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PubMed1982

Changes in mouse oocyte membrane potential and permeability during meiotic maturation.

Mouse oocytes spontaneously undergo meiotic maturation when removed from the ovary and cultured in vitro. This paper describes the changes in cell surface membrane potential from the germinal vesicle (GV) stage (- 46 mV, inside negative), through germinal vesicle breakdown (GVBD) (- 31 mV), to the polar body (PB) stage (- 17 mV). Radioisotope tracer flux experiments established the total exchangeable internal K at the GV stage in 190 mM, the K efflux rate coefficient as 6.7 X 10(-5) sec-1) and the K permeability as 46.7 X 10(-8) cm sec-1. In comparison with previous results with PB stage oocytes, this suggests that the membrane potential depolarization is caused largely by a decrease in K permeability. When GVBD is blocked with 0.11 mM dibutyryl cyclic AMP, the membrane potential does not depolarize. This suggests a linkage between depolarization and GVBD. However, incubation in 80 mM K medium, which depolarizes the oocyte, does not trigger GVBD. It is concluded that membrane depolarization by itself is not sufficient to cause GVBD.

Animals↗
PubMed1989

Effect of membrane potential on cytosolic calcium of bovine aortic endothelial cells.

The effect of bradykinin on membrane potential of cultured bovine aortic endothelial cells (BAECs) was estimated by measuring the uptake of the lipophilic cation, tetra[3H]phenylphosphonium ([3H]TPP+). Uptake of [3H]TPP+ was found to be 1) a function of extracellular K+ concentration, 2) sensitive to valinomycin, and 3) decreased by the K+ channel inhibitor, Ba2+, suggesting that the uptake of [3H]TPP+ responds to changes in membrane potential of the BAEC. Bradykinin (50 nM) produced an increase in [3H]TPP+ uptake in low K+ buffer consistent with a bradykinin-induced membrane hyperpolarization. The effect of membrane depolarization with high K+ buffer on the bradykinin-stimulated changes in cytosolic Ca2+ was determined using the fluorescent Ca2+ indicator, fura-2. The results of these experiments demonstrated that both basal cytosolic Ca2+ and bradykinin-stimulated release of Ca2+ from internal stores were not affected by membrane depolarization. However, bradykinin-stimulated influx of Ca2+ from the extracellular space decreased with membrane depolarization in a manner consistent with the movement of Ca2+ through a channel.

Animals↗
PubMed1977

Potassium activity and plasma membrane potentials in epithelial cells of toad bladder.

Intracellular potassium activity (aki), mucosal and serosal membrane potential (mEm, sEm), short-circuit current (Isc), and transepithelial potential difference in the epithelium of the toad bladder were measured with a potassium-sensitive liquid ion exchanger and an ordinary microelectrode. Under basal conditions, aki was 41.2 +/- 0.5 mM, corresponding to 54.4 mM in free potassium concentration, so half or more of the intracellular potassium may be of bound form or sequestrated within subcellular organelles. The sEm cannot be explained by only the potassium equilibrium potential (Eeq), because the sEm was markedly lower than the Eeq and no relation was found between them. Ouabain and rotenone decreased the aki, but ethacrynic acid, which also inhibited the Isc and the membrane potentials, did not show any effect on aki. Vasopressin decreased aki with an elevation in mEm, whereas prostaglandin E1 increased the aki with elevation in the sEm. These characteristic changes may afford an insight into the mechanisms by which transcellular electrolyte transport occurs.

Animals↗
PubMed1999

Hydrogen peroxide, potassium currents, and membrane potential in human endothelial cells.

BACKGROUND: Hydrogen peroxide (H2O2) and reactive oxygen species are implicated in inflammation, ischemia-reperfusion injury, and atherosclerosis. The role of ion channels has not been previously explored. METHODS AND RESULTS: K+ currents and membrane potential were recorded in endothelial cells by voltage- and current-clamp techniques. H2O2 elicited both hyperpolarization and depolarization of the membrane potential in a concentration-dependent manner. Low H2O2 concentrations (0.01 to 0.25 micromol/L) inhibited the inward-rectifying K+ current (KIR). Whole-cell K+ current analysis revealed that H2O2 (1 mmol/L) applied to the bath solution increased the Ca2+-dependent K+ current (KCa) amplitude. H2O2 increased KCa current in outside-out patches in a Ca2+-free solution. When catalase (5000 micro/mL) was added to the bath solution, the outward-rectifying K+ current amplitude was restored. In contrast, superoxide dismutase (1000 u/mL) had only a small effect on the H2O2-induced K+ current changes. Next, we measured whole-cell K+ currents and redox potentials simultaneously with a novel redox potential-sensitive electrode. The H2O2-mediated KCa current increase was accompanied by a whole-cell redox potential decrease. CONCLUSIONS: H2O2 elicited both hyperpolarization and depolarization of the membrane potential through 2 different mechanisms. Low H2O2 concentrations inhibited inward-rectifying K+ currents, whereas higher H2O2 concentrations increased the amplitude of the outward K+ current. We suggest that reactive oxygen species generated locally increases the KCa current amplitude, whereas low H2O2 concentrations inhibit KIR via intracellular messengers.

Calcium↗
PubMed2006

Phase-locking of hippocampal interneurons' membrane potential to neocortical up-down states.

During quiet wakefulness and sleep, and under anesthesia, the membrane potentials of neocortical pyramidal neurons show synchronous, slow oscillations, so-called up-down states (UDS), that can be detected in the local field potential (LFP). The influence of this synchronized, spontaneous neocortical activity on the hippocampus is largely unknown. We performed the first in vivo whole-cell recordings from hippocampal dorsal CA1 interneurons and found that their membrane potentials were phase-locked to neocortical up-down states with a small delay. These results provide strong evidence for cortico-hippocampal interaction and suggest that neocortical activity drives hippocampal interneurons during UDS.

Action Potentials↗
PubMed1992

Effect of diclofop on the membrane potentials of herbicide-resistant and -susceptible annual ryegrass root tips.

Electrophysiological measurements were made on root tip cells in the elongation zone of diclofop-methyl-resistant (SR4/84) and -susceptible (SRS2) biotypes of annual ryegrass (Lolium rigidum Gaud.) from Australia. The phytotoxic action of diclofop-methyl (methyl 2-[4-(2',4'-dichlorophenoxy)phenoxy]propanoate) on susceptible whole plants was completely reversed by a simultaneous application of 2,4-dichlorophenoxyacetic acid (dimethylamine salt). The phytotoxic acid metabolite, diclofop (50 micromolar), depolarized membrane potentials of both biotypes to a steady-state level within 10 to 15 minutes. Repolarization of the membrane potential occurred only in the resistant biotype following removal of diclofop. The resistant biotype has an intrinsic ability to reestablish the electrogenic membrane potential, whereas the susceptible biotype required an exogeneous source of IAA to induce partial repolarization. Both biotypes were susceptible to depolarization by carbonylcyanide-m-chlorophenylhy-drazone (CCCP), and their membrane potentials recovered upon removal of CCCP. A 15-minute pretreatment with p-chloromercuribenzenesulphonic acid (PCMBS) blocked the depolarizing action of diclofop in both biotypes. However, PCMBS had no effect on the activity of CCCP. The action of diclofop appears to involve a site-specific interaction at the plasmalemma in both Lolium biotypes to cause the increased influx of protons into sensitive cells. The differential response of membrane depolarization and repolarization to diclofop treatment may be a significant initial reaction in the eventual phytotoxic action of the herbicide.

Journal Article↗
PubMed1998

Intramitochondrial [Ca2+] and membrane potential in ventricular myocytes exposed to anoxia-reoxygenation.

The aim of this study was to investigate the role of mitochondrial ionic homeostasis in promoting reoxygenation-induced hypercontracture in cardiac muscle. Mitochondrial membrane potential and intramitochondrial Ca2+ concentration ([Ca2+]) were measured using confocal imaging in guinea pig ventricular myocytes exposed to anoxia and reoxygenation. Anoxia produced a variable, but often profound, mitochondrial depolarization. Some cells mounted a recovery of their mitochondrial membrane potential during reoxygenation; the depolarization was sustained in other cells. Recovery of the mitochondrial membrane potential seemed essential to avoid reoxygenation-induced hypercontracture. Reoxygenation also caused a sizable elevation in intramitochondrial [Ca2+], the amplitude of which was correlated with the likelihood of a cell undergoing hypercontracture. A sustained Ca2+ load analogous to that seen during reoxygenation was imposed on cardiac mitochondria through permeabilization of the plasma membrane. Elevation of intracellular [Ca2+] to 800 nM caused a substantial mitochondrial depolarization. We propose that the conditions seen in guinea pig ventricular myocytes during reoxygenation are well suited to produce Ca2+-dependent mitochondrial depolarization, which may play a significant role in promoting irreversible cell injury.

Animals↗
PubMedDate not supplied

Altered membrane properties of cerebral vascular smooth muscle following subarachnoid hemorrhage: an electrophysiological study. I. Changes in resting membrane potential (Em) and effect on the electrogenic pump potential contribution to Em.

Subarachnoid hemorrhage was produced experimentally in cats by intracisternal injection of non-heparinized autologous arterial blood obtained by cardiac puncture under ketamine and xylazine anesthesia. Cats were sacrificed at varying time intervals between 30 min and 7 days post ictus. Measurements of resting membrane potential were recorded from smooth muscle cells of the basilar artery. These measurements were obtained by impalement from the adventitial surface of isolated but otherwise intact segments of the artery using glass microelectrodes with tip sizes less than 0.1 micron. The resting membrane potential recorded in vitro from animals previously subjected to subarachnoid hemorrhage in vivo was consistently and significantly depolarized when compared to normal controls. This depolarization was present as early as 30 min post ictus. Addition of the cardiac glycoside, ouabain, in a concentration of 10(-5)M depolarized cells from both control and experimental animals. There is a significant electrogenic pump potential contribution to the resting membrane potential of vascular smooth muscle cells. Ouabain is a potent blocker of Na+, K+-ATPase, the enzyme responsible for maintaining the cation electrochemical gradients. The depolarization recorded in these cells following subarachnoid hemorrhage is not, therefore, due to impairment of the electrogenic pump. The significance and implications of these findings are discussed.

Animals↗
PubMed1987

Alterations in hepatic membrane potentials in vivo during early and late sepsis.

To determine whether alterations in hepatocyte membrane electrical responses might play a role in glucose dyshomeostasis during sepsis, hepatocyte membrane potentials were measured in vivo in rats made septic by cecal ligation and puncture (CLP). In both early-septic (8-10 hr after CLP) and late-septic (18-20 hr after CLP) rats, resting hepatocyte membrane potentials were significantly depressed compared to those in sham-operated rats. In addition, the hyperpolarization response to glucagon administration in vivo which was observed in the sham-operated rats was significantly attenuated in both early- and late-sepsis rats. To determine whether this blunted hyperpolarization response was related to defects in stimulation of gluconeogenesis, livers from sham-operated and early-sepsis rats were isolated and perfused. The livers from sham-operated rats responded to 1 nM glucagon by increasing glucose release by 53%, while those from septic rats increased by only 20%. These results suggest that a defect associated with the plasma membrane may be an early event in the development of glucose dyshomeostasis during sepsis.

Animals↗
PubMed1993

Membrane potential oscillations and corticothalamic connectivity in rat associational thalamic neurons in vitro.

Thalamic relay neurons were recorded from the dorsolateral and lateroposterior nuclei of the rat thalamus in a superfused explant preparation. The mean membrane potential of these cells was -67 +/- 7 mV, input resistance 114 +/- 31 M omega and spike amplitude 75 +/- 6 mV. Low-threshold slow membrane potential oscillations (1-4 Hz) were present in about 46% of the neurons. They occurred either spontaneously or following a membrane potential perturbation. In a subpopulation of cells, we also observed a high-threshold membrane oscillation when cells were depolarized above -45 mV. This oscillation consisted of bursts of low-amplitude spikes interrupted by rhythmic after-hyperpolarizations. Stimulation of the corticothalamic pathway elicited prolonged inhibitory postsynaptic potentials in associational thalamic neurons. In the presence of picrotoxin, corticothalamic input evoked prominent excitatory postsynaptic responses that showed marked short-term synaptic plasticity. Our results suggest that associational thalamic neurons maintained in vitro have a strong tendency to exhibit membrane oscillations. In addition, they receive a direct excitatory cortical input that remained functional in explant preparation.

Animals↗
PubMed2001

Mitochondrial membrane potential in density-separated trout erythrocytes exposed to oxidative stress in vitro.

Previous literature reports have demonstrated that nucleated trout erythrocytes in condition of oxidative stress are subjected to DNA and membrane damage, and inactivation of glutathione peroxidase. The present study was undertaken to investigate if mitochondrial membrane potential in stressed conditions was also influenced. Density-separated trout erythrocyte fractions, obtained using a discontinuous Percoll gradient, were submitted to stress conditions and the mitochondrial membrane potential was determined by means of cytofluorimetric analysis after incubation of each subfraction with JC-1, a mitochondrial specific fluorescent probe. The results clearly show that the mitochondrial membrane potential decreased significantly in all erythrocyte fractions, also if the oxidative effect on mitochondria is more severe with increased density (age) of the cell. Ebselen was very effective in preventing mitochondrial depolarization in young as well as in old erythrocytes.

Animals↗
PubMed1972

Ionic basis of membrane potentials of epithelial cells in rat small intestine.

1. Potentials across the mucosal and serosal membranes of the epithelial cells of rat jejunum together with transmural potentials were recorded using everted sac preparations.2. Ionic changes in either mucosal or serosal fluids affect mucosal or serosal membrane potentials respectively with comparable changes in the transmural potential. The contralateral membrane potential is relatively unaffected.3. Replacement of mucosal sodium chloride by potassium chloride or lithium chloride had little effect on potentials, but its replacement by mannitol or Tris chloride increased the negativity of the mucosal potential, giving linear relationships against log(10)[Na](m) with slopes of 41.4 and 30.7 mV respectively for tenfold change in [Na](m).4. At constant [Na](m), potassium or lithium increased the mucosal potential by 25.7 and 19.8 mV respectively for tenfold concentration changes.5. Qualitatively similar changes occurred in the serosal potential when the ionic composition of the serosal fluid was varied.6. Mucosal potential changes in response to modifications of the ionic composition of the mucosal fluid were the same in the presence and absence of galactose.7. Sodium and potassium diffusion potentials largely determine both the mucosal and serosal membrane potentials. For the mucosal membrane, P(K):P(Na) is 1.26:1, and is probably higher for the serosal membrane. Chloride makes no significant contribution to membrane potentials.8. Potentials generated by the electrogenic sodium pump are superimposed on diffusion potentials across the serosal membrane.

Animals↗
PubMed1996

Membrane potential regulates sea urchin sperm adenylylcyclase.

Adenylylcyclase (AC) from sea urchin sperm does not appear to be regulated by G proteins [Hildebrandt, J. D., Tash, J. S., Kirchick, H. J., Lipschunits, L., Secra, R. D., & Birmbaumer, L. (1985) Endocrinology 116, 1357-1366]. During sperm activation and the acrosome reaction, membrane potential changes and cAMP increases. Here we explore if membrane potential can modulate the sperm AC. Hyperpolarization of Lytechinus pictus sea urchin sperm either with valinomycin in artificial sea water (ASW) without K+ or with dilution in ASW without Na+ increased the [c-AMP] (2.2- and 5.8-fold, respectively). This increase also occurred in the absence of extracellular Ca2+ (1.9- and 3.1-fold, respectively) and was enhanced by 100 microM IBMX, a phosphodiesterase inhibitor. It has been suggested that sea urchin sperm AC is stimulated by increases in intracellular Ca2+ and intracellular pH. In ASW without Na+ and Ca2+ (0Na0CaASW), sea urchin sperm intracellular pH decreases, and intracellular Ca2+ cannot increase. Therefore, these observations taken together indicate that AC in these cells in modulated by membrane potential. Dilution of Strogylocentrotus purpuratus sperm in 0Na0CaASW hyperpolarized them and increased their cAMP levels (1.3-fold). This stimulation was enhanced by IBMX (1.6-fold). Addition of the egg peptide speract under this condition further hyperpolarized S. purpuratus sperm and synergistically increased [cAMP] above 0Na0CaASW. This stimulation became larger in the presence of IBMX (from 1.6- to 5.2-fold). Since speract cannot elevate intracellular pH or [Ca2+] in 0Na0CaASW, the increase in [cAMP] it causes must be due to sperm hyperpolarization.

1-Methyl-3-isobutylxanthine↗
PubMed2001

UCP2 muscle gene transfer modifies mitochondrial membrane potential.

OBJECTIVE: The aim of this work was to evaluate the effect of uncoupling protein 2 (UCP2) muscle gene transfer on mitochondrial activity. DESIGN: Five week-old male Wistar rats received an intramuscular injection of plasmid pXU1 containing UCP2 cDNA in the right tibialis anterior muscles. Left tibialis anterior muscles were injected with vehicle as control. Ten days after DNA injection, tibialis anterior muscles were dissected and muscle mitochondria isolated and analyzed. RESULTS: There were two mitochondrial populations in the muscle after UCP2 gene transfer, one of low fluorescence and complexity and the other, showing high fluorescence and complexity. UCP2 gene transfer resulted in a 3.6 fold increase in muscle UCP2 protein levels compared to control muscles assessed by Western blotting. Furthermore, a significant reduction in mitochondria membrane potential assessed by spectrofluorometry and flow cytometry was observed. The mitochondria membrane potential reduction might account for a decrease in fluorescence of the low fluorescence mitochondrial subpopulation. CONCLUSION: It has been demonstrated that UCP2 muscle gene transfer in vivo is associated with a lower mitochondria membrane potential. Our results suggest the potential involvement of UCP2 in uncoupling respiration. International Journal of Obesity (2001) 25, 68-74

Animals↗
PubMed1979

Cellular energy metabolism, trans-plasma and trans-mitochondrial membrane potentials, and pH gradients in mouse neuroblastoma.

A method for quantitative evaluation of transmembrane electrical potential and pH gradients across a subcellular compartment in an intact cell is presented. This approach has been applied in studies of mouse neuroblastoma C-1300 clone NB41A3, in which the transmembrane electrical potential and pH gradients and the mitochondrial volume percent have been determined. Membrane potentials and pH gradients were measured by two different methods. Equilibrium distributions of [(3)H]triphenylmethyl phosphonium and [(14)C]-thiocyanate ions gave calculated apparent membrane potentials of -77.0 and -29.6 mV, respectively, at 20-25 degrees C; a value of -60.8 mV was obtained from microelectrode measurements. Equilibrium distributions of weak acids ([(14)C]trimethylacetic acid and 5,5-di[(14)C]methyl-2,4-oxazolidine-dione) and of weak bases ([(14)C]dimethylamine and [(14)C]trimethylamine) gave calculated upper and lower limits of the pH gradient (Delta pH = pH(e) - pH(i)) of -0.14 and -0.21 pH unit, respectively. The microelectrode measurements showed that the intracellular pH is within 0.1 of a pH unit or less of the extracellular pH over the extracellular pH range of 7.35-6.85. The mitochondrial volume percent calculated on the basis of the measured cytochrome c content is 5.6 +/- 1.2% and compares well with estimates of 5.4 +/- 1.1% obtained from 25 electron micrographs. Measurements of the cellular energetic parameters gave values within the range found in other cells and perfused organs. Comparison of the results of the microelectrode and equilibrium measurements permits estimates of the electrical potential and pH gradients across the mitochondrial membrane (mitochondria-to-cytoplasm gradients) to be made and suggests that the trans-mitochondrial membrane protonmotive force in the intact cell cannot be greater than -143 mV.

Animals↗
PubMed1971

The effect of potassium and chloride ions on the volume and membrane potential of single barnacle muscle cells.

1. In single barnacle skeletal muscle cells cell diameter has been measured as a function of external osmolality, and cell diameter and membrane potential have been measured during changes of external K and Cl concentrations ([K](o) and [Cl](o)) like those described in frog muscle by Hodgkin & Horowicz (1959). The diameter was monitored microscopically with a precision of 0.2-0.4% (S.D.). [K](o) was varied from 1 to 18 mM, a range of concentrations which does not cause contracture.2. At pH 8.0 the Cl permeability was so low that net KCl and water movements were absent. Such net movements were present at pH 4.5, corresponding to a change in the ratio (Cl conductance/K conductance) from approximately 1/12 at pH 8.0 to 1/2 at pH 4.5.3. Characteristically long time constants were observed for membrane potential responses to a change in [K](o) and/or [Cl](o), even at constant [K](o).[Cl](o). This phenomenon is attributed to a delayed equilibration by diffusion within the system of sarcolemmal invaginations and T-tubules. The delay in the response was increased by introducing polyvinylpyrrolidone (PVP) into this system, presumably because PVP raises intratubular viscosity.4. At pH 4.5 anomalous rectification for net movements of K was demonstrated by measurements of cell diameter and of membrane potential.

Animals↗
PubMedDate not supplied

[Ca 2+ outflow from sarcoplasmic reticulum vesicles during changes in membrane potential, Ca2+ concentration and pH].

The concentration gradient Ca2+ outflux from the vesicles of the fragmented sarcoplasmic reticulum of rabbit skeletal muscles has been studied under conditions of the induced membrane potential, the concentrations of Ca2+ and H+ in the medium washing over the vesicles being different. The Ca2+ outflux from vesicles is shown to be the same with a decrease of the membrane potential from--80 down to -10 mV and gets higher with the zero and subsequent positive values of the latter. A significant intensification of the Ca2+ outflux from vesicles under the effect of external-vesicular Ca2+ has been observed at its concentration of 10(-5) M. Against this background of external-vesicular Ca2+ and zero value of the membrane potential either exogenous AMP or the pH increase from 6.5 up to 7.8 favour a release of more than 70% of passively accumulated Ca2+. The pH effect grows with a decrease in the external-vesicular concentration of Ca2+. A conclusion is drawn on the significance of protons in the regulation of the Ca2+ release from the sarcoplasmic reticulum.

Adenosine Monophosphate↗