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PubMed2006

Tonic activity of parasympathetic efferent nerve fibers hyperpolarizes the resting membrane potential of frog taste cells.

We investigated the relationship between the membrane potential of frog taste cells in the fungiform papillae and the tonic discharge of parasympathetic efferent fibers in the glossopharyngeal (GP) nerve. When the parasympathetic preganglionic fibers in the GP nerve were kept intact, the mean membrane potential of Ringer-adapted taste cells was -40 mV but decreased to -31 mV after transecting the preganglionic fibers in the GP nerve and crushing the postganglionic fibers in the papillary nerve. The same result occurred after blocking the nicotinic acetylcholine receptors on parasympathetic ganglion cells in the tongue and blocking the substance P neurokinin-1 (NK-1) receptors in the gustatory efferent synapses. This indicates that the parasympathetic nerve (PSN) hyperpolarizes the membrane potential of frog taste cells by -9 mV. Repetitive stimulation of a transected GP nerve revealed that a -9-mV hyperpolarization of taste cells maintained under the intact GP nerve derives from an approximately 10-Hz discharge of the PSN efferent fibers. The mean frequency of tonic discharges extracellularly recorded from PSN efferent fibers of the taste disks was 9.1 impulses/s. We conclude that the resting membrane potential of frog taste cells is continuously hyperpolarized by on average -9 mV by an approximately 10-Hz tonic discharge from the parasympathetic preganglionic neurons in the medulla oblongata.

Action Potentials↗
PubMed1987

Synchronous occurrence of spontaneous localized calcium release from the sarcoplasmic reticulum generates action potentials in rat cardiac ventricular myocytes at normal resting membrane potential.

Under certain conditions, spontaneous release of Ca2+ from the sarcoplasmic reticulum occurs in resting mammalian myocardium. In single rat ventricular myocytes, such spontaneous Ca2+ release appears localized rather than homogeneous. When the increase in cytosolic Ca2+ is present in a single locus within a cell, it causes a small depolarization, which, at the normal resting potential, is subthreshold for generating an action potential. However, when spontaneous Ca2+ release occurs simultaneously at more than a single discrete locus, the resultant sarcolemmal depolarization is augmented to levels that can induce an action potential, even when this depolarization begins at the normal resting membrane potential. Thus, the synchronous occurrence of multifocal localized increases in cytosolic Ca2+ due to spontaneous Ca2+ release from the sarcoplasmic reticulum within ventricular myocytes is a mechanism for "abnormal automaticity."

Action Potentials↗
PubMed1985

Influence of Ca2+ on the plasma membrane potential and electrogenic uptake of glycine by myeloma cells. Involvement of a Ca2+-activated K+ channel.

The involvement of Ca2+-activated K+ channels in the regulation of the plasma membrane potential and electrogenic uptake of glycine in SP 2/0-AG14 lymphocytes was investigated using the potentiometric indicator 3,3'-diethylthiodicarbocyanine iodide. The resting membrane potential was estimated to be -57 +/- 6 mV (n = 4), a value similar to that of normal lymphocytes. The magnitude of the membrane potential and the electrogenic uptake of glycine were dependent on the extracellular K+ concentration, [K+]o, and were significantly enhanced by exogenous calcium. The apparent Vmax of Na+-dependent glycine uptake was doubled in the presence of calcium, whereas the K0.5 was not affected. Ouabain had no influence on the membrane potential under the conditions employed. Additional criteria used to demonstrate the presence of Ca2+-activated K+ channels included the following: (1) addition of EGTA to calcium supplemented cells elicited a rapid depolarization of the membrane potential that was dependent on [K+]o; (2) the calmodulin antagonist, trifluoperazine, depolarized the membrane potential in a dose-dependent and saturable manner with an IC50 of 9.4 microM; and (3) cells treated with the Ca2+-activated K+ channel antagonist, quinine, demonstrated an elevated membrane potential and depressed electrogenic glycine uptake. Results from the present study provide evidence for Ca2+-activated K+ channels in SP 2/0-AG14 lymphocytes, and that their involvement regulates the plasma membrane potential and thereby the electrogenic uptake of Na+-dependent amino acids.

Animals↗
PubMed1988

Flow cytometric analysis of membrane potential in embryonic rat spinal cord cells.

Flow cytometric analysis of membrane potential in suspensions of embryonic rat spinal cord cells was carried out in a fluorescence-activated cell sorter (FACS) using anionic voltage-sensitive, fluorescent dyes (oxonols). The FACS or flow cytometer is an analytical instrument that measures optical properties of large cell populations at a single cell level of resolution. The incorporation of oxonol allows relative measurements of membrane potential, since the partition of oxonol within the plasmalemma is directly related to the degree of cell depolarization. Incubation of cells in elevated K+ concentrations or with the Na+ channel agonist batrachotoxin (BTX) changed the fluorescence intensity distribution pattern of the live-cell population; these changes were consistent with the depolarizing effects of these manipulations. Fluorescence shifts were either undetectable or minimal in the dead-cell population. The BTX-induced shift was blocked by tetrodotoxin (TTX) and was reversed in Na+-free medium, indicating embryonic expression of functional Na+ channels. Fluorescence microscopy of sorted cells showed that live cells typically exhibited circumferential ring-like patterns, whose intensities were enhanced under depolarizing conditions. The results show that flow cytometry combined with oxonol dyes can be used to measure the relative membrane potential of large numbers of individual central nervous system cells. The analysis of the changes in the distributions of these membrane potentials can be used to reveal the development of functional ion conductance mechanisms.

Animals↗
PubMed1979

Membrane potential oscillations in molluscan "burster" neurones.

Membrane potential oscillations can be induced in molluscan neurones under a variety of artificial conditions. In the so-called 'burster' neurones oscillations are generated even in isolated cells. A likely mechanism for 'bursting' involves the following ionic currents: 1. A transient inward current carried by Na+ and Ca2+. This current is responsible for the upstroke of the action potentials. 2. A delayed outward current carried by K+. This current is voltage-sensitive and is responsible for the downstroke of the action potential during the early part of the burst. It becomes progressively inactivated during the burst. Its amplitude depends on the intracellular pH. 3. A rapidly developing outward current carried by K+ which is inactivated at potentials close to action potential threshold. This current tends to hold the membrane in the hyperpolarized state and is involved in spacing the action potentials. 4. A prolonged inward current which may not inactivate. It is probably carried by both Na+ and Ca2+. This current is responsible for the depolarizing phase of the burst but also contributes to the action potential. 5. A slowly developing outward current, carried by K+. This current appears as a result of a slow increase in intracellular ionized calcium and is responsible for the hyperpolarizing phase of the burst. Note that a transient increase in this current may also contribute to the falling phase of the action potential during the later stages of the burst. It is also sensitive to intracellular pH. One of the more significant features of this system of producing membrane potential oscillations is that the frequency of the bursts depends on the rate at which the intracellular ionized calcium returns to its resting level. This process depends on the metabolic state of the animal which can thereby exert a considerable influence on the electrical activity of burster neurones.

Animals↗
PubMed1959

The effect of the ovarian steroids on the membrane potential of uterine muscle.

Measurements with flexible intracellular microelectrodes show that the rabbit myometrium when insufficiently stimulated by estrogen has a low membrane potential of about 30 to 35 mv. Estrogen (endogenous or exogenous) increases this value up to 43 to 48 mv., whereas progesterone increases it still further up to 55 to 60 mv. Between the 20th and 29th days of rabbit pregnancy the membrane potential at placental implantation sites is about 10 mv. higher than between these sites. Progesterone treatment increases the value at the interplacental sites to the level of the placental sites. The onset of labor is preceded by a drop in membrane potential at the placental sites to the level of the interplacental sites. This change results in a more or less uniform potential of 45-50 mv. along the length of the uterine horn at term. The membrane potential of the uterus is a log function of the [K](0) at values greater than 12 mM/liter, as is the case in other excitable tissues. In Ca-free Krebs the membrane potential of the estrogen-dominated uterus drops to a low level; the progesterone-dominated myometrium exhibits only a transient and lesser decrease. The membrane potential of the myometrial cell is influenced by endocrine regulation. The correlation between membrane potential and threshold only holds for the estrogen-dominated uterus, however, in other endocrine conditions the relationship breaks down.

Animals↗
PubMed1997

Hypoxia in striatal and cortical neurones: membrane potential and Ca2+ measurements.

Simultaneous measurements of membrane potential and intracellular Ca2+ were used to study the effects of hypoxia on striatal and cortical neurones. Striatal neurones responded to hypoxia with a reversible membrane depolarization coupled with a transient increase in intracellular Ca2+. Thirty minutes of hypoxia caused an irreversible membrane depolarization associated with a massive raise in Ca2+ levels, leading to cell death. Conversely, cortical neurones were more resistant to O2 deprivation. Hypoxia (4-10 min) induced minimal changes in both membrane potential and Ca2+ signals. Longer periods (20-30 min) caused an initial membrane hyperpolarization followed by a large but reversible depolarization coupled with a transient increase in Ca2+ signals. These results support the hypothesis of a differential sensitivity of central neurones to hypoxia, suggesting that striatal neurones are more vulnerable than cortical cells.

Animals↗
PubMed1987

Mitochondrial membrane potential estimated with the correction of probe binding.

Lipophilic ions are widely used as the probe for estimation of the membrane potential. It is suggested that the correction of the probe binding to the membrane and/or intracellular constituents is a problem to be solved in order to evaluate the membrane potential accurately. Previously, we proposed a method for the correction of the probe binding (Demura, M., Kamo, N. and Kobatake, Y. (1985) Biochim. Biophys. Acta 820, 207-215). In this paper, the method was applied to the determination of the membrane potential of intact mitochondria. The probes used constitute a homologous series of (Phe)3-P+-(CH2)n-CH3 (n = 0-4) and tetraphenylphosphonium (TPP+). Binding of these probes to de-energized mitochondria followed the Langmuir isotherm. However, values of parameters determined at high (50-800 microM) and low (under 20 microM) probe concentrations were different, suggesting the existence at least two, high- and low-affinity, binding sites. With extrapolation to the 'state of no binding', the membrane potential of intact mitochondria was estimated to be -147 mV (interior-negative) when they were energized by 5 mM succinate in medium consisting of 125 mM KCl, 10 mM MgCl2, 5 mM phosphate, 0.4 mM EDTA and 50 mM Tris-HCl (pH 7.5) at 25 degrees C. Parameters appearing in the equation for the correction of probe binding were determined with the use of this value of the membrane potential. The validity of the equation and the value of the parameters were revealed by the fact that after the correction, all probes used gave approximately the same value under the same conditions. We expanded the method so as to include the langmuir adsorption isotherm. When the modified equation is used, the estimated membrane potentials were less dependent on a probe concentration less than 10 microM.

Animals↗
PubMed1983

Inhibition by tosyl-L-phenylalanyl chloromethyl ketone of membrane potential changes in rat neutrophils. Correlation with the inhibition of biological activity.

A plasma membrane-associated serine esterase (protease) has previously been reported to be required during stimulation of a variety of cell types. In this study we have examined the role of such a protease on membrane potential changes using an optical probe of membrane potential 3,3'-dipropylthiodicarbocyanine iodide. The irreversible chymotrypsin-like protease inhibitor TPCK (tosyl-L-phenylalanyl chloromethyl ketone) inhibited membrane potential changes in rat neutrophils in response to phorbol myristate acetate, N-formylmethionylleucylphenylalanine and the calcium ionophore A23187 in a time- and dose-dependent manner. This inhibition was correlated with the known inhibitory effects on superoxide (O-2) generation and enzyme release (lysozyme and beta-glucuronidase). High external calcium concentrations overcame the inhibitory effects of TPCK on A23187-induced stimulation but had no effect on the inhibition of N-formylmethionylleucylphenylalanine stimulation. These results suggest that a TPCK-inhibitable activity is required for the development of the membrane potential changes that are coupled to subsequent secretory events and precede a calcium requiring activity.

Acetates↗
PubMed1978

Changes in membrane potential during calcium ion influx and efflux across the mitochondrial membrane.

1. A depolarisation of the membrane of rat liver mitochondria, as measured with the safranine method, is seen during Ca2+ uptake. The depolarisation is followed by a slow repolarisation, the rate of which can be increased by the addition of EGTA or phosphate. 2. Plots relating the initial rate of calcium ion (Ca2+) uptake and the decrease in membrane potential (delta psi) to the Ca2+ concentration show a half-maximal change at less than 10 micron Ca2+ and a saturation above 20 micron Ca2+. 3. Plots relating the initial rate of Ca2+ uptake to delta psi are linear. 4. Addition of Ca2+ chelators, nitriloacetate or EGTA, to deenergized mitochondria equilibrated with Ca2+ causes a polarisation of the mitochondrial membrane due to a diffusion potential created by electrogenic Ca2+ efflux. 5. If the extent of the response induced by different nitriloacetate concentrations is plotted against the expected membrane potential a linear plot is obtained up to 70 mV with a slope corresponding to two-times the extent of the response induced by valinomycin in the presence of different potassium ion gradients. This suggests that the Ca2+ ion is transferred across the membrane with one net positive charge in present conditions.

Acetates↗
PubMed1999

Evaluation of gravity-dependent membrane potential shift in Paramecium.

It is still debated whether or not gravity can stimulate unicellular organisms. This question may be settled by revealing changes in the membrane potential in a manner depending on the gravitational forces imposed on the cell. We estimated the gravity-dependent membrane potential shift to be about 1 mV G-1 for Paramecium showing gravikinesis at 1-5 G, on the basis of measurements of gravity-induced changes in active propulsion and those of propulsive velocity in solutions, in which the membrane potential has been measured electrophysiologically. The shift in membrane potential to this extent may occur from mechanoreceptive changes in K+ or Ca2+ conductance by about 1% and might be at the limit of electrophysiological measurement using membrane potential-sensitive dyes. Our measurements of propulsive velocity vs membrane potential also suggested that the reported propulsive force of Paramecium measured in a solution of graded densities with the aid of a video centrifuge microscope at 350 G was 11 times as large as that for -29 mV, i.e., the resting membrane potential at [K+]o = 1 mM and [Ca2+]o = 1 mM, and, by extrapolation, that Paramecium was hyperpolarized to -60 mV by gravity stimulation of 100-G equivalent, the value corrected by considering the reduction of density difference between the interior and exterior of the cell in the graded density solution. The estimated shift of the membrane potential from -29 mV to -60 mV by 100-G equivalent stimulation, i.e., 0.3 mV G -1, could reach the magnitude entirely feasible to be measured more directly.

Animals↗
PubMed1991

Patterns of membrane potentials and distributions of the medullary respiratory neurons in the decerebrate rat.

We analyzed the membrane potential of 161 respiratory neurons in the medulla of decerebrate rats which were paralyzed and ventilated. Three types of inspiratory (I) neurons were observed: those displaying progressive depolarization in inspiration (augmenting I neurons), those which gradually repolarized after maximal depolarization at the onset of inspiration (decrementing I neurons) and those exhibiting a plateau or bell-shaped membrane potential trajectory throughout inspiration (I-all neurons). Three types of expiratory (E) neurons were also encountered: those in which the membrane potential progressively depolarized (augmenting E neurons), those in which the membrane potential repolarized during the interval between phrenic bursts (decrementing E or post-I neurons) and those exhibiting a plateau or bell-shaped membrane potential trajectory throughout expiration (E-all neurons). Axonal projections of these medullary neurons were identified in the cranial nerves (n = 34), or in the spinal cord (n = 19) as revealed by antidromic stimulation and/or by reconstruction following horseradish peroxidase (HRP) labeling. The other 108 neurons were not antidromically activated (NAA) by the stimulations tested, or had their axons terminating inside the medulla as revealed by HRP labeling. All these respiratory neurons, except for 3 which were hypoglossal motoneurons, had their somata within the ventrolateral medulla, in the region of the nucleus ambiguus, homologous to the ventral respiratory group (VRG) of the cat. No dorsal respiratory group (DRG) was detected within the medulla of the rats. Due to this absence of a DRG, it is concluded that the neural organization of respiratory centers is quite different in cats and rats.

Animals↗
PubMed1994

Smooth muscle cells affect endothelial membrane potential in rat aorta.

The effects of vasoconstrictors on membrane potential of endothelium of intact rat aorta were investigated using the patch-clamp technique. Norepinephrine, endothelin (ET)-1, 5-hydroxytryptamine (5-HT), vasopressin, and angiotensin II evoked depolarization and oscillations in membrane potential. The alpha 1-adrenoreceptor agonist phenylephrine (PE), but not the alpha 2-agonist clonidine or the beta-agonist isoproterenol, evoked oscillations. The antagonist of 5-HT2-receptors, ketanserin, inhibited 5-HT-evoked oscillations. ET-3, unlike ET-1, did not evoke oscillations. The antagonists of voltage-operated Ca2+ channels, nifedipine and verapamil, inhibited vasoconstrictor-evoked oscillations, and the Ca2+ channel agonist BAY K 8644 enhanced oscillations. Acetylcholine and sodium nitroprusside inhibited PE-evoked oscillations. The inhibitors of NO synthase, N omega-nitro-L-arginine and NG-methyl-L-arginine, as well as methylene blue, enhanced oscillations. The intima of rat aorta with endothelium was removed from underlying smooth muscle. In this preparation, acetylcholine evoked a response similar to that in the intact vessel, but PE and ET-1 were without effect. These data suggest that vasoconstrictors acting on receptors on aortic smooth muscle evoke a response that is transferred to the endothelium and evokes depolarization and oscillations in endothelial membrane potential.

Animals↗
PubMed1991

Permselectivity of sound and carious human dental enamel as measured by membrane potential.

A microwell technique was used for determination of the permselectivities of sound and carious enamel in the same slice of tooth. The permselectivity determination was accomplished by drilling microwells in the enamel and filling them with a simulated plaque fluid containing lactate, carbonate, and inorganic ions at concentrations similar to those in resting plaque fluid, but with different concentrations of KCl. The electrical potentials developed across the enamel membrane were measured with microreference electrodes placed in the wells or in the solution outside the tooth. The results showed that the membrane potential was a function of the composition of the solutions separated by the enamel membrane and was independent of the composition of the solutions in the adjacent wells. The enamel was found to be cation-permselective, and sound enamel was more permselective than carious enamel. The flux rate of K+ was estimated from the change in the K+ concentration of the well solution as a function of time. The flux rate and the membrane potential data were used in the Nernst-Planck Flux Equation for calculation of the diffusion coefficient of K+ through enamel. The results indicate that the permselectivity of enamel can greatly influence the diffusion of ions through enamel membranes.

Carbonic Acid↗
PubMed1990

Membrane potential dependence of intracellular pH regulation by identified glial cells in the leech central nervous system.

1. We have measured the intracellular pH (pHi) and membrane potential of identified glial cells in the central nervous system of the leech, Hirudo medicinalis, using double-barrelled pH-sensitive microelectrodes. 2. When extracellular K+ concentration was increased, the glial membrane potential decreased and pHi increased; lowering the extracellular K+ concentration hyperpolarized the glial membrane and decreased pHi. These pHi changes were largely dependent upon the presence of CO2-HCO3-; in nominally CO2-HCO3(-)-free saline solution, they were 50-80% smaller. 3. The steady-state pHi of the glial cells in CO2-HCO3(-)-buffered saline solution strongly correlated with the membrane potential between -40 and -90 mV. The slope of this relationship was 60 mV/pH unit. 4. The neurotransmitter 5-hydroxytryptamine (50 microM), which hyperpolarizes the glial membrane, also produced a large, CO2-HCO3(-)-dependent decrease in pHi. The size of the pHi change depended upon the amplitude of the membrane hyperpolarization. 5. The increase in pHi produced by the membrane depolarization in 20 mM-K+ was abolished in Na(+)-free saline. Removal of external Na+ in the presence of 20 mM-K+ reversed the pHi increase. 6. The pHi increase in 20 mM-K+ was also inhibited by the stilbene 4,4-diisothiocyanostilbene-2'-disulphonic acid (DIDS, 0.5 mM). In a DIDS-poisoned preparation a small decrease of pHi was observed in 20 mM-K+ both in the presence and nominal absence of CO2-HCO3-. 7. In neurones, neither CO2-HCO3- nor 20 mM-K+ produced an intracellular alkanization. The steady-state pHi of several identified neurones was not correlated with the membrane potential. 8. We conclude that in glial cells, but not in neurones, the pHi is dependent upon the membrane potential. This membrane potential dependence is due to the activity of the electrogenic Na(+)-HCO3- co-transporter in the glial cell membrane.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1993

Lack of voltage sensitive potassium channels and generation of membrane potential by sodium potassium ATPase in murine T lymphocytes.

Voltage sensitive K+ channels, which are responsible for generation of membrane potential in most cells, are functionally absent in about one-third of peripheral murine T cells and greatly reduced in the rest as shown by resistance of their membrane potential to changes in extracellular potassium concentration and failure of K+ channel dependent volume regulation. Despite the absence of voltage- sensitive K+ channels, the membrane potential of peripheral T cells is between -60 and -70 mV, the same as thymocytes. A total of 40 to 70 mV of the membrane potential of peripheral T cells is produced by the direct electrogenic action of the asymmetric Na+K+ ATPase pump because the cells are depolarized by ouabain, an inhibitor of the pump, removal of extracellular potassium or reduction of temperature. The residual, ouabain-resistant membrane potential, is sensitive to the K+ channel blocker, quinine, and thus due to electrodiffusion through K+ channels. Na+ and K+ turnover, and sensitivity to ouabain, are the same in peripheral T cells and thymocytes. The predominant mechanism of membrane potential generation changes during T lymphocyte differentiation from electrodiffusion in the thymus to electrogenic in peripheral T cells and back to electrodiffusion upon peripheral cell activation.

Animals↗
PubMed1968

A contribution of an electrogenic Na+ pump to membrane potential in Aplysia neurons.

The resting membrane potential (RMP) of Aplysia neurons is very temperature-dependent, and in some cells increases with increasing temperature by as much as 2 mv/ degrees C. RMP at room temperature may significantly exceed the potassium equilibrium potential, which can be determined by measurement of the equilibrium point of the spike after potential. The hyperpolarization on warming is completely abolished by ouabain, replacement of external Na(+) by Li(+), removal of external K(+), and by prolonged exposure to high Ca(++), while it is independent of external chloride but is increased by cocaine (3 x 10(-3)M). In an identified cell that shows a marked temperature dependence of RMP, both the potassium equilibrium potential and the membrane resistance were found to be relatively independent of temperature. The hyperpolarization on warming, which may increase RMP by as much as 50%, can most reasonably be ascribed to the activity of an electrogenic Na(+) pump.

Action Potentials↗
PubMed1989

Effect of cold temperature on membrane potential responses in opossum esophageal circular muscle.

The effects of cold temperature on resting membrane potential (RMP) and membrane potential responses to depolarizing electrical current and intramural nerve stimulation were examined in opossum esophageal circular smooth muscle. Intracellular recordings were made in smooth muscle strips obtained from 7 to 8 cm (proximal site) and 1 to 2 cm (distal site) above the lower esophageal sphincter. RMP was not affected by changes in temperature between 34 and 22 degrees C. Cooling caused progressive inhibition of the amplitude and a slight increase in the duration of the spike potential produced by depolarizing current. Cooling did not modify the threshold for spike potential generation but decreased the spike amplitude from 34.0 +/- 0.5 mV at 34 degrees C to 14.1 +/- 2.2 mV at 22 degrees C (P less than 0.01). Electrical field stimulation with single electrical pulses (1.0 ms) produced tetrodotoxin-sensitive biphasic membrane responses consisting of initial hyperpolarization, or an inhibitory junction potential followed by depolarization that increased in amplitude as temperature was decreased from 34 to 26 degrees C and then decreased in amplitude as temperature was further decreased. At both proximal and distal sites cooling from 34 to 22 degrees C caused more than a twofold increase in the duration of hyperpolarization and time to peak depolarization. However, the increase in the absolute time of the duration of hyperpolarization and the time to peak depolarization was significantly greater at the distal than proximal esophageal site. Cooling to 16 degrees C decreased RMP and nearly abolished the biphasic membrane potential response.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗