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PubMed2001

Simulating the spread of membrane potential changes in arteriolar networks.

OBJECTIVE: Our aim was to simulate the spread of membrane potential changes in microvascular trees and then make the simulation programs accessible to other researchers. We have applied our simulations to demonstrate the implications of electrical coupling between arteriolar smooth muscle and endothelium. METHODS: A two-layered, cable-like model of an arteriole was used, and the assumptions involved in the approach explicitly stated. Several common experimental situations that involve the passive spread of membrane potential changes in microvascular trees were simulated. The calculations were performed using NEURON, a well-established computer simulation program that we have modified for use with vascular trees. RESULTS: Simulated results show that membrane potential changes would probably not spread as far in the endothelium as they would in the smooth muscle of arterioles. Where feed arteries are connected to larger distributing arteries, passive spread alone may not explain the physiologically observed spread of diameter changes. CONCLUSIONS: Simulated results suggest that the morphology of an arteriole, in which the muscle layer is much thicker than the endothelium, favors electrical conduction along smooth muscle rather than the endothelium. However, it seems that passive electrical spread is insufficient to explain the apparent spread of membrane potential changes in experimental situations. Active responses involving voltage-dependent conductances may be involved, and these can also be included in our simulation.

Animals↗
PubMed1980

The effects of digoxin on resting membrane potentials of skeletal muscles in dystrophic mice.

To clarify the abnormality of skeletal muscles in dystrophic mice, we studied the potassium content, resting membrane potential and especially the effects of digoxin on the membrane potential. Both the potassium content and the resting membrane potential of dystrophic muscles were significantly lower than those of normal mice. The resting membrane potential of dystrophic muscles was less reduced by digoxin than that of normal mice. It was suggested that there was a change in membrane permeability of skeletal muscles in dystrophic mice and that membrane permeability was less sensitive to digoxin than normal mice.

Animals↗
PubMed1983

Sleep-related variations of membrane potential in the lateral geniculate body relay neurons of the cat.

Membrane potential of lateral geniculate body relay neurons was monitored in chronic cats during the sleep-waking cycle. Neurons were tonically depolarized throughout paradoxical (P) sleep and the maximal level of polarization occurred during slow (S) sleep (mean difference of membrane potential between S and P sleep: + 10.2 +/- 1.3 mV, n = 6, range: 8-12 mV). Some features of the spontaneous activity of S and P sleep are briefly discussed in relation to the level of membrane potential. In particular it is suggested that the phasic depolarizations underlying the bursts of action potentials during S sleep, and which are reproduced retinal cell axons impinging upon the hyperpolarized membrane.

Animals↗
PubMed1999

Redistribution of cytochrome c precedes the caspase-dependent formation of ultracondensed mitochondria, with a reduced inner membrane potential, in apoptotic monocytes.

Apoptosis was induced in human monocytic THP.1 cells by the use of chemicals with disparate mechanisms of action. Apoptotic cells were characterized by a reduced inner mitochondrial membrane potential, increased cytosolic cytochrome c, ultracondensed mitochondria, condensed chromatin, cytoplasmic inclusions of beta-actin, and fragmentation of the Golgi apparatus. All of these changes, except the release of cytochrome c, were prevented by caspase inhibition. Cells were separated into two populations, with either normal or low inner mitochondrial membrane potential, using fluorescence-activated cell sorting. Ultracondensed mitochondria were observed only in the cells with low inner mitochondrial membrane potential, whereas noncondensed mitochondria were found in the cells with a normal inner mitochondrial membrane potential. We have demonstrated a sequence of related biochemical and ultrastructural changes, commencing with the release of mitochondrial cytochrome c, followed by activation of caspases and a reduction of inner mitochondrial membrane potential. These changes involved the formation of ultracondensed but not swollen mitochondria. Thus the release of mitochondrial cytochrome c was not the result of the mitochondrial permeability transition, reduction of inner mitochondrial membrane potential, or rupture of the outer mitochondrial membrane. Discontinuities in the outer membrane of ultracondensed mitochondria may, however, facilitate the further release of caspase-activating proteins, thereby amplifying the apoptotic process.

Actins↗
PubMed1982

The use of fluorescent dyes to measure membrane potentials: a critique.

Under controlled conditions, fluorescent cyanine dyes can be used to measure membrane potentials of cell suspensions. Similar changes in membrane potential can be followed both with fluorescent dyes and electrophysiological probes in response to changes in the ion composition of the medium. Recent reports that attempt to abrogate the use of the cyanine dyes in measurements of the membrane potential are misleading.

Adenosine Triphosphate↗
PubMed1996

Heat-induced changes in intracellular sodium and membrane potential: lack of a role in cell killing and thermotolerance.

Hyperthermia induces transient changes in intracellular free sodium levels and membrane potential. The possible role of these changes in cell killing by hyperthermia and thermotolerance has been evaluated using Chinese hamster ovary IS1 and HeLa cells. Intracellular sodium was measured with Sodium Green and SBFI, while membrane potential was measured with the oxonol dye diBAC4(3). Heating at either 42.0 or 45.0 degrees C caused nearly the same decrease in free [Na+]i from about 20 mM in unheated cells to 5-7 mM in heated cells. However, survival differed by over two orders of magnitude after heating for 30 min at these two temperatures. In addition, blockage of the heat-induced decrease in [Na+]i using ouabain and/or amiloride did not affect the survival curves for heated cells. Hyperthermia also induced a membrane hyperpolarization of 15 mV after 15 min at 42.0 degrees C or 35 mV after 15 min at 45.0 degrees C which could be blocked with ouabain and amiloride. Both the free [Na+]i and membrane potential recovered to near baseline levels within 30-40 min after heating. Induction of thermotolerance using a 45.0 degrees C, 10-min heat treatment also was not affected by ouabain and/or amiloride. Finally, thermotolerant cells experienced the same heat-induced changes in free [Na+]i and membrane potential as non-thermotolerant cells. We conclude that the heat-induced changes in free [Na+]i and membrane potential are not directly related to cell killing by hyperthermia or thermotolerance.

Amiloride↗
PubMed1996

Kinetic study of the plasma-membrane potential in procyclic and bloodstream forms of Trypanosoma brucei brucei using the fluorescent probe bisoxonol.

The characteristics of the plasma-membrane potential of procyclic and bloodstream forms of Trypanosoma brucei brucei (cultured cells) were investigated using the fluorescent anionic probe bisoxonol. Observation of a stable and representative plasma-membrane potential in the resting state required careful washing, centrifugation and maintenance of the cells at room temperature before measurement. Bloodstream forms were more prone to depolarization during washing at 4 degrees C than procyclic cells. The higher fluorescence observed in the presence of long slender cells than in the presence of procyclic cells shows that the plasma-membrane potential is more negative in the insect form. Healthy dilute cells can sustain their plasma-membrane potential for hours in the presence of external glucose. The presence of a high K+ concentration in the medium did not promote by itself the depolarization of either type of cell. Study of bisoxonol fluorescence as a function of time allowed us to follow the kinetics of the action of metabolic inhibitors in the presence of various ions. o-Vanadate (1 mM) was found to depolarize bloodstream-form cells rapidly but only in a phosphate-free NaCl buffer. Omeprazole and strophanthidin also specifically depolarized bloodstream-form trypanosomes. However, NN'-dicyclohexylcarbodi-imide depolarized both types of cell, but more rapidly for bloodstream-form cells. Bloodstream-form trypanosomes appear to use mainly a vanadate-sensitive Na+ pump to maintain their Na+-diffusion gradient. However, most of the ATPase inhibitors tested had little or no effect on the plasma-membrane potential of procyclics suggesting that this form of trypanosome may rely on several regulation mechanisms.

Animals↗
PubMed1996

Effects of density and gating of delayed-rectifier potassium channels on resting membrane potential and its fluctuations.

The aim of this study is to evaluate directly, using a reduced experimental system, the nature of interactions between voltage-gated potassium channels and the resting membrane potential. Xenopus oocytes were injected with various concentrations of cRNA coding for a delayed-rectifier potassium channel Shaker-IR. The effects of the density and kinetics of the expressed channels on resting membrane potential is explored in isolated ("inside-out") patches. The channel density is given in terms of maximal conductance (Gmax), measured from the maximal slope of the I-V curve under voltage clamp conditions. The capacitance of the experimental setup is approximately 1 pF. At high channel densities (Gmax > 10 pA/mV) the mean membrane potential is stabilized at approximately -60 mV. This resting membrane potential is more than 35 mV positive to the reversal potential for potassium ions under the same experimental conditions. Analyses of voltage clamp experiments indicate that at high channel densities the mean membrane potential is determined by the rates of channel activation and deactivation, but is not affected by the rates involved in the process of slow (C-type) inactivation. In contrast, at lower channel densities membrane potential is very unstable, and its mean value and amplitude of fluctuations are strongly affected by the process of slow (C-type) inactivation.

Animals↗
PubMed1978

Ionic effects on the membrane potential of hyperpolarizing photoreceptors in scallop retina.

1. The effects of different external ionic conditions and of metabolic inhibitors on the membrane potential of hyperpolarizing photoreceptors in the retina of the scallop Pecten irradians were examined in the presence and absence of light.2. Changes in extracellular K(+) have a greater effect on membrane potential in the light than in darkness. The receptor potential is increased in amplitude when [K](o) is reduced and decreased when [K](o) is elevated. It is hyperpolarizing when [K](o) is less than the estimated value for [K](i) and depolarizing when this condition is reversed.3. The complete replacement of [Na](o) causes a significant hyperpolarization of membrane potential in darkness, whereas it has a much smaller hyperpolarizing effect on the peak of the receptor potential.4. The ratio of Na(+) to K(+) permeabilities (P(Na)/P(K)) decreases during bright illumination. Our results suggest that P(K) is seven times that for P(Na) in the dark but is 57 times greater than P(Na) in light.5. The metabolic inhibitors DNP and NaCN cause membrane potential in the dark to hyperpolarize. This hyperpolarization is associated with a decrease in the P(Na)/P(K) ratio similar to that found during illumination.6. High [Ca(+)](o) also causes membrane potential in the dark to hyperpolarize. This hyperpolarization is associated with an increase in membrane conductance.7. The results indicate that the hyperpolarizing receptor potential of the distal photoreceptor is produced by a light-evoked increase in K(+) permeability.

Animals↗
PubMed1986

Pyronin G as a fluorescent probe for quantitative determination of the membrane potential of mitochondria.

Added to mitochondrial suspension, pyronin G changes the intensity of its fluorescence depending on the membrane potential (energy state) of the mitochondria. The mechanism of this effect is studied and a dependence is obtained between the membrane potential and the fluorescence intensity. This permits quantitative determination of the membrane potential by the changes in the fluorescence of the suspension. A method is proposed for measuring the membrane potential of vesicles in the -120 to -220 mV interval.

Animals↗
PubMed1985

Effects of probes of membrane potential on metabolism in synaptosomes.

Effects of three probes for measuring membrane potential, tetraphenylphosphonium (TPP+), rhodamine 6G and 3,3'-dipropylthiocarbocyanine (diS-C3-(5)) on energy metabolism in synaptosomes were investigated. None of the three probes had any effect on lactate production in synaptosomes. TPP+ and rhodamine 6G did not inhibit the respiration of synaptosomes with pyruvate and succinate as exogenous substrate and were only weakly inhibitory with endogenous substrates. In contrast, diS-C3-(5) markedly inhibited the respiration of synaptosomes with glucose, pyruvate and endogenous substrates. All three probes reduced ATP content in synaptosomes and depolarized the membrane potential in synaptosomes with increasing concentrations of the probes. It is, therefore, preferable to estimate membrane potential with TPP+ or rhodamine 6G at their low concentrations where their effect on metabolism is negligible.

Adenosine Triphosphate↗
PubMed1985

Mitochondrial and plasma membrane potentials cause unusual accumulation and retention of rhodamine 123 by human breast adenocarcinoma-derived MCF-7 cells.

Quantitative studies of MCF-7 cells (derived from human breast adenocarcinoma) and CV-1 cells (from normal African green monkey kidney epithelium), using the permeant cationic compound tetraphenylphosphonium (TPP), in conjunction with fluorescence microscopy using rhodamine 123 (Rh123), indicate that the mitochondrial and plasma membrane potentials affect both uptake and retention of these compounds. Under conditions that depolarize the plasma membrane, uptake and retention of TPP and Rh123, driven only by the mitochondrial membrane potential, is greater in MCF-7 than in CV-1. An ionophore that dissipates the mitochondrial membrane potential of MCF-7 cells causes them to resemble CV-1 cells by decreasing uptake and retention. Hyperpolarizing the mitochondrial membrane of CV-1 increases accumulation and prolongs retention; hyperpolarization of the plasma membrane further heightens this effect, causing the uptake of CV-1 cells to resemble that of MCF-7 cells even more closely. The greater uptake and retention by MCF-7 appears to be a consequence of elevated mitochondrial and plasma membrane potentials. The plasma membrane potential affects mitochondrial retention of TPP and Rh123 and its role in enhancing the effect of a difference in mitochondrial membrane potential is explained.

Adenocarcinoma↗
PubMed1989

Mechanisms and significance of calcium entry at positive membrane potentials in guinea-pig ventricular muscle cells.

Possible mechanisms for calcium entry at positive membrane potentials were investigated in single cells isolated from guinea-pig ventricular muscle. The cells were voltage clamped and contraction was measured by an optical technique. When prolonged (200 ms to 2 s) depolarizations at +60 mV were applied, contraction amplitude increased with pulse duration, in contrast to the contraction at 0 mV. When a 'pre-pulse' to 0 mV was applied for 200 ms to inactivate current through 'L-type' calcium channels, contraction nevertheless increased with membrane potential during a subsequent test pulse applied over the range -40 to +60 mV. Contraction during the test pulse at +60 mV was abolished when extracellular calcium was reduced to zero. This effect developed more rapidly than abolition of the contraction in response to the pre-pulse to 0 mV. Reduction of extracellular calcium from 2.5 to 1 mM reduced the contraction at +60 mV to a greater extent than that at 0 mV and caused an inward shift in the current at +60 mV. Nifedipine (5 microM) substantially reduced the contraction during the test pulse to 0 mV but had little effect on the contraction at +60 mV. Conversely, dodecylamine (20 microM) caused little or no decrease in the contraction at 0 mV but substantially reduced the contraction at +60 mV. Following a conditioning pre-pulse to 0 mV the contraction at +60 mV was not consistently reduced by exposure to 3 microM-ryanodine. The interpolation of a single 200 ms pulse to +60 mV in a train of pulses to 0 mV potentiated the following contraction to 0 mV. This potentiation decayed over the first four steps to 0 mV following an interpolated pulse and increased with the voltage of the interpolated pulse over the range -20 to +60 mV. Potentiation was abolished on exposure to 3 microM-ryanodine. These observations are consistent with entry of calcium at positive membrane potentials through voltage-dependent, non-inactivating pathways which are insensitive to nifedipine but inhibited by dodecylamine. The observations support the hypothesis that calcium entry via this mechanism may contribute, at least under some conditions, to the loading of intracellular stores of calcium during the late plateau of the action potential, and thus influence subsequent contraction. Calcium entry through Na+-Ca2+ exchange is a possibility which would allow calcium entry to increase over the range of membrane potentials at which contraction was increased. However, additional calcium entry through other nifedipine-insensitive pathways, such as calcium-activated non-selective channels, cannot be excluded.

Amines↗
PubMed2006

Effect of solanine on the membrane potential of mitochondria in HepG2 cells and [Ca2+]i in the cells.

AIM: To observe the effect of solanine on the membrane potential of mitochondria in HepG(2) cells and [Ca(2+)](i) in the cells, and to uncover the mechanism by which solanine induces apoptosis. METHODS: HepG(2) cells were double stained with AO/EB, and morphological changes of the cells were observed using laser confocal scanning microscopy (LCSM). HepG(2) cells were stained with TMRE, and change in the membrane potential of mitochondria in the cells were observed using LCSM. HepG(2) cells were double stained with Fluo-3/AM, and change of [Ca(2+)](i) in the cells were observed using LCSM. HepG(2) cells were double stained with TMRE and Fluo-3/AM, and both the change in membrane potential of mitochondria and that of [Ca(2+)](i) in the cells were observed using LCSM. RESULTS: Cells in treated groups showed typical signs of apoptosis. Staining with TMRE showed that solanine could lower membrane potential; staining with Fluo-3/AM showed that solanine could increase the concentration of Ca(2+) in tumor cells; and those of double staining with TMRE and Fluo-3/AM showed that solanine could increase the concentration of Ca(2+) in the cells at the same time as it lowered the membrane potential of mitochondria. CONCLUSION: Solanine opens up the PT channels in the membrane by lowering the membrane po-tential, leading to Ca(2+) being transported down its concentration gradient, which in turn leads to the rise of the concentration of Ca(2+) in the cell, turning on the mechanism for apoptosis.

Apoptosis↗
PubMed1988

Effects of Cl- deficiency on the membrane potential in mouse pancreatic beta-cells.

The membrane potential of mouse pancreatic beta-cells was measured with microelectrodes. In the resting cell (3 mM D-glucose), the membrane potential was -63 +/- 3 mV (mean +/- S.E. for four experiments). In the presence of 3 mM D-glucose, total Cl- substitution by isethionate induced a depolarization by 3-4 mV, and readmission of Cl- induced a hyperpolarization by 3-5 mV. At 10 mM glucose, reduction of Cl- to 12 mM by substituting isethionate for Cl- reversibly shifted the repolarization potential by 6-9 mV in the positive direction and stimulated the burst activity during the initial 2-3 min by increasing the fraction of plateau phase. This was followed by a gradual inhibition of electrical activity, including decrease in fraction of plateau phase and slow wave amplitude. Total substitution of Cl- by isethionate or methyl sulphate reversibly shifted the repolarization potential by 3-4 mV in the positive direction and rapidly inhibited the electrical burst pattern without any initial stimulation. Glucose-induced (10 mM) insulin release (15 min) and 45Ca2+ uptake (3 min) were strongly inhibited by reducing the Cl- concentration to 10 mM (isethionate as substitute) and were further inhibited by further reduction of the Cl- concentration. It is suggested that beta-cells are equipped with on electrogenic Cl- flux, which can affect the burst pattern of electrical activity. The inhibitory effects of Cl- substitution may be explained by an influence of Cl- on the voltage-controlled Ca2+ channels.

Animals↗
PubMed1987

Further analysis of spontaneous membrane potential activity and the hyperpolarizing response to parathyroid hormone in osteoblastlike cells.

Whole cell voltage clamp measurements using the patch technique on well-attached and well-spread cells of an osteoblastlike line (ROS 17/2.8) show the same spontaneous membrane potential activity as measurements with inserted microelectrodes. Furthermore, membrane potential measurements during the first 80 milliseconds (ms) following microelectrode penetration of the cell membrane usually show no decay. There is also good agreement between values of cell membrane resistance obtained by the microelectrode technique, the whole cell patch clamp technique, and the single channel patch clamp technique. These results indicate that our microelectrode measurements are not dominated by leak-induced artifacts, and that the spontaneous membrane potential activity is not induced by Ca2+ leakage around the microelectrode. The spontaneous membrane potential activity is eliminated in the presence of the Ca2+ ionophore A23187, also in serum-free medium, and by K+ and Ca2+ channel blockers, but it is not affected by the hyperpolarizing responses to parathyroid hormone (PTH) and dibutyryl cAMP, which persist under all of these conditions. These results support the hypothesis that the spontaneous membrane potential activity is related to repeated fluctuations of internal [Ca2+] and that such fluctuations result from a feedback loop involving Ca2+ channels or Ca2+ pumps in the cell membrane.

Animals↗