced junction potentials were recorded from the circular and longitudinal muscle cells. 3. Localized distension with a small balloon caused relaxation of the circular muscle on the anal side of the distended region (descending relaxation). Relaxation of the longitudinal muscle was also induced by EFS. 4. Inhibitory junction potentials (i.j.ps) were recorded from all circular muscle cells tested, but rarely from the longitudinal muscle cells. 5. The i.j.ps were recorded only in the presence of atropine but relaxations of both muscles were induced even in the absence of atropine. 6. Apamin (100 nM) completely abolished the i.j.ps recorded in both circular and longitudinal muscle cells, but had no significant effect on the relaxations of either. 7. In contrast to apamin, Ng nitro-L-arginine (10 microM) inhibited the relaxations of both muscles, but did not affect the i.j.ps. 8. Exogenously added nitric oxide (0.1-10 microM) induced relaxations of both muscles concentration-dependently, but did not affect the membrane potentials at these concentrations. 9. These data strongly suggest that nitric oxide-mediated relaxation of rat proximal colon is not associated with the i.j.ps of the cell membrane.

Animals↗
PubMed2001

Radiation-induced apoptosis of human peripheral T cells: analyses with cDNA expression arrays and mitochondrial membrane potential assay.

We examined sequential changes in post-irradiated peripheral blood T cells taken from normal volunteers, by using targeted Atlas cDNA Expression Arrays and mitochondrial membrane potential assay. At 1 and 3 hours after 5 Gy irradiation, changes of gene expression were examined by targeted Atlas cDNA Expression Arrays using Apoptosis Array. The Atlas Human Apoptosis Array includes 205 key genes that are known to control apoptosis, including extracellular and cytoplasmic effectors. Concerning Fas, no significant changes of spot intensities were identified between irradiated T cells and non-irradiated ones at both 1 h and 3 h after 5 Gy irradiation. Caspase families, including caspases 9 and 3 also showed no changes between these two groups. An apoptosis regulator bclw showed a remarkable decrease in irradiated T cells. These results suggested that irradiation induced direct apoptosis of T cells by changing the membrane potential of mitochondria. Using a CCD camera-equipped fluorescence microscope and MitoCapture, a mitochondrial membrane potential indicator, we demonstrated 5 Gy radiation induced loss of membrane potential, i.e., an early stage of apoptosis, in human peripheral blood T cells at 10 hours after irradiation.

Apoptosis↗
PubMed1983

[Membrane potential, permeability coefficients and the ratio of the influx/efflux rates for alkaline cations across the muscle fiber membrane of the frog in a bi-ionic system].

Membrane potential and 42K, 22Na, 86Rb fluxes were measured in frog muscles immersed in sucrose--sulfate media with cation of one type. For elimination of the internal sodium and chloride ions muscles were preincubated in sucrose solution. It was found that dependence of membrane potential on the cation concentration deviated from the Goldman--Hodgkin--Katz relation. The variation in the permeability coefficients which should be assumed to correlate to experimental dependence with the Goldman--Hodgkin--Katz formula, were estimated. The required values of the permeability, coefficients were shown to differ from those found by fluxes. The influx/efflux rate constants ratio for all of the cations tested did not obey the Ussing criterion for independent passive movement of ion across membrane. It is concluded that the Goldman--Hodgkin--Katz formula cannot be used for a description of passive ion movement in the systems similar to those studied in this work.

Animals↗
PubMedDate not supplied

[Effect of creatine phosphate synthesis on the membrane potential of mitochondria].

The method of the penetrating ions allows to observe the creatine phosphokinase function of heart mitochondria in steady state conditions. The addition of ADP to respiring mitochondria decreases the membrane potential in the course of the ATP synthesis. The subsequent addition of creatine decreases the membrane potential for a long period of time because of ADP formation in creatine phosphokinase reaction. It was shown in the experiments with maintainance of the constant concentration of ADP or ATP in the medium that the ADP concentration in the medium acts mainly on the membrane potential during the creatine phosphate synthesis. There is no effect of creatine on the membrane potential of liver mitochondria which have no creatine phosphokinase.

Adenosine Diphosphate↗
PubMed1982

Relation between membrane potential and lactate in gastrocnemius and soleus muscle of the cat during tourniquet ischemia and postischemic reflow.

The relation between the lactate content and the membrane potential was investigated in the gastrocnemius and soleus muscle of the cat during and after a 4h period of ischemia. The skeletal muscle content of ATP and glucose was also measured. No change occurred in the ATP content of the gastrocnemius muscle during ischemia and increased above initial values after reflow in both muscles. The lactate content increased, and the membrane potential decreased linearly in both muscles during the ischemic period. The final lactate accumulation was higher and the decrease in membrane potential was less in the gastrocnemius than in the soleus. After release of the tourniquet both variables returned to normal or near normal values within 1.5 h in both muscles. A significant correlation was found between the lactate content and the membrane potential in both muscles during the entire experimental period. It is suggested that the depolarisation occurring in skeletal muscle during hypoxia is partly caused by changes in intracellular pH.

Adenosine Triphosphate↗
PubMed1988

Effects of reinnervation with normal and tetrodotoxin-inactive nerves on resting membrane potential of rat skeletal muscle.

Resting membrane potentials (RMPs) have been recorded in vitro near the end-plate region of rat soleus muscles reinnervated with tetrodotoxin-inactive nerves and compared with those of denervated muscles whose reinnervation had been prevented. The two muscle groups exhibited the same low values of RMP typical of denervated muscles. In control muscles of rats in which impulse conduction was left unimpaired, reinnervation induced the expected increase in RMP values towards normal. It is suggested that, at least for this property, reinnervation restores to normal the muscle fibre membrane essentially through the return of activity.

Animals↗
PubMed2002

Ionic basis of the resting membrane potential and action potential in the pharyngeal muscle of Caenorhabditis elegans.

The pharynx of C. elegans is a rhythmically active muscle that pumps bacteria into the gut of the nematode. This activity is maintained by action potentials, which qualitatively bear a resemblance to vertebrate cardiac action potentials. Here, the ionic basis of the resting membrane potential and pharyngeal action potential has been characterized using intracellular recording techniques. The resting membrane potential is largely determined by a K(+) permeability, and a ouabain-sensitive, electrogenic pump. As previously suggested, the action potential is at least partly dependent on voltage-gated Ca(2+) channels, as the amplitude was increased as extracellular Ca(2+) was increased, and decreased by L-type Ca(2+) channel blockers verapamil and nifedipine. Barium caused a marked prolongation of action potential duration, suggesting that a calcium-activated K(+) current may contribute to repolarization. Most notably, however, we found that action potentials were abolished in the absence of external Na(+). This may be due, at least in part, to a Na(+)-dependent pacemaker potential. In addition, the persistence of action potentials in nominally free Ca(2+), the inhibition by Na(+) channel blockers procaine and quinidine, and the increase in action potential frequency caused by veratridine, a toxin that alters activation of voltage-gated Na(+) channels, point to the involvement of a voltage-gated Na(+) current. Voltage-clamp analysis is required for detailed characterization of this current, and this is in progress. Nonetheless, these observations are quite surprising in view of the lack of any obvious candidate genes for voltage-gated Na(+) channels in the C. elegans genome. It would therefore be informative to re-evaluate the data from these homology searches, with the aim of identifying the gene(s) conferring this Na(+), quinidine, and veratridine sensitivity to the pharynx.

4-Aminopyridine↗
PubMed1984

Mitochondrial membrane potential monitored in situ within isolated guinea pig brown adipocytes by a styryl pyridinium fluorescent indicator.

2-( Dimethylaminostyryl )-l-methyl pyridinium, a fluorescent indicator of mitochondrial membrane potential, is accumulated up to 400-fold by intact, isolated brown adipocytes from cold-adapted guinea pigs. The indicator can be optically localized within the in situ mitochondria. Ionophores which would be predicted to lower or increase the in situ mitochondrial membrane potential lead to decreased and increased uptake, respectively, of the radio-labelled indicator. Noradrenaline induces a 15 mV decrease in the sum of mitochondrial and plasma membrane potentials. The results indicate that the mitochondria within isolated brown adipocytes maintain a substantial membrane potential in the resting state, rather than being artifactually depolarized.

Adipose Tissue, Brown↗
PubMed1989

The dependence of sodium pump current on internal Na concentration and membrane potential in cardioballs from sheep Purkinje fibres.

The effect of various intracellular Na concentrations (CiNa) and membrane potentials on the Na pump current (Ip) was studied in isolated, cultured sheep cardiac Purkinje cells ('cardioballs'). Ip was identified as cardiac steroid sensitive current. The dependence of Ip on CiNa was investigated at a membrane potential of -40 mV by means of whole-cell recording from cardioballs internally perfused with media containing various Na concentrations. Internal perfusion with a Na free solution abolished Ip. The amplitude of Ip as a function of CiNa displayed saturation kinetics. Half maximal activation of Ip occurred at a CiNa of about 9 mM. The maximal Ip density was estimated to be 1.1 microA/cm2. The potential dependence of Ip was studied by conventional whole-cell recording under various ionic conditions. Generally Ip displayed little voltage dependence at membrane potentials positive to -20 mV. Ip declined at more negative potentials. The pump cycle probably includes only one voltage sensitive step. The potential dependence of Ip was more pronounced at lower CiNa or lower concentrations of the external pump activator Cs+. The findings are in line with the idea that increasingly steeper ionic gradients against which the cations are pumped strengthen the voltage dependence of Ip in the potential range studied. Other factors probably affecting the pump current-voltage (Ip-V) relation are discussed. The results suggest that Ip varies during electrical activity.

Animals↗
PubMed1989

Effect of membrane potential on divalent cation transport catalyzed by the "electroneutral" ionophores A23187 and ionomycin.

Depolarization of plasma membrane potential has a potent inhibitory effect on divalent cation influx catalyzed by the carboxylic ionophores ionomycin and A23187. This effect is observed in different cell models and does not depend on either inhibition of Ca2+-activated cation channels or activation of Ca2+ extrusion mechanisms as suggested previously. A dependence of divalent cation influx on the magnitude of membrane potential is observed also in artificial liposomes. The inhibition of ionophore-dependent divalent cation transport by membrane potential depolarization can be modified varying the ionophore concentration and the external pH. These findings suggest that both neutral and positively charged ionophore-cation complexes can cross the plasma membrane and that their contribution to the overall transport process can be varied according to the experimental conditions.

Adrenal Gland Neoplasms↗
PubMed1989

The membrane potential changes polarity during capacitation of murine epididymal sperm.

The membrane potential in murine epididymal sperm was determined with a voltage-sensitive, fluorescent probe. In freshly collected sperm, the potential was inside-negative, viz., -13 mV, and was associated with an intracellular K+ concentration of about 122 mM. Following incubation of sperm in a medium capable of sustaining capacitation and fertilization efficacy, the potential became gradually positive. An inside-positive potential, +24 mV, was obtained after 40 min of incubation, concomitant with an intracellular K+ concentration of approximately 30 mM. At this time, about 70 percent of sperm had capacitated. An inside-positive membrane potential may play a role in facilitating the acrosome reaction.

Animals↗
PubMed2005

Mitochondrial membrane potential is reduced in copper-deficient C2C12 cells in the absence of apoptosis.

Mitochondrial membrane potential is reduced in copper-deficient rat hearts, but it is uncertain if this will lead to the onset of apoptosis. To determine if copper deficiency per se leads to apoptosis, C2C12 cells were made copper deficient by treatment with the copper chelator tetraethylenepentamine (TEPA). In TEPA-treated cells, the activity of Cu, Zn-superoxide dismutase and cytochrome-c oxidase decreased dramatically. The protein levels of nuclear-encoded subunits of the cytochromie-c oxidase decreased, but the mitochondrial-encoded subunits remained unchanged. Decreased mitochondrial membrane potential was indicated in TEPA-treated cells, but further investigation of the potential induction of apoptosis by measuring caspase-3 activity, protein concentrations of Bcl-2 and Bax, and DNA fragmentation suggested that apoptosis is not induced in TEPA-treated C2C12 cells. Cells with decreased mitochondrial membrane potential were not destined to apoptosis as a result of copper deficiency.

Animals↗
PubMed1984

The effect of membrane potential on initial velocity of GABA uptake and steady state distribution ratio in rat cortical synaptosomes.

Initial velocity of synaptosomal GABA uptake and steady state distribution ratio (DR) have been measured as a function of medium potassium concentration [( K]o) and in the presence of veratridine. Previous studies of the effect of [K]o and veratridine on membrane potential have been utilized to relate GABA uptake to membrane potential. Both initial velocity of uptake and steady state DR are functions of membrane potential; initial velocity and in DR are linearly related to membrane potential. Final DR is determined by the electrochemical potential gradient for the transported ions. Previous studies of the relation of [Na]o to uptake have shown that either one or two sodium ions may be translocated with each GABA molecule. Present results are consistent with this assumption if it is also assumed that an anion is co-transported with each GABA molecule.

Animals↗
PubMed1999

Membrane potential and time requirements for detection of weak signals by voltage-gated ion channels.

The question of minimum detection limits for biological processes sensitive to membrane potential perturbations has arisen in various contexts. Of special interest are the prediction of theoretical limits for sensory perception processes and for possible biological effects of environmental or therapeutic electric and magnetic fields. A new method is presented here, addressing the particular case in which perturbations of membrane potential affect the gating rate probability of voltage-sensitive ion channels. Using a two-state model for channel gating, the influence of the perturbing potential on the mean fraction of open channels is approximated by a Boltzmann distribution, and integrated over time to obtain a quantity proportional to the net change in expected charge transfer through the membrane. This change in net charge transfer (the signal, S) is compared to the expected root mean variance in charge transfer (the noise, N) due to random channel gating. Using a nominal criterion of S/N = 1, a model is developed for predicting the minimum time and number of ion channels necessary to detect a given membrane potential. Example calculations, carried out for a gating charge of 6, indicate that a 1 microV induced membrane potential can be detected after 10 ms by an ensemble of less than 10(8) ion channels.

Algorithms↗
PubMed1989

The effect of epidermal growth factor on membrane potential. Rapid hyperpolarization followed by persistent fluctuations.

The effects of epidermal growth factor (EGF) on membrane potential were investigated in suspensions of the following three cell types endowed with a large complement of specific receptors: EGFR-T17 (a clone of mouse NIH-3T3 fibroblasts overexpressing EGF receptors); A431 and KB (two human carcinoma lines). In all these lines EGF induced a rapid and marked hyperpolarization constituted by an initial peak (in all three cell lines) and a subsequent sustained plateau phase, concomitant with the well-known increase of [Ca2+]i. The time course and phorbol ester inhibitability of the membrane potential effects were the same as for the [Ca2+]i response. Experiments with Na+-free and chloride-free media excluded a major role of the latter ions in the EGF-induced hyperpolarization. In contrast, experiments with high K+ media, with the monovalent cation ionophore gramicidin and with Ca2+-free media together with either a Ca2+ ionophore (ionomycin, in A431 and EGFR-T17), or an agonist (bradykinin, in A431) addressed to a receptor coupled to phosphoinositide hydrolysis, were consistent with the involvement of Ca2+-activated K+ channels. The EGF-induced hyperpolarization was completely blocked by the K+ channel blocker, quinidine, and unaffected by a variety of other drugs. Patch clamping of individual EGFR-T17 cells confirmed the initial hyperpolarization (from approximately -30 mV, the resting potential, to -60, -80 mV) was due to activation of an outward current. This initial hyperpolarization was followed by fluctuations (period approximately 1 min) persisting as long as the cells could be analyzed. Thus, the changes of membrane potential appear to be not only novel members of the group of early events triggered by EGF in target cells but also long-lasting effects of the growth factor, which continue for unexpectedly long periods of time after EGF application.

Animals↗
PubMed2000

Imaging membrane potential with voltage-sensitive dyes.

Membrane potential can be measured optically using a variety of molecular probes. These measurements can be useful in studying function at the level of an individual cell, for determining how groups of neurons generate a behavior, and for studying the correlated behavior of populations of neurons. Examples of the three kinds of measurements are presented. The signals obtained from these measurements are generally small. Methodological considerations necessary to optimize the resulting signal-to-noise ratio are discussed.

Animals↗