Correlations between membrane potential and inhibitory post-synaptic potential in spinal motor neurones.
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Animals↗
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[Changes in membrane potentials and resistance of muscle membranes in the crayfish Astacus fluviatilis induced by changes in pH].
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Animals↗
Functional maturation of membrane potential changes and superoxide-producing capacity during differentiation of human granulocytes.
The alterations of stimulus-induced membrane potential changes, superoxide (O2-)-producing capacity and phagocytic activity during differentiation of human granulocytes were investigated in the human leukemia cell lines HL-60 and KG-1 differentiating in vitro and in human leukemic granulocytes obtained from chronic myelogenous leukemia patients. HL-60 cells incubated with dimethyl sulfoxide or with retinoic acid showed progressively increasing O2- production as well as membrane potential changes (depolarization) on contact with phorbol myristate acetate or the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine, with a concomitant increase in the proportion of mature cells of the granulocytic type. Phagocytosis of latex particles, yeast, and oil droplets appeared 24 h after incubation with dimethyl sulfoxide and anteceded the increment of O2- production and membrane potential changes, both of which appeared concomitantly 3 d after incubation with dimethyl sulfoxide. Similar findings were observed when immature and mature granulocytes obtained from chronic myelogenous leukemia patients were stimulated by phorbol ester, the chemotactic peptide, or calcium ionophore A23187, and the amount of O2- production was parallel to the magnitude of membrane potential changes. HL-60 and KG-1 cells incubated for 1-6 d with phorbol myristate acetate showed neither O2- production nor membrane potential changes on contact with phorbol ester, chemotactic peptide, or A23187, although such cells resembled macrophages morphologically, and their phagocytic activity was significantly increased. O2- production and membrane potential changes in normal granulocytes induced by phorbol ester, chemotactic peptide and A23187 were inhibited by 2-deoxyglucose. These findings indicate that the O2--producing system and the system provoking membrane potential changes may develop concomitantly as human granulocytes mature and differentiate, and that the development of these systems and of phagocytic activity may be independently regulated.
Adult↗
Resting membrane potentials and excitability at different regions of rat dorsal root ganglion neurons in culture.
To study the role of electrical membrane processes in neuronal regeneration and growth, resting membrane potentials and action potentials of sensory (dorsal root ganglion) neurons growing in culture were measured at the soma, neurite and growth cone using the whole-cell patch-clamp technique. Our results show that resting membrane potentials measured at the soma (-56.8 +/- 8.8 mV), neurite varicosity (-55.8 +/- 5.2 mV) and growth cone (-57.2 +/- 4.1 mV) of growing neurons were not statistically different. The membrane resistance measured around the resting membrane potential at the neurite varicosity (160 +/- 70 M omega) was smaller than those at the soma (687 +/- 540 M omega) and growth cone (922 +/- 825 M omega). The resting membrane potential measured at the soma using a perforated patch (-60.3 +/- 4.4 mV) was not different from that measured in the normal whole cell. In both configurations, isotonic KCl (140 mM) depolarized the membrane potential to above 0 mV. The K+ channel blockers quinine, Cs+, 4-aminopyridine and tetraethylammonium depolarized the membrane potential by 10-40 mV, while Na(+)-free extracellular solution hyperpolarized it by about 10 mV. Extracellularly applied ouabain, intracellular Na(+)-free or low Cl(-)-containing solutions did not affect the resting membrane potential. Similar results were obtained for growth cones. Action potentials could be evoked by current pulses in 81% of somata and in all growth cones, but not in neurite varicosities. Current-induced repetitive firing was found in 19% of somata and in 65% of growth cones.(ABSTRACT TRUNCATED AT 250 WORDS)
Action Potentials↗
Subacinar distribution of hepatocyte membrane potential response to stimulation of gluconeogenesis.
Isolated rat livers were perfused and the membrane potentials of matched periportal and pericentral hepatocytes were determined using glass microelectrodes. O2 uptake and gluconeogenesis were increased by both phenylephrine and glucagon and the extent of the increase was not affected by the direction of perfusion. With no exogenous substrate, hepatocyte membrane potentials were approximately -27 mV. No gradients were found. Substrate produced hyperpolarization in all hepatocytes, with a small but significant gradient produced. Phenylephrine-induced hyperpolarization was higher in periportal than in pericentral hepatocytes during anterograde perfusion, but reversed during retrograde perfusion. Similar effects on membrane potential were produced by phorbol myristate acetate (PMA). Glucagon hyperpolarized homogeneously during both anterograde and retrograde perfusion with no gradients across the acinus. Octanol addition during glucagon stimulation, however, resulted in heterogeneity similar to phenylephrine or PMA. Thus when hepatocytes are stimulated by substrate or hormones, the degree of hepatocyte membrane potential heterogeneity across the acinus is highly dependent on the nature of the stimulus. We propose that the differential hormone effects on hepatocyte membrane potential may be mediated at least in part by differential modulation of cell to cell communication via gap junctions.
Animals↗
Role of membrane potential in the accumulation of quaternized ellipticines by human tumor cell lines.
9-Methoxy-N2-methylellipticinium acetate (MMEA) is representative of a series of quaternized ellipticines that exhibited selective cytotoxicity for human brain tumor cell lines of glial origin in the in vitro primary screen of the U.S. National Cancer Institute. The present investigation was initiated to determine whether membrane potential contributes to the cellular accumulation of this lipophilic cation by selected brain tumor and non-brain tumor cell lines. The results indicate that accumulation of MMEA by drug-sensitive cell lines, but not drug-resistant cell lines, is reduced by experimental conditions that depolarize the plasma membrane, e.g., stepped increases in the extracellular potassium concentration. These experimental conditions result in increased cellular fluorescence of cells stained with the voltage-sensitive anionic dye bis(1,3-dibutylbarbituric acid)trimethine oxonol, suggesting that decreased accumulation of MMEA is the result of decreased membrane potential. Membrane potential measurements using the null point method indicated that the mean membrane potential of selected MMEA-sensitive cell lines (-39.4 +/- 6.8 mV) was significantly lower (P < .005) than MMEA-resistant cell lines (-17 +/- 3.8 mV). Ultrastructural studies with the MMEA-sensitive U-251 glioblastoma indicated that the first morphological effects of MMEA occurred in mitochondria, where dissolution of cristae was observed, followed by engulfment of mitochondria in multilamellar phagocytic vesicles. Electron microscopic autoradiographic studies with tritium-labeled MMEA revealed that the drug was localized in mitochondria and nuclei.
Antineoplastic Agents↗
Contribution of an electrogenic sodium pump to the membrane potential in the intestinal epithelial cell.
The transmural potential difference of isolated rat duodenum and the membrane potential of its epithelial cell were examined during changes of the ionic medium at both warm (31--35 degrees C) and cold temperatures (2--5 degrees C). In the range of low external K+ concentrations, cooling produced an immediate and reversible depolarization of the membrane potential (around -10 mV) greater than that estimated from a simple thermodynamic temperature effect (RT/F). Such a temperature sensitive component of the membrane potential at 31 degrees C was completely abolished by anoxia and serosal ouabain. Readmission of K+ to the bathing fluid of duodenum previously deprived of K+ and loaded by Na+ caused a remarkable transient hyperpolarization of the epithelial membrane, which was abolished by serosal ouabain. Decreases in the value of transmural potential difference were also produced by cooling, anoxia and serosal ouabain, but these were so small that concurrent changes in the membrane potential could be regarded as chiefly reflecting changes in the effective emf of the cell. Thus, an electrogenic Na+-K+ exchange pump located on the serosal membrane of the duodenal epithelial cells was shown to contribute significantly to the membrane potential under normal conditions (up to around -7 mV). The coupling ratio of Na+-efflux and K+-influx associated with this pump was estimated by the Mullins-Noda equation (1963) to be approximately 4:3 under the physiological steady-state conditions.
Animals↗
Slow oscillations of membrane potential in interneurons that control heartbeat in the medicinal leech.
In the preceding paper (Arbas and Calabrese, 1987), we identified several properties that contribute to the activity of neurons (HN cells) that control heartbeat in the medicinal leech. Premotor HN (7) interneurons, which do not generate the heartbeat rhythm, exhibit Na+-dependent fast action potentials, Ca2+-mediated plateau potentials in the absence of Na+, and hyperpolarization-activated "restorative" changes in membrane potential that depolarize the membrane potential on hyperpolarization due to injected currents or synaptic inhibition. HN interneurons of ganglia 3 and 4 (i.e., timing oscillator interneurons) exhibit all of the properties described for HN (7) interneurons and have the additional characteristic that they are connected in oscillatory circuits. Reciprocal oscillations in membrane potential occurred in the bilateral HN interneurons (3) and (4) in the presence of elevated Ca2+ that were independent of Na+ -mediated action potentials. Their ability to oscillate in this way is based on 3 parameters: (1) production of a regenerative plateau potential by one of the pair of HN neurons in either ganglion, (2) inhibition of the contralateral HN neuron by the HN neuron in plateau, and (3) a phase transition mediated by escape from inhibition by the hyperpolarized HN neuron. The conductances responsible for restorative membrane potential shifts activated by hyperpolarization during synaptic inhibition may mediate the escape from inhibition that times the phase transition of the 2 HN neurons.
Action Potentials↗
Effect of calcium on the membrane potential of Amphiuma red cells.
An increase in extracellular Ca concentration causes the membrane of giant red cells of the salamander, Amphiuma means, to undergo a marked, transient hyperpolarization. This hyperpolarization is caused by an increase in K permeability of the membrane as judged from the K sensitivity of the membrane potential and from the rate of K loss under influence of raised extracellular Ca concentration. At constant external pH, the induction of hyperpolarization by increased extracellular Ca has a relatively well-defined threshold concentration. Furthermore the phenomenon is of an "all or none" type with most of the cells having membrane potential values either in the normal range (about -15 mV) or in the range -40 to -70mV. Shortly after suspension in Ringer's with 15 mm Ca, most if not all of the individual cells are hyperpolarized. Upon continued exposure (5-20 min) to the higher Ca concentration the membrane potential returns to the normal value in a fashion compatible with an "all or none" response. The observed Ca effect is sensitive to the pH of the suspending medium. At pH 6.2 the response is absent whereas the hyperpolarization is markedly stronger at pH 8.2 than at PH 7.2. It is argued that a reliable transport number for K under influence of Ca cannot be estimated from the slope of membrane potential vs. log (extracellular K concentration). This is probably related to the fact that the membrane potentials of the cells in the population do not stay constant in time. The above phenomenon is compared with the Ca-induced K permeability in poisoned human red cells or red cell ghosts. It is important to note that the cells employed in the present study are neither poisoned nor mechanically disrupted. This study emphasizes that the role of Ca in regulating cell membrane permeability to K seems to be a general feature.
Animals↗
Effect of sugars and amino acids on membrane potential in two clones of sugarcane.
Sugarcane (Saccharum officinarum L.) leaf parenchyma cells bathed in 1X solution maintained an average membrane potential of -135 millivolts in the dark. No difference in membrane potential was found between clones 51 NG 97 and H50 7209. An electrogenic pump appears to contribute to membrane potential in these cells. Sugars (25 millimolar) added externally caused the following membrane potential depolarizations (in millivolts) in clone 51 NG 97: glucose, 18 +/- 4; galactose, 24 +/- 7; 3-O-methylglucose, 10 +/- 4; sucrose, 22 +/- 3; fructose, 21 +/- 7; raffinose, 9 +/- 3; mannitol, 0; lactose, 0; melibiose, 0; and 1-O-methyl-alpha-galactose, 0. Glycine (25 millimolar) and serine (10 millimolar) caused depolarizations of 47 +/- 7 and 23 +/- 2 millivolts, respectively. Depolarization shows saturation kinetics with respect to glucose concentration, with a K(m) of 3 to 6 millimolar. The metabolic inhibitors KCN and salicyl hydroxamic acid together caused depolarization of the membrane potential and greatly inhibited depolarization by 25 millimolar glucose and 25 millimolar raffinose. In a series of substitution experiments, glucose (25 millimolar) caused almost total inhibition of depolarization by raffinose, sucrose, and 3-O-methylglucose (all 25 millimolar), but only partial inhibition of depolarization to 25 millimolar glycine. Glycine (25 millimolar), also, only partially inhibited depolarization by 25 millimolar glucose. Total depolarization to 25 millimolar glycine and 25 millimolar glucose was comparable to the amount of depolarization of membrane potential caused by 1 millimolar KCN plus 1 millimolar salicyl hydroxamic acid. The results are consistent with a co-transport mechanism of membrane transport, with sugars and amino acids being transported by separate carrier systems.
Journal Article↗
Gamma-frequency fluctuations of the membrane potential and response selectivity in visual cortical neurons.
Fluctuations at frequencies of 25-70 Hz is an inherent property of cortical activity. These rapid, gamma-range fluctuations are apparent in the local field potentials, in spiking of cells and cell groups, and in the membrane potential of neurons. To investigate stimulus dependence of the gamma-frequency fluctuations of the membrane potential, we have recorded intracellularly responses of cells in cat visual cortex to presentation of moving gratings. We found gamma-range fluctuations of the membrane potential in both simple and complex cells. The strength of the gamma-frequency fluctuations correlated with the stimulus optimality. Furthermore, the amplitude of the gamma-frequency fluctuations correlated with the phase of stimulus-imposed slow changes of the membrane potential. The combination of these features makes cortical neurons capable of encoding the slow changes in the visual world in a kind of amplitude modulation of the high frequency fluctuations. This assures reliable transformation of the membrane potential changes into spike responses without compromising the temporal resolution of visual information encoding in the low frequency range.
Action Potentials↗
Transport system ASC for neutral amino acids. An electroneutral sodium/amino acid cotransport sensitive to the membrane potential.
The influx of L-threonine through system ASC does not influence the membrane potential in cultured human fibroblasts although comparable fluxes of amino acids through another Na(+)-dependent agency, system A, effectively depolarize the cells. The membrane potential, however, stimulates the influx of amino acids through system ASC with a maximal effect at -50 mV. The sensitivity of amino acid influx through system ASC to the membrane potential is not constant, but rather, is dependent on intracellular and extracellular concentrations of the substrates, Na+ and amino acids, of the system. Conditions which favor the loading of the ASC carrier at the external surface reduce the sensitivity of ASC-mediated amino acid influx to the membrane potential; in contrast, the sensitivity of this amino acid influx increases under conditions which favor loading of the carrier at the internal surface. Trans-stimulation, a well-known characteristic of system ASC, also varies with the concentrations of the substrates of the system and, in fact, this characteristic is not observed when external Na+ is low. These data may be accommodated by a model in which an electrically silent mode of operation of the transporter is dominant. The influence of the membrane potential on the transport system is dependent on the extent to which a charge-translocating step in the cycling of the carrier is rate limiting (relative rate limitance).
Adolescent↗
[3H]tetraphenylphosphonium accumulation in cerebral cortical synaptosomes as a measure of nicotine-induced changes in membrane potential.
The effect of nicotine on synaptosomal membrane potential in P2 preparations of rat cerebral cortex was investigated using a membrane permeant, lipophilic cation, [3H]tetraphenylphosphonium ([3H]TPP+). [3H]TPP+ accumulated in synaptosomes in a time-dependent manner and its accumulation was decreased when the extracellular potassium concentration was increased and in the presence of the sodium channel toxin, veratridine. Nicotine (1-1000 microM) decreased the accumulation of [3H]TPP+ in both P2 synaptosomal preparations and in synaptosomes purified using Percoll gradients. This effect of nicotine was mimicked by other nicotinic agonists (1,1-dimethyl-4-phenylpiperazinium iodide, cytisine, suberyldicholine and acetylcholine) and was partially blocked by 10 microM mecamylamine and 30 microM hexamethonium. Atropine (1 microM) and the removal of calcium from the incubation mixture both enhanced the effect of nicotine while the addition of physostigmine (10 microM) reduced the nicotine-induced decrease in [3H]TPP+ accumulation, evidence that acetylcholine released from the synaptosomes by nicotine may produce hyperpolarization of synaptosomes via stimulation of presynaptic muscarinic receptors. It is concluded that the effect of nicotine on [3H]TPP+ accumulation is mediated by nicotine stimulation of a ganglionic-type nicotinic cholinergic receptor and that this method of determining synaptosomal membrane potential will provide a functional measure of presynaptic nicotinic receptor activation.
Animals↗
Membrane potentials of differentiating enterocytes.
A positional analysis of enterocyte membrane potential has been carried out using in vitro preparations of rabbit distal ileum. Young enterocytes were found to possess a microvillar membrane potential significantly less than that seen in older enterocytes. The length of enterocyte microvilli was also found to be significantly less in younger enterocytes. It is suggested that developmental changes in membrane potential, occurring during the early stages of enterocyte differentiation, probably reflect a changed permeability to ions associated with the establishment of a fully developed microvillar membrane. Other explanations for the observed findings are also considered.
Age Factors↗
The binding and release of the inhibitor protein are governed independently by ATP and membrane potential in ox-heart submitochondrial vesicles.
(1) The effects of membrane potential (delta psi) and nucleotides on the interaction between the F1-ATP synthase and its natural inhibitor protein (IF1) are studied in ox-heart submitochondrial vesicles. (2) Membrane potential causes displacement of IF1 from submitochondrial vesicles, as shown by measuring both delta psi-dependent stimulation of ATPase capacity and release of 125I-labelled IF1 from the vesicles. These effects are abolished if ATP is included in the incubation. (3) There is a linear increase in the steady-state ATPase capacity of oxidising vesicles as delta psi is increased from 100 mV to 135 mV. Increasing delta psi above 140 mV leads to no further change. (4) At a constant membrane potential, ATP suppresses the increase in ATPase capacity, with a concentration for half maximal effect of 140 microM. This value is close to the Km for ATP hydrolysis by membrane-bound F1. This suppression is related to ATP concentration rather than to delta Gp or ATP/ADP ratio. (5) The unidirectional on- and off-rates of IF1 were measured separately. The off-rate of IF1 is increased by membrane potential but unaffected by ATP. The on-rate, conversely, is increased by ATP. Thus, the suppression of the potential-dependent net release of IF1 from submitochondrial vesicles by ATP results from an increase of the IF1 on-rate above the off-rate.
Adenosine Triphosphate↗
Recovery of membrane potentials from diamide-induced depolarization in frog lens fibers.
Measurement of membrane potentials in isolated frog lens fibers was made by means of intracellular microelectrode techniques. The membrane potentials of lens fibers were depolarized to various degrees after exposure to diamide, an -SH inhibitor. When the degree of diamide-induced depolarization was less than 20 mV, the membrane potentials almost fully recovered to the control level within 12 h after immersion in a Ringer's solution containing dithiothreitol (DTT), a -SH protector. A similar tendency was also recognized in some lenses (57%) whose depolarization was 30 mV. When the degree of depolarization was 40 mV, the membrane potentials further depolarized in all cases tested in spite of treatment with DTT. From this study, it is considered that frog lens fibers could not recover their function if the damage was so severe as to produce a membrane depolarization of more 40 mV. Determination of ionic concentrations in lens fibers revealed a highly significant correlation between the degree of diamide-induced depolarization and changes in concentration ratio of Na+/K+.
Animals↗
A near-zero membrane potential in transporting corneal endothelial cells of rabbit.
1. When rabbit corneal endothelial cells are impaled with 3 M-KCl-filled microelectrodes (Rt = 20-70 M omega) a stable membrane potential of -28.7 +/- 4.8 mV (mean +/- S.D., n = 400) is measured. 2. Varying the [KCl] of the filling solution causes a change in measured membrane potential; 154 mM gives typically -2 mV, 10 mM typically +37 mV. 3. Variation in membrane potential with different [KCl] cannot be ascribed to tip potential. Double-barrelled microelectrodes containing a different [KCl] in each barrel both give the same membrane potential when inserted into a cell. 4. Microelectrodes filled with a reference liquid ion exchanger (RLIE) give a membrane potential of +2 mV. 5. Impaling a cell with a double-barrelled microelectrode, one barrel containing KCl and the other RLIE, showed that the ion exchanger is not having a toxic effect on the cell and does not affect membrane potential measured by the KCl-filled barrel. 6. We suggest that microelectrodes containing non-isotonic concentrations of KCl generate a significant and artifactual change in membrane potential of corneal endothelial cells caused by the movement of excess KCl (originating from the microelectrode tip) across the plasma membrane where a liquid-junction potential is generated. 7. We further suggest that the physiological membrane potential of corneal endothelial cells is around zero. This could result from a solution of the constant field equation where: 0.9 PNa congruent to PK congruent to 3.2 PCl.
Animals↗
Effect of bilirubin on the membrane potential of rat brain synaptosomes.
The effect of the neurotoxic pigment bilirubin on the membrane potential of rat brain synaptosomes was studied by using the tetraphenylphosphonium ion (TTP+) technique. Bilirubin induces a rapid depolarization of synaptosomes, as reflected by an efflux of previously accumulated [3H]TTP+. This phenomenon persisted when the membrane potential across either the plasma membrane of the synaptosome or the inner membrane of the entrapped mitochondria was selectively depressed, thus indicating that both components of the synaptosomal membrane potential were affected by bilirubin. Bovine serum albumin, used at a albumin/bilirubin molar ratio of 1:1, had the capacity to completely prevent and reverse the effect of bilirubin. This fact demonstrates that the bilirubin-induced TPP+ release from synaptosomes is a reversible process that requires the presence of bilirubin interacting with the synaptosomal membranes. These results, together with the inhibition by bilirubin of [3H]TPP+ and [2-14C]acetate uptake by synaptosomal plasma membrane vesicles isolated from rat brain, suggest that bilirubin depresses the membrane potential across the synaptosomal plasma membrane by a mechanism involving alterations in ion permeability. This effect could be of relevance in the pathogenesis of bilirubin encephalopathy.
Animals↗