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PubMed1999

Effects of bicarbonate ion on chick retinal pigment epithelium: membrane potentials and light-evoked responses.

The purpose of this study was to determine how changes in [HCO3-] alter the electrical properties of the retinal pigment epithelium (RPE). Experiments were conducted on the isolated chick retina-RPE-choroid preparation. The chamber holding the preparation allowed independent perfusion of the retinal and the choroidal surfaces. The light-evoked trans-tissue potential (TTP), the trans-epithelial potential (TEP), the trans-retinal potentials, and the intracellularly-recorded apical and basal membrane potentials were studied. Increasing the [HCO3-]0 in the choroidal bath from 25 to 40 mEq/1 led to an increase in the TTP and TEP. The same change in the retinal bath decreased the TTP because of a biphasic change of the RPE membrane potentials. There was also an increase in the amplitudes of the TEP, the c-wave and the slow PIII. The light-evoked subretinal K+ decrease was greater which is consistent with an increase in the photoreceptor light response. These observations indicated that the decrease of TTP resulted from a basal membrane hyperpolarization followed by an apical membrane depolarization induced by an increase in retinal [HCO3-]0. The relationship of these potential changes to the human bicarbonate responses is discussed.

Animals↗
PubMed1977

The effect of the CO2/HCO3- buffer system on the membrane potential of frog skeletal muscle.

1. The membrane potential of frog skeletal muscle was measured in various solutions, in the presence and in the absence of the CO2/HCO3- buffer. 2. The CO2/HCO3- buffer (PCO2 = 38-593 mm Hg; [HCO3-] = 5-25 mM/1) generally induced a reversible depolarization. 3. In the presence of C1-, there was a slowly developing but marked depolarization. 4. In the absence of C1-, there was an early depolarization which increased in high-PCO2 or low-K+ solutions, and decreased in low-PCO2, high-K+ or Na+-free solutions. Changing the HCO3- concentration did not modify the depolarization. 5. The early depolarization and contractions observed in C1--free Ringer persisted in presence of tubocurarine chloride (2.5-10(-5) M/1). 6. Possible mechanisms for the depolarization are discussed.

Animals↗
PubMed1984

Myocardial metabolic inhibition and membrane potential, contraction, and potassium uptake.

Interruption of synthesis of ATP during hypoxia or ischemia can produce membrane depolarization that may be related to inhibition of Na+-K+-ATPase. To examine this hypothesis, the effects of exposure of cultured chick embryo ventricular cells to 1 mM cyanide (CN), to 20 mM 2-deoxy-D-glucose (2-DG), to CN + 2-DG, and to ouabain (10(-3) M) on contraction, membrane potential, and 42K uptake were determined. CN produced moderate membrane depolarization and electromechanical uncoupling within 2 min. 2-DG caused marked membrane depolarization with a transient negative inotropic effect. Exposure to CN + 2-DG produced marked depolarization (-38 mV) and mechanical arrest of the cells in a relaxed state. Ouabain produced marked depolarization (-39 mV) and contracture of the cells. Uptake of 42K was inhibited by 10(-3) M ouabain within seconds. However, CN + 2-DG produced no inhibition of 42K uptake within the first 2 min of exposure, and inhibition of the Na pump by CN + 2-DG required 30 min to develop fully. Exposure to CN alone produced no inhibition of 42K uptake, whereas moderate inhibition was produced by 2-DG alone even when substrate for oxidative phosphorylation was provided. We conclude that the acute effects of inhibition of glycolysis and oxidative phosphorylation on membrane potential and contraction in these cells are not due to inhibition of the Na pump and that during partial metabolic inhibition active univalent cation transport in these cells is relatively dependent on ATP derived from glycolysis, whereas contraction is more dependent on ATP supplied by oxidative phosphorylation.

Animals↗
PubMed1989

Effects of substance P, calcitonin gene-related peptide and capsaicin on tension and membrane potential of pig coronary artery in vitro.

The effects of substance P (SP), calcitonin gene-related peptide (CGRP) and capsaicin were studied on isometric tension and membrane potential of pig coronary arterial strips in vitro. CGRP induced an endothelium-independent relaxation without change in the smooth muscle membrane potential whereas SP relaxed and hyperpolarized the strip via the endothelium. Applied together, the mechanical effects of SP plus CGRP were additive. CGRP did not affect the hyperpolarization due to SP. In order to examine a possible role of endogenous SP and CGRP, capsaicin was used. It provoked a contraction which was adventitia-dependent, and was inhibited by indomethacin. In presence of indomethacin, capsaicin caused a relaxation. It was accompanied by a hyperpolarization of smooth muscle membrane potential only when the strip had an intact endothelium. When the strip was de-endothelialized capsaicin relaxation subsisted. This indicates that capsaicin produced a relaxation of indomethacin-treated strip by releasing a hyperpolarizing endothelial factor and probably endogenous CGRP.

Animals↗
PubMed1988

Factors responsible for oscillations of membrane potential recorded with tight-seal-patch electrodes in mouse fibroblasts.

In giant fibroblastic L cells, penetration of a conventional microelectrode brought about marked decreases in the membrane potential and input resistance measured with a patch electrode under tight-seal whole-cell configuration, and repeated hyperpolarizations were often observed upon penetration. Therefore, the question arose whether such leakage artifact is a causal factor for generation of the membrane potential oscillation even in giant L cells. During whole-cell recordings, however, regular potential oscillations were observed in the cells that had not been impaled with a conventional microelectrode, as far as the Ca2+ buffer was not strong in the pipette solution. Oscillatory changes in the intracellular potential were detected by extracellular recordings with a tight-seal patch electrode in the cell-attached configuration. Thus, the potential oscillation occurs even in the absence of penetration-induced leakage or without rupture of the patch membrane. Withdrawal of a micropipette from one cell was often found to induce marked cell damage and elicit oscillatory hyperpolarizations in a neighboring cell with a certain time lag. The longer the distance between the injured and recorded cells, the greater was the time lag. Application of the cell lysate on the cell surface also gave rise to oscillatory hyperpolarizations. After repeated applications of the lysate, the membrane became unresponsive (desensitized), suggesting the involvement of receptors for the lysate factor. The lysates of different cell species (mouse lymphoma L5178Y cells or human epithelial Intestine 407 cells) produced similar effects. The effective component was heat stable and distinct from ATP. Lysate-induced hyperpolarizations were inhibited by deprivation of extracellular Ca2+ and by application of a Ca2+ channel blocker (nifedipine) or a K+ channel blocker (quinine) in the same manner as spontaneous oscillatory hyperpolarizations. It is concluded that the mouse fibroblast exhibits membrane potential oscillations, when the cell was activated, presumably via receptor systems, by some diffusible factors released from damaged cells.

Animals↗
PubMed2003

A cuvette-based fluorometric analysis of mitochondrial membrane potential measured in cultured astrocyte monolayers.

Mitochondrial membrane potential (Deltapsi(M)) plays a key role in coordinating mitochondrial function and cell biology in general. In astrocytes, Deltapsi(M) is an important indicator of the health of these brain cells and their response to traumatic and hypoxic injury. We have shown previously how fluorescent signals can be measured from cells attached to a coverslip in a standard cuvette with a fluorometer and modulated using a cuvette perfusion system (Pflugers Arch-Eur. J. Physiol. 421 (1992) 400). Here we report on how this method can be employed to characterize the actions of a number of potentiometric fluorescent cationic dyes, including JC-1, Rh123 and TMRM, for their ability to monitor Deltapsi(M) in primary cultures of intact astrocytes. All dyes detected the reversible depolarization produced by brief exposure to the mitochondrial uncoupler protonophore FCCP, which short circuits and dissipates Deltapsi(M). Qualitatively similar responses were measured after treatment with either azide, an inhibitor of complex IV in the mitochondrial respiratory chain, or the oxidant H(2)O(2). Cell depolarization with high potassium modified the responses to FCCP. The time courses of these responses differed in a manner dependent on the particular dye used and in a way that correlated with expected permeation rate. The merits and pitfalls of these different potentiometric dyes for monitoring Deltapsi(M) are discussed.

Animals↗
PubMed1980

Ca2+ uptake and membrane potential in sarcoplasmic reticulum vesicles.

The rate of calcium uptake by sarcoplasmic reticulum vesicles isolated from rabbit skeletal muscle was stimulated by inside-negative membrane potential generated by K+ gradients in the presence of valinomycin. The increase in the calcium transport rate was accompanied by a proportional increase in the rate of calcium-dependent ATP hydrolysis, without significant change in the steady state level of the phosphorylated enzyme intermediate. Changes in the sarcoplasmic reticulum membrane potential during calcium transport were monitored with the optical probe, 3,3'-diethylthiadicarbocyanine. The decrease in the absorbance of 3,3'-diethylthiadicarbocyanine at 660 nm following generation of inside-negative membrane potential was reversed during ATP-induced calcium uptake. These observations support an electrogenic mechanism for the transport of calcium by the sarcoplasmic reticulum.

Adenosine Triphosphatases↗
PubMed1999

A role for a glibenclamide-sensitive, relatively ATP-insensitive K+ current in regulating membrane potential and current in rat aorta.

OBJECTIVE: ATP-sensitive K+ channels have been classified based on their inhibition by cytoplasmic ATP. Recent evidence in vascular smooth muscle has suggested that these channels show weak sensitivity to intracellular ATP. However, it is not known whether these channels regulate the resting K+ conductance in vascular smooth muscles. Therefore, the aim of the present investigation was to characterize this current in rat aorta myocytes and to examine whether it contributes to setting the membrane potential. METHODS: The conventional and nystatin-permeablised whole cell patch clamp techniques were used to characterize the effect of glibenclamide on membrane potential and K+ current in enzymatically dispersed rat aorta myocytes. RESULTS: The mean resting potential measured in current clamp mode using the permeabilized patch approach was -54 +/- 5 mV (n = 8). Glibenclamide (10 microM) caused a reversible 24-mV depolarization in these cells. In symmetrical K+ (135 mM) solution an inward glibenclamide-sensitive (10 microM) current (-4.1 +/- 0.7 pA/pF; n = 5), hereafter termed Iglib, was observed at a membrane potential of -80 mV when cells held at -60 mV were ramped from -80 to +80 mV. In the absence of any nucleotide in the pipette solution, Iglib measured by the conventional whole-cell method was -23.69 +/- 4.65 pA/pF (n = 9). With 1 and 3 mM ATP in the pipette, the average current density was -25 +/- 6.3 pA/pF (n = 8), and -9.4 +/- 2.7 pA/pF (n = 9), respectively. In the absence of ATP, 1 mM GDP significantly (P < 0.01) increased Iglib (-44.8 +/- 8.4 pA/pF; n = 13). Inclusion of 1 mM ATP in the GDP-containing pipette solution had no significant effect on the current amplitude (-56.4 +/- 10.7 pA/pF; n = 7). Iglib fell to -11.0 +/- 2.9 pA/pF (n = 10) if 1 mM GDP and 3 mM ATP were present. In symmetrical K+, the Iglib observed in the presence of 1 mM ATP in the pipette was increased by more than two-fold in the presence of 10 microM levcromakalim. In PSS containing 5 mM K+, a significant glibenclamide-sensitive current was observed at -45 mV membrane potential when cells dialyzed with 1 mM ATP were ramped between -80 to 30 mV. CONCLUSION: These results demonstrate that Iglib channels in rat aorta myocytes differ from classical KATP channels, being relatively insensitive to intracellular ATP. Iglib therefore appears to have an important role in contributing to the maintenance of the resting potential in rat aortic smooth muscle.

Adenosine Triphosphate↗
PubMed1990

Calcium influx into endothelial cells and formation of endothelium-derived relaxing factor is controlled by the membrane potential.

We studied the role of the membrane potential in the control of the intracellular free calcium concentration ([Ca2+]i) and release of the two autacoids endothelium-derived relaxing factor (EDRF = nitric oxide) and prostaglandin I2 in endothelial cells. ATP (3 mumol/l) and bradykinin (1 nmol/l) evoked rapid increases (sixfold) in [Ca2+]i in cultured endothelial cells. [Ca2+]i remained elevated over several minutes. When the cells were depolarized, either by K+ (70-90 mmol/l) or by preincubation with the blocker of K+ channels tetraethylammonium (3 mmol/l), the initial peak of [Ca2+]i remained unaffected but [Ca2+]i returned significantly faster to resting levels, indicating a reduction in Ca2+ influx. In native, freshly isolated endothelial cells, K+ abolished increases in [Ca2+]i induced by acetylcholine (3 mumol/l). Release of EDRF in response to bradykinin (cultured cells) and acetylcholine (native cells) was inhibited by K+ (by 70%), whereas release of prostaglandin I2 was not significantly reduced. Preincubation of cultured endothelial cells with the receptor-independent stimulus thimerosal (5 mumol/l, 40 min) evoked a long-lasting release of EDRF and small elevations of [Ca2+]i (twofold) after washout of the drug. Depolarization with K+ decreased thimerosal-induced EDRF release and [Ca2+]i in a reversible manner. In patch-clamped endothelial cells, bradykinin (1 nmol/l) induced transient hyperpolarizations that were significantly prolonged by BRL 34915 (1 mumol/l), an activator of K+ channels. BRL 34915 also elicited increases in [Ca2+]i, particularly in thimerosal-stimulated endothelial cells. These effects were abolished by K+. We conclude that the initial rise in [Ca2+]i in response to receptor-binding agonists, caused by mobilization of Ca2+ from intracellular stores, activates K+ channels, thereby inducing hyperpolarization.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed2006

Simultaneous monitoring of ionophore- and inhibitor-mediated plasma and mitochondrial membrane potential changes in cultured neurons.

Although natural and synthetic ionophores are widely exploited in cell studies, for example, to influence cytoplasmic free calcium concentrations and to depolarize in situ mitochondria, their inherent lack of membrane selectivity means that they affect the ion permeability of both plasma and mitochondrial membranes. A similar ambiguity affects the interpretation of signals from fluorescent membrane-permeant cations (usually termed "mitochondrial membrane potential indicators"), because the accumulation of these probes is influenced by both plasma and mitochondrial membrane potentials. To resolve some of these problems a technique is developed to allow simultaneous monitoring of plasma and mitochondrial membrane potentials at single-cell resolution using a cationic and anionic fluorescent probe. A computer program is described that transforms the fluorescence changes into dynamic estimates of changes in plasma and mitochondrial potentials. Exploiting this technique, primary cultures of rat cerebellar granule neurons display a concentration-dependent response to ionomycin: low concentrations mimic nigericin by hyperpolarizing the mitochondria while slowly depolarizing the plasma membrane and maintaining a stable elevated cytoplasmic calcium. Higher ionomycin concentrations induce a stochastic failure of calcium homeostasis that precedes both mitochondrial depolarization and an enhanced rate of plasma membrane depolarization. In addition, the protonophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone only selectively depolarizes mitochondria at submicromolar concentrations. ATP synthase reversal following respiratory chain inhibition depolarizes the mitochondria by 26 mV.

ATP Synthetase Complexes↗
PubMed1975

Relationship between membrane potential and external potassium in human glioblastoma cells in tissue culture.

Cells from a human glioblastoma (TC 526) maintained in tissue culture for ten years had a mean membrane potential of 27 +/- 0.9 mV at an external potassium concentration [Ko] of 5.3 mM. When [Ko] was varied between 2.5 and 5.3 mM, membrane potential changes were close to those predicted by the Nernst equation. At higher [Ko], the Nernstian slope was approached only in the presence of 10(-5) M ouabain, which did not affect membrane potential at a [Ko] of 5.3 mM. An electrogenic sodium pump activated by high [Ko] could explain these findings; such a mechanism has been demonstrated in other tissues.

Biological Transport, Active↗
PubMed1979

Effects of mercuric chloride on the resting membrane potentials of blue crab (Callinectes sapidus) muscle fibers.

The effects of concentrations of mercuric chloride ranging from 3.68 to 368 microM (1--100 ppm) on the resting membrane potentials of muscle fibers in the extensor muscle of the carpopodite in walking legs of adults blue crabs were investigated in vitro. Glass micropipettes filled with saturated solutions of potassium chloride and conventional electronic equipment were used. Resting membrane potentials in uncontaminated artificial sea water averaged -78 mV +/- 4 mV (S.E.M.). Mercuric chloride added to the control bath at 3.68 or 9.2 microM did not affect the resting membrane potentials. At 18.4 microM threshold effects were obtained in 50% of the preparations. At concentrations ranging from 25.7 to 368 microM progressive deterioration of membrane polarization occurred as the mercury concentration was increased. This effect was irreversible despite multiple washes with normal sea water. We conclude that mercuric chloride has very powerful toxic effects at the peripheral motor effector elements in blue crabs. These results do not, of course, rule out more central effects on enzymatic systems or neuronal networks.

Animals↗
PubMed1978

Charge shift optical probes of membrane potential. Theory.

The chromophores of a series of known and unknown probes of membrane potential are subjected to molecular orbital calculations. These calculations are used to characterize the charge distribution and excitation-induced shift of electron density in the chromophores. This is used to predict or rationalize the magnitude of an electrochromic response to membrane potential. The predictions are consistent with more rigorous calculations on several selected systems as well as with the available experimental data. Emerging from the survey is a variation on previously considered forms of electrochromism involving a simple migration of the charge in an ionic chromophore. The intrinsic amphipathic structures of some of these systems may make them especially well suited for the construction of well oriented, highly responsive probes. A particularly promising charge-shift chromophore is the 4-(p-aminostyryl) pyridinium cation.

Coloring Agents↗
PubMed1981

Effect of 2-nicotinamidethyl nitrate (SG-75) on membrane potentials of canine Purkinje fibers.

In canine Purkinje fibers firing spontaneously at a cycle length of about 2.7 sec, 2-nicotinamidethyl nitrate (SG-75) (10(-6)-10(-4)M) increased the cycle length and in high concentrations (10(-5)-10(-4)M) abolished the spontaneous firing. The increase in cycle length was due entirely to that decrease in slope of the diastolic depolarization which was more marked during late diastole than during early diastole. Neither the maximum diastolic potential nor the take-off potential was changed. When the membrane potential failed to reach the take-off potential, it polarized again after the early diastolic depolarization, in some fibers. The depth of the notch was increased and the peak value of the plateau of the action potential was decreased by SG-75, however, the maximum rate of rise of the action potential remained unchanged. Shortening of the action potential duration was evident when Purkinje fibers were stimulated at a cycle length of 2 sec. These fibers remained excitable at 10(-4) M SG-75 and when stimulated at a cycle length of 2 sec, the action potential occurred with a duration of less than half of control. These results can be interpreted as being due to an increase in the background K current induced by SG-75.

Animals↗
PubMed2004

Dynamics of rat entorhinal cortex layer II and III cells: characteristics of membrane potential resonance at rest predict oscillation properties near threshold.

Neurones generate intrinsic subthreshold membrane potential oscillations (MPOs) under various physiological and behavioural conditions. These oscillations influence neural responses and coding properties on many levels. On the single-cell level, MPOs modulate the temporal precision of action potentials; they also have a pronounced impact on large-scale cortical activity. Recent studies have described a close association between the MPOs of a given neurone and its electrical resonance properties. Using intracellular sharp microelectrode recordings we examine both dynamical characteristics in layers II and III of the entorhinal cortex (EC). Our data from EC layer II stellate cells show strong membrane potential resonances and oscillations, both in the range of 5-15 Hz. At the resonance maximum, the membrane impedance can be more than twice as large as the input resistance. In EC layer III cells, MPOs could not be elicited, and frequency-resolved impedances decay monotonically with increasing frequency or has only a small peak followed by a subsequent decay. To quantify and compare the resonance and oscillation properties, we use a simple mathematical model that includes stochastic components to capture channel noise. Based on this model we demonstrate that electrical resonance is closely related though not equivalent to the occurrence of sag-potentials and MPOs. MPO frequencies can be predicted from the membrane impedance curve for stellate cells. The model also explains the broad-band nature of the observed MPOs. This underscores the importance of intrinsic noise sources for subthreshold phenomena and rules out a deterministic description of MPOs. In addition, our results show that the two identified cell classes in the superficial EC layers, which are known to target different areas in the hippocampus, also have different preferred frequency ranges and dynamic characteristics. Intrinsic cell properties may thus play a major role for the frequency-dependent information flow in the hippocampal formation.

Animals↗
PubMed1999

Organelle-specific probe JC-1 identifies membrane potential differences in the mitochondrial function of bovine sperm.

The mitochondrial probe 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolyl-carbocyan ine iodide (JC-1) not only identifies mitochondria exhibiting low membrane potentials by the emission of green fluorescence (range, 510-520 nm) but also differentiates these from mitochondria exhibiting relatively high membrane potentials. This discrimination occurs because JC-1 forms aggregates at high membrane potentials. These J-aggregates emit a bright red-orange fluorescence at 590 nm. In this study, JC-1 was combined with the classical dead cell stain, propidium iodide (PI), to identify a spectrum of functional sperm along with degenerate sperm. Flow cytometric analysis of bull sperm showed that the aggregate:monomer ratio differed among bulls before cryopreservation (P < 0.001) but not afterwards (P > 0.05). The effects of stain equilibration time, sperm concentration, and live:dead ratios were examined. The addition of SYBR-14 to the JC-1 and PI combination enhanced the distinction between the red PI-stained and red-orange JC-1-stained populations. This discrimination between J-aggregates and the PI-stained sperm was affected by sperm concentration. These studies show that JC-1 can be useful in monitoring mitochondrial function in bovine sperm.

Animals↗
PubMed2001

Resting membrane potential as a marker of apoptosis: studies on Xenopus oocytes microinjected with cytochrome c.

Observation of the electrical potential difference across the cell membrane is described as a new method for monitoring apoptosis of a single cell. The resting membrane potential (DeltaPsi) of Xenopus oocytes has been recorded in real time following microinjection of cytochrome c. Soon after microinjection, DeltaPsi becomes less negative and attains a new constant value with a half time, t(m), of about 35 (+ /- 5) min at all cytochrome c concentrations greater than 1 microM. The cytosol extract of cytochrome c-injected oocytes shows DEVD proteolytic activity characteristic of aspartate specific proteases, implicating an apoptotic death pathway. In response to the delivery of cytochrome c into the cytosol, caspases are activated within 7 min while the changes in DeltaPsi begin to occur after about 30 min. The method described here will be potentially useful to assess the effectiveness of cell death regulators and modulators of synthetic and biological origin, and the results presented shed light on the currently debated issue of the importance of the redox state of cytochrome c in the initiation of apoptosis.

Animals↗
PubMedDate not supplied

Effects of nicotine and ethanol on rat atrial membrane potentials.

The purpose of this research was to study the effects of nicotine and ethanol, alone and in combination, on cardiac membrane potentials (MP). Rat atrial preparations driven at 5 Hz were superfused with Tyrode's solution (37 degrees C) while recording MP with intracellular microelectrodes. Nicotine concentrations below and including 6.2 x 10(-5) M did not affect MP. Within 15 s, nicotine 3.1 x 10(-3) M shortened the action potential duration (APD) and depressed the overshoot of the action potential (OS). This action was blocked by atropine. After 3 min, nicotine prolonged the APD and depressed Vmax of phase O, OS and the amplitude of the action potential (AAP), without affecting the resting membrane potential (RMP). Nifedipine blocked the depression of the OS while tetraethylammonium chloride blocked the prolongation of the APD. Acute exposure to ethanol depressed OS and AAP and shortened APD, but it did not affect RMP or Vmax of phase O. When nicotine and ethanol were administered simultaneously, the APD-prolonging effects of nicotine prevailed. The influence of chronic ethanol ingestion on the acute action of nicotine and/or ethanol was studied in rats pair-fed a liquid diet with (ER) or without (NR) ethanol (35% of total caloric intake) for 24 weeks. Chronic ethanol ingestion accentuated the depressant effect of nicotine 3.1 x 10(-3) M on OS and AAP, but it did not modify the APD-prolonging action of nicotine. The same results were observed when ER and NR were exposed to nicotine and ethanol simultaneously.

Action Potentials↗