SEARCH · Search PubMed

Results for “Membrane Potentials”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources

PubMed1980

Quantitative measurements of membrane potential in Escherichia coli.

By use of giant cells of Escherichia coli induced by growth in the presence of 6-amidinopenicillanic acid, membrane potentials have been measured by two completely independent techniques: directly with intracellular microelectrodes and indirectly from the steady-state distribution of [3H]tetraphenylphosphonium. Under a variety of conditions, the two methods yield values that agree very closely. Thus, with both techniques, the membrane potential approximates -85 mV (interior negative) at pH 5.0 and -142 mV at pH 8.0, with an average slope of -22 mV/pH unit over the range pH 5.0-7.0. A parallel study of membrane vesicles prepared from giant cells was undertaken using tetraphenylphosphonium distribution alone as a measure of membrane potential. The vesicles were found to exhibit a much smaller slope of membrane potential vs. extracellular pH (about -6 mV/pH unit) than intact giant cells. The results indicate that distribution studies with these lipophilic cations provide an excellent measure of membrane potential and are discussed in relation to calculations of H+/substrate stoichiometry for protonsymport systems in E. coli.

Amdinocillin↗

PubMedDate not supplied

Characterising neural representation in terms of the dynamics of cell membrane potential activity: a control theoretic approach using differential geometry.

Experimental and theoretical results seem to demand that the study of neural representations in the brain considers both the subthreshold and suprathreshold dynamic activity of the neural membrane potential, rather than be solely focussed on stimulus representation in trains of action potentials. In a dynamical systems formulation, the membrane potential can be regarded as the "state" of the neuron, evolving continuously over time and space, within an infinite dimensional space, in response to ever changing inputs. Formally, the state of the neuron, together with future inputs, is sufficient to fully determine the future behaviour of the neuron. In this paper, the characterisation of membrane potential activity is approached from a control theoretic viewpoint as a "reachability" problem, in which the effect of particular stimulus-evoked synaptic inputs is seen as driving the cell from some initial state of the neuron to a particular terminal state on a given manifold. It is shown that a fluctuating subthreshold membrane potential induced by synaptic background activity, and the cooperative interaction of excitatory and inhibitory inputs, may be important factors in allowing the cell to "reach" a maximal subset of all possible membrane potential states, through the action of its synaptic inputs.

Cell Membrane↗

PubMed1974

Pancreatic acinar cells: membrane potential and resistance change evoked by acetylcholine.

1. Membrane potential and input resistance measurements were made on segments of pancreas from mice or rats, whereas potential measurements alone were made on pancreas from cats or rabbits placed in a tissue bath which was perfused with a Krebs-Henseleit solution.2. The acinar cell membrane potential was about -40 mV and the input resistance 4-8 MOmega. Spontaneous miniature depolarization potentials were occasionally observed superimposed upon the resting potential. In these cases synchronous reductions in input resistance were observed.3. The immediate effect of stimulation with ACh was always a depolarization and a concomitant reduction in input resistance and time constant. In some cases a secondary depolarization was observed accompanied by an increase in input resistance. The time constant, however, remained as short as in the first phase of depolarization.4. In the rabbit pancreas ACh evoked biphasic potential changes: depolarization followed by hyperpolarization. A similar pattern could sometimes also be observed in the mouse pancreas following a brief pulse of ACh addition. In these cases the depolarization was followed by a small but relatively long lasting hyperpolarization. The depolarization was accompanied by a reduction in input resistance.5. Pancreozymin caused depolarization of the acinar cell membrane and a marked reduction in input resistance and time constant.6. In the presence of atropine (1.4 x 10(-6)M) depolarization of the acinar cell membrane by an elevated K concentration (50 mM) in the bathing fluid did not reduce the input resistance.7. It is concluded that the two physiological stimulants of pancreatic protein secretion, ACh and pancreozymin, act on the acinar cells by increasing the permeability of the plasma membrane.

Acetylcholine↗

PubMed2006

ATP synthase is responsible for maintaining mitochondrial membrane potential in bloodstream form Trypanosoma brucei.

The mitochondrion of Trypanosoma brucei bloodstream form maintains a membrane potential, although it lacks cytochromes and several Krebs cycle enzymes. At this stage, the ATP synthase is present at reduced, although significant, levels. To test whether the ATP synthase at this stage is important for maintaining the mitochondrial membrane potential, we used RNA interference (RNAi) to knock down the levels of the ATP synthase by targeting the F1-ATPase alpha and beta subunits. RNAi-induced cells grew significantly slower than uninduced cells but were not morphologically altered. RNAi of the beta subunit decreased the mRNA and protein levels for the beta subunit, as well as the mRNA and protein levels of the alpha subunit. Similarly, RNAi of alpha subunit decreased the alpha subunit transcript and protein levels, as well as the beta-subunit transcript and protein levels. In contrast, alpha and beta RNAi knockdown resulted in a 60% increase in the F0 complex subunit 9 protein levels without a significant change in the steady-state transcript levels of this subunit. The F0-32-kDa subunit protein expression, however, remained stable throughout induction of RNAi for alpha or beta subunits. Oligomycin-sensitive ATP hydrolytic and synthetic activities were decreased by 43 and 44%, respectively. Significantly, the mitochondrial membrane potential of alpha and beta RNAi cells was decreased compared to wild-type cells, as detected by MitoTracker Red CMXRos fluorescence microscopy and flow cytometry. These results support the role of the ATP synthase in the maintenance of the mitochondrial membrane potential in bloodstream form T. brucei.

Animals↗

PubMedDate not supplied

Influence of cell membrane potential, and selectivity of the Na+/H+ exchanger and Cl-/HCO3- exchanger on the intracellular accumulation of adriamycin.

Intracellular accumulation of adriamycin (ADR) has been reported to be influenced by cell membrane potential. We first evaluated intracellular accumulation of ADR and 3,3'-(di-n-hexyl)-2,2'-oxacarbocyanine iodide (NK-2280), an indicator of cell membrane potential, and found a good correlation between ADR and NK-2280 intracellular accumulation in several cell lines. This suggests that ADR accumulation may be influenced by cell membrane potential or the mechanisms of NK-2280 accumulation may be similar to those of ADR accumulation. Next, we observed the influence of the NA+/H+ exchanger and Cl-/HCO3- exchanger on the intracellular accumulation of ADR and NK-2280, and found that ADR accumulation decreased with increasing concentrations of 3,5-diamino-6-chloro-N-(diaminomethylene)pyrazinecarboxamide (amiloride), an inhibitor of the Na+/H+ exchanger, and 4,4'-diisothiocyanato-stilbene-2,2'-disulfonic acid (DIDS), an inhibitor of the Cl-/HCO3- exchanger, however, NK-2280 accumulation was increased by amiloride, and decreased by DIDS. The increased accumulation of NK-2280 induced by amiloride may be due to the increased cell membrane potential caused by the inhibition of H+ ion efflux and NA+ ion influx due to the inhibition of the Na+/H+ exchanger. The decreased accumulation of NK-2280 may be also due to the decreased cell membrane potential caused by the inhibition of Cl- ion efflux due to the inhibition of the Cl-/HCO3- exchanger by DIDS. However, the decreased rate caused by DIDS was greater than the increased rate caused by amiloride. Therefore, it is suggested that the decreased accumulation of NK-2280 by DIDS may be influenced by other factors apart from cell membrane potential. These results suggest that the Cl-/HCO3- exchanger may be related to both ADR accumulation, and NK-2280 accumulation, and that the Na+/H+ exchanger may be related to ADR accumulation, but not NK-2280. This suggests that the Cl-/HCO3- exchanger is of low selectivity.

3T3 Cells↗

PubMed1985

ADP induced depolarization of human platelet membrane potential.

The transmembrane potential of human blood platelets suspended in plasma was investigated by studying the distribution of a radiolabeled permeant ion [14C] thiocyanate. The membrane potential of resting platelets was found to be -54.50 mV +/- 9.23 S.D. with a range of -39 to -76 mV (n = 27). The possibility that platelet activation alters membrane potential or that changes in membrane potential serve as an activation trigger was investigated. Stimulation by ADP (10 microM) resulted in a significant (p less than 0.05) depolarization of the membrane potential. Preincubation with 6 mM EGTA failed to inhibit ADP-induced depolarization even though EGTA effectively prevented primary and secondary aggregation but not shape change. Preincubation with PGE1 inhibited shape change, aggregation, and the ADP-induced depolarization. No significant change in membrane potential was observed following stimulation by epinephrine (50 microM). These results suggest that the initial interaction of ADP and its receptor may involve an inward positive current which can be determined by thiocyanate distribution.

Adenosine Diphosphate↗

PubMed1987

Oxonol VI as an optical indicator for membrane potentials in lipid vesicles.

Experiments with large unilamellar dioleoylphosphatidylcholine vesicles were carried out in order to study the effect of membrane potential on the fluorescence of Oxonol VI. A partition equilibrium of dye between membrane and water was found to exist with a partition coefficient gamma identical to c lipid/c water of about 19,000 (at zero voltage). In the presence of an inside-positive membrane potential, the negatively charged dye accumulates in the intravesicular aqueous space according to a Nernst equilibrium. This leads to an increased adsorption of dye to the inner lipid monolayer and to a concomitant increase of fluorescence. The fluorescence change can be calibrated as a function of transmembrane voltage by generating a potassium diffusion potential in the presence of valinomycin. The intrinsic fluorescence of the membrane-bound dye is not affected by voltage; the whole influence of voltage on the fluorescence results from voltage-dependent partitioning of the dye between water and membrane. The voltage dependence of the apparent partition coefficient can be quantitatively described by a three-capacitor model in which the dye is assumed to bind to adsorption planes located on the hydrocarbon side of the membrane/solution interface. Oxonol VI was found to be suitable for detecting changes of membrane potential associated with the activity of the (Na+ + K+)-ATPase in reconstituted vesicles. When ATP is added to the external medium, pump molecules with the ATP-binding side facing outward become activated; this results in a translocation of net positive charge towards the vesicle interior. Under this condition, fluorescence changes corresponding to (inside-positive) potentials of up to 150-200 mV are observed. After the build-up of the membrane potential, a quasi-stationary state is reached in which the pump current is compensated by a back-flow of charge through passive conductance pathways.

Adsorption↗

PubMed1996

Membrane currents and the resting membrane potential in cultured bovine pulmonary artery endothelial cells.

1. We have used the whole-cell patch-clamp technique to characterize the ionic conductances that determine the resting membrane potential in cultured endothelial cells from calf pulmonary artery (CPAE cells). 2. Resting membrane potentials were scattered between -88 and +5 mV with a mean +/- S.E.M. of -26 +/- 3 mV (n = 104). 3. The most prominent membrane current in resting cells was an inwardly rectifying K+ current. This current showed Na(+)-dependent inactivation and was efficiently blocked by external Ba2+ (EC50 = 2.2 microM), but was relatively insensitive to quinine, quinidine and TEA. 4. Hypertonic cell shrinkage inhibited an outwardly rectifying Cl- current, which was also efficiently blocked by 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB; 100 microM), quinine (500 microM) and quinidine (500 microM). 5. A linear, time-independent background current remained after elimination of these two currents. This current was dependent on extracellular monovalent cations with a permeability sequence of Cs+ > Na+ > Li+ >> N-methyl-D-glucamine. It was partially blocked by millimolar concentrations of the divalent cations Ca2+, Ni2+ and Ba2+. Gd3+ (200 microM) had no significant effect on this background current. 6. Continuous measurements of the membrane potential confirm that the three described conductances are the major determinants of the membrane potential. Due to the low slope conductance in the region between -70 and 0 mV, small changes in one of the current components can evoke large depolarizations or hyperpolarizations, which explains the large scattering of the resting membrane potentials.

Animals↗

PubMed1981

The effect of herpes virus infection on the membrane potential of parotid acinar cells.

Monolayers of feline parotid acinar cells were infected with feline rhinotracheitis herpes virus. Membrane potentials and input resistances were measured before and during infection. Uninfected acinar cells had an average membrane potential of -51 mV and resistances from 6 to 120 mega-ohms; cells infected for more than 18 h had an average membrane potential of -19 mV and resistances from 30 to 100 mega-ohms. The time course of the decrease in membrane potential was studied and was found to commence about ten to 14 h after infection.

Animals↗

PubMed1990

Opposite cardiac actions of the enantiomers of Bay K 8644 at different membrane potentials in guinea-pig papillary muscles.

The influence of membrane potential on the effects of the enantiomers and the racemate of Bay K 8644 [1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluor-methylphenyl)-p yri dine-5-carboxylate] on force of contraction and on action potentials were studied in guinea-pig papillary muscles in order to detect possible changes in the direction of drug action or in potency. Membrane potential was varied by changing the potassium concentration ([K+]o) in the bathing solution. At normal resting potential, (-)-Bay K 8644 enhanced force of contraction and prolonged the action potential duration measured at 50% of repolarization (APD) to the same extent as the racemate and with similar pD2 values. After membrane depolarization by raising [K+]o from 5.4 to 17.4 mmol/l, the (-)-enantiomer and the racemate prolonged the APD to a similar degree but enhanced force to a lesser extent. The maximum rate of depolarization of slow action potentials, Vmax, was increased at the highest concentrations (10(-5) mol/l). The effects of (+)-Bay K 8644 were more complicated. At high concentrations (10(-5) mol/l) it decreased force of contraction and APD, the pD2 values were one order of magnitude lower than for the (-)-enantiomer and the racemate. A high concentration (+)-Bay K 8644 (10(-5) mol/l) virtually abolished contractile activity at all membrane potentials, the extent of shortening in APD increased with membrane depolarization in elevated [K+]o. Vmax of slow action potentials was decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1979

Further studies of the membrane potential of the stria cells of the guinea pig in vitro.

Negative membrane potentials from the stria vascularis of the guinea pig have been recorded in vivo. Stable negative membrane potentials from the stria cells have also been recorded for as long as 2 minutes in vitro. They varied from -20 mV to -49 mV, irrespective of whether the stria vascularis was immersed in Ringer's solution for in K-Ringer's solution (approximately to the composition of an endolymph). Labelling of the inserted stria cells from which the membrane potential had been recorded demonstrated that the microelectrode tip was inside the cell. These cells will continue to show electrical activity for some time when immersed in suitable media.

Animals↗

PubMed1990

Analysis of the membrane potential of rat- and mouse-liver mitochondria by flow cytometry and possible applications.

Washed and purified rat- or mouse-liver mitochondria exhibiting high membrane integrity and metabolic activity were studied by flow cytometry. The electrophoretic accumulation/redistribution of cationic lipophilic probes, rhodamine 123, safranine O and a cyanine derivative, 3,3'-dihexyloxadicarbocyanine iodide, during the energization process was studied and was consistent with the generation of a negative internal membrane potential. An exception to this was nonylacridine orange which spontaneously bound to the mitochondrial membrane by hydrophobic interactions via its hydrocarbon chain. Energized purified mitochondria stained with potentiometric dyes exhibited both higher fluorescence and population homogeneity than the non-energized or deenergized (nigericin plus valinomycin) mitochondria. By contrast, under non-energized or deenergized conditions, the mitochondrial population exhibited fluorescence intensity heterogeneity related to the residual membrane potential; two subpopulations were evident, one of low fluorescence which may be related to the autofluorescence of the mitochondria (plus non-specific dye binding) and a second population which exhibited high fluorescence. Flow cytometry of the unpurified, simply washed, rat-liver mitochondria stained with rhodamine 123, a classically used dye, provided evidence of their heterogeneity in terms of light-scattering properties and membrane-potential-related fluorescence. One third of the washed mitochondria were found to be non-functional by such assays. The fluorescence of purified rat-liver mitochondria due to the membrane potential built up by endogenous substrates indicates heterogeneity of the mitochondrial population with respect to levels of endogenous substrates. The low-angle light scattering increases upon energization and provides some original information about the shape and modification of the inner mitochondrial conformation accompanying the energization. The heterogeneity of the rat liver mitochondrial population, from a structural, metabolic (existence of endogenous substrates) and functional (active and non-active mitochondrial population dispersion) point of view could thus be demonstrated by flow-cytometry analysis. Two animal models were examined with regard to the alteration of the mitochondrial membrane potential under the effects of drugs (rat-liver mitochondria), and the effects of ammonium toxicity (mouse-liver mitochondria). These results are promising and open new perspectives in the study of mitochondriopathies.

Ammonia↗

PubMed1986

Peptidergic modulation of the membrane potential of the Schwann cell of the squid giant nerve fibre.

The effects of a range of neuropeptides were investigated on the membrane potential of the Schwann cells of the giant nerve fibre of the tropical squid. Vasoactive intestinal peptide (VIP) produced a dose-dependent, long-lasting hyperpolarization of the Schwann-cell membrane potential. Among peptides structurally related to VIP, similar effects were produced by peptide histidine isoleucine (PHI) but not by secretin and glucagon. Substance P and somatostatin also hyperpolarized the Schwann-cell membrane potential but via receptor systems distinct from those activated by VIP. Methionine enkephalin ([Met]-enkephalin) blocked the actions of all the above peptides as well as the effects of DL-octopamine and carbachol. The actions of [Met]-enkephalin upon the VIP responses were antagonized by naloxone. VIP produces its effects on the Schwann-cell membrane potential via a receptor system that is independent from those described previously which mediate the effects of carbachol and DL-octopamine. However, VIP can potentiate the effects of the latter systems. The actions of VIP on the Schwann cell are unlikely to be mediated via changes in adenosine 3',5'-cyclic monophosphate (cyclic AMP) levels and are insensitive to changes in the level of extracellular calcium in the superfusate. The actions of VIP are, however, potentiated in the presence of low concentrations of lithium ions suggesting that the VIP receptor may mediate its effects by inducing the hydrolysis of polyphosphatidylinositols in the Schwann-cell membrane. Evidence is presented for the existence of an endogenous VIP-like component in the normal hyperpolarizing action of giant-axon activity on the membrane potential of the Schwann cell.

Animals↗

PubMed1987

The Bulla ocular circadian pacemaker. I. Pacemaker neuron membrane potential controls phase through a calcium-dependent mechanism.

In an effort to understand the cellular basis of entrainment of circadian oscillators we have studied the role of membrane potential changes in the neurons which comprise the ocular circadian pacemaker of Bulla gouldiana in mediating phase shifts of the ocular circadian rhythm. We report that: 1. Intracellular recording was used to measure directly the effects of the phase shifting agents light, serotonin, and 8-bromo-cAMP on the membrane potential of the basal retinal neurons. We found that light pulses evoke a transient depolarization followed by a smaller sustained depolarization. Application of serotonin produced a biphasic response; a transient depolarization followed by a sustained hyperpolarization. Application of a membrane permeable analog of the intracellular second messenger cAMP, 8-bromo-cAMP, elicited sustained hyperpolarization, and occasionally a weak phasic depolarization. 2. Changing the membrane potential of the basal retinal neurons directly and selectively with intracellularly injected current phase shifts the ocular circadian rhythm. Both depolarizing and hyperpolarizing current can shift the phase of the circadian oscillator. Depolarizing current mimics the phase shifting action of light, while hyperpolarizing current produces phase shifts which are transposed approximately 180 degrees in circadian time to depolarization. 3. Altering BRN membrane potential with ionic treatments, depolarizing with elevated K+ seawater or hyperpolarizing with lowered Na+ seawater, produces phase shifts similar to current injection. 4. The light-induced depolarization of the basal retinal neurons is necessary for phase shifts by light. Suppressing the light-induced depolarization with injected current inhibits light-induced phase shifts. 5. The ability of membrane potential changes to shift oscillator phase is dependent on extracellular calcium. Reducing extracellular free Ca++ from 10 mM to 1.3 X 10(-7) M inhibits light-induced phase shifts without blocking the photic response of the BRNs. The results indicate that changes in the membrane potential of the pacemaker neurons play a critical role in phase shifting the circadian rhythm, and imply that a voltage-dependent and calcium-dependent process, possibly Ca++ influx, shifts oscillator phase in response to light.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2001

Effect of lithium and sodium valproate ions on resting membrane potentials in neurons: an hypothesis.

In an attempt to understand the therapeutic effects of lithium and sodium valproate in stabilizing the moods in manic depressive illness, the well-known Goldman-Hodgkin-Katz (G-H-K) equation is modified to include a fourth ion, such as a lithium ion or a sodium ion. The modified G-H-K equation is used to calculate the resting membrane potential in neurons. These calculations show that the resting membrane potential is depolarized depending upon the relative concentration of the lithium ion and upon its relative permeability. These calculations suggest that the resting membrane potential may be hyperpolarized in bipolar patients before treatment, and that the lithium ion perhaps depolarizes the resting membrane potential back to the normal level. They further support the prevailing hypothesis that manic-depressive illness may be caused by the hyperpolarization of the resting membrane potential, which, in turn, may be caused by the changes in ionic conductance (permeability) of the membranes. Sodium ions in sodium valproate do not significantly affect the resting membrane potential since they do not significantly change in the serum.

Bipolar Disorder↗

PubMed1983

Cell-to-cell channels with two independently regulated gates in series: analysis of junctional conductance modulation by membrane potential, calcium, and pH.

We study cell-to-cell channels, in cell pairs isolated from Chironomus salivary gland, by investigating the dependence of junctional conductance (gj) on membrane potentials (E1, E2), on Ca2+, and on H+, and we explore the interrelations among these dependencies; we use two separate voltage clamps to set the membrane potentials and to measure gj. We find gj to depend on membrane potentials whether or not a transjunctional potential is present. The pattern of gj dependence on membrane potentials suggests that each channel has two closure mechanisms (gates) in series. These gates pertain, respectively, to the two cell faces of the junction. By treating the steady-state gj as the resultant of two simultaneous but independent voltage-sensitive open/closed equilibria, one within each population of gates (i.e., one on either face of the junction), we develop a model to account for the steady-state gj vs. E relationship. Elevation of cytosolic Ca2+ or H+ at fixed E lowers gj, but at moderate concentrations of these ions this effect can be completely reversed by clamping to more negative E. Overall, the effect of a change in pCai or pHi takes the form of a parallel shift of the gj vs. E curve along the E axis, without change in slope. We conclude (1) that the patency of a cell-to-cell channel is determined by the states of patency of its two gates; (2) that the patency of the gates depends on membrane potentials (not on transjunctional potential), on pCai, and on pHi; (3) that pCai and pHi determine the position of the gj vs. E curve on the E axis; and (4) that neither Ca2+ nor H+ at moderate concentrations alters the voltage sensitivity of gj.

Animals↗

PubMed1986

Transport of F1-ATPase subunit beta into mitochondria depends on both a membrane potential and nucleoside triphosphates.

Transport of cytoplasmically synthesized precursor proteins into or across the inner mitochondrial membrane requires a mitochondrial membrane potential. We have studied whether additional energy sources are also necessary for protein translocation. Reticulocyte lysate (containing radiolabelled precursor proteins) and mitochondria were depleted of ATP by pre-incubation with apyrase. A membrane potential was then established by the addition of substrates of the electron transport chain. Oligomycin was included to prevent dissipation of delta psi by the action of the F0F1-ATPase. Under these conditions, import of subunit beta of F1-ATPase (F1 beta) was inhibited. Addition of ATP or GTP restored import. When the membrane potential was destroyed, however, the import of F1 beta was completely inhibited even in the presence of ATP. We therefore conclude that the import of F1 beta depends on both nucleoside triphosphates and a membrane potential.

Adenosine Triphosphate↗

PubMed1989

Dual-wavelength ratiometric fluorescence measurements of membrane potential.

This work shows that the voltage across membranes in two very different preparations, lipid vesicles in suspension and individual HeLa cells under a microscope, is linearly related to the ratio of fluorescence excited from the two wings of the absorption spectrum of a voltage-sensitive dye. The dye di-4-ANEPPS [1-(3-sulfonatopropyl)-4-[beta-[2-(di-n-butylamino)-6-naphthyl] vin yl]pyridinium betaine] is well characterized from earlier investigations and responds via a rapid (less than millisecond) spectral shift to membrane potential changes. The resultant small change in fluorescence intensity monitored at a single wavelength is useful for measurements of temporally well-defined voltage transients such as action potentials. The dual-wavelength approach described in this work extends the usefulness of this fast potentiometric dye by filtering out complex or artifactual changes in fluorescence intensity and providing a voltage-dependent signal that is internally standardized. Thus, rapid measurements of membrane potential are made possible in nonexcitable cells.

Electric Conductivity↗