Generation of resting membrane potential

2004 ◽  
Vol 28 (4) ◽  
pp. 139-142 ◽  
Author(s):  
Stephen H. Wright

This brief review is intended to serve as a refresher on the ideas associated with teaching students the physiological basis of the resting membrane potential. The presentation is targeted toward first-year medical students, first-year graduate students, or senior undergraduates. The emphasis is on general concepts associated with generation of the electrical potential difference that exists across the plasma membrane of every animal cell. The intention is to provide students a general view of the quantitative relationship that exists between 1) transmembrane gradients for K+ and Na+ and 2) the relative channel-mediated permeability of the membrane to these ions.

1988 ◽  
Vol 255 (6) ◽  
pp. G822-G825 ◽  
Author(s):  
R. A. Weisiger ◽  
J. G. Fitz

The electrical potential difference across the plasma membrane was compared in paired livers from male and female rats perfused single-pass with Krebs-bicarbonate buffer. Variability in the membrane potential measured for different cells within the same liver was small (SD = 1.3 mV). The mean membrane potential was 5.1 mV more negative for male livers than for female livers (-30.3 +/- 0.6 vs. -25.2 +/- 1.0 mV, P less than 0.001), and the male liver had a more negative membrane potential than the female liver in all nine pairs studied. No correlation between membrane potential and perfusion rate was seen. Variability among female livers was more than twice as great (range -19.6 to -30.0 mV) as for male livers (range -26.7 to -31.9 mV). These results suggest that hepatic membrane potential may be modulated by sex hormone levels, which are more variable in female animals. Because the hepatic uptake of bile acids such as taurocholate and organic anions such as bilirubin may involve net movement of electrical charge across the plasma membrane, the current results may explain previously reported sex differences in the uptake of these and other electrogenically transported molecules.


Weed Science ◽  
1994 ◽  
Vol 42 (2) ◽  
pp. 285-292 ◽  
Author(s):  
John P. Wright

All actively metabolizing cells have an electrical potential difference, negative on the interior, across their membranes. This electrochemical potential gradient is generated primarily by proton-pumping ATPases and provides the driving force for the transport of various ionic and neutral solutes. It is a key element in the energy metabolism of cells. Such factors as alteration of transport processes, energy metabolism, cytoplasmic pH, and membrane permeability have a direct effect on the magnitude of the membrane potential. In a brief survey, diclofop-methyl, diclofop, hydroxydiclofop, CGA 82725, haloxyfop-methyl, haloxyfop, bentazon, dinoseb, 4-hydroxy CIPC, and 2-hydroxy CIPC caused rapid depolarizations of the membrane potential of oat coleoptiles. Chlorsulfuron, dimethipin, propham, CIPC, dicamba, alachlor, metolachlor, napthalic anhydride, and paraquat had no measurable effects. The depolarizing effects of diclofop-reported earlier are used to illustrate the methods and interpretation of plant cell membrane potential measurements. Diclofop and diclofop-methyl affect the membrane properties of sensitive plant cells. Diclofop irreversibly depolarized the membrane potential and increased the proton permeability of sensitive cells but not resistant cells. It also increased the ATPase activity of isolated membrane vesicles. The mechanism through which diclofop exerted its effect is not fully understood. The equipment and techniques required for the intercellular recording of membrane potentials and resistance are described as well as the limitations of the techniques. A method not used in herbicide studies but with great potential for studies of herbicide interactions with membranes is patch clamp. A brief introduction to the methods will be given.


1990 ◽  
Vol 258 (2) ◽  
pp. C336-C343 ◽  
Author(s):  
M. E. Duffey ◽  
D. C. Devor

Intracellular pH (pHc) was measured in the short-circuited epithelium of rabbit distal colon using H(+)-selective microelectrodes. pHc was 6.91 +/- 0.02 (SE) when the bath pH was 7.4. Intracellular HCO3- activity (acHCO3-) was estimated from these measurements to be 8 +/- 0 mM. When we replaced all Cl- in the tissue bathing solutions with the impermeant anion gluconate, pHc rose to 7.44 +/- 0.08 and acHCO3- increased to 30 +/- 6 mM. These results demonstrate that this tissue contains a Cl(-)-HCO3- exchange mechanism. During the Cl- replacement the apical membrane electrical potential difference hyperpolarized from -55 +/- 1 to -74 +/- 3 mV, suggesting that membrane ionic conductance had changed. Elevation of either the apical or basolateral membrane bathing solution K+ concentration produced a greater depolarization of membrane potential during Cl- replacement than when tissues were bathed in normal electrolyte solutions. In additional experiments, pHc was raised by lowering the bath CO2 concentration while the bath Cl- concentration was kept normal. Under these conditions, membrane potential hyperpolarized and was more sensitive to the elevation of bath K+ concentration than when pHc was normal. These results suggest that membrane K+ conductance in this tissue is increased by intracellular alkalinization.


1984 ◽  
Vol 83 (2) ◽  
pp. 175-192 ◽  
Author(s):  
W J Betz ◽  
J H Caldwell ◽  
S C Kinnamon

In an attempt to determine the mechanism by which rat skeletal muscle endplates generate a steady outward current, we measured the effects of several drugs (furosemide, bumetanide, 9-anthracene carboxylic acid [9-AC]) and changes in external ion concentration (Na+, K+, Cl-, Ba++) on resting membrane potential (Vm) and on the steady outward current. Each of the following treatments caused a 10-15-mV hyperpolarization of the membrane: replacement of extracellular Cl- with isethionate, addition of furosemide or bumetanide, and addition of 9-AC. These results suggest that Cl- is actively accumulated by the muscle fibers and that the equilibrium potential of Cl- is more positive than the membrane potential. Removal of external Na+ also caused a large hyperpolarization and is consistent with evidence in other tissues that active Cl- accumulation requires external Na+. The same treatments greatly reduced or abolished the steady outward current, with a time course that paralleled the changes in Vm. These results cannot be explained by a model in which the steady outward current is assumed to arise as a result of a nonuniform distribution of Na+ conductance, but they are consistent with models in which the steady current is produced by a nonuniform distribution of GCl or GK. Other treatments (Na+-free and K+-free solutions, and 50 microM BaCl2) caused a temporary reversal of the steady current. Parallel measurements of Vm suggested that in none of these cases did the electrochemical driving force for K+ change sign, which makes it unlikely that the steady current arises as a result of a nonuniform distribution of GK. All of the results, however, are consistent with a model in which the steady outward current arises as a result of a nonuniform distribution of Cl- conductance, with GCl lower near the endplate than in extrajunctional regions.


1985 ◽  
Vol 225 (3) ◽  
pp. 815-819 ◽  
Author(s):  
M Höfer ◽  
A Künemund

In the yeast Rhodotorula glutinis, accumulation of the tetraphenylphosphonium ion (TPP+) was increased under conditions of osmotic stress, indicating a hyperpolarization of the negative membrane potential (delta psi). The following observations were consistent with the occurrence of hyperpolarized delta psi: enhanced accumulation of glucosamine, the uptake of which is also driven by delta psi; increased respiratory rate. The accumulation of TPP+ was gradually decreased by lowering the pH of cell suspensions. At pH values below 4.5, no TPP+ was taken up, but instead thiocyanate (SCN-) was accumulated, indicating a positive delta psi. The pH-dependent influx of glucosamine followed the pattern of TPP+ accumulation both in the wild-type and in the nystatin-resistant mutant, M67, which displayed a negative delta psi down to pH 3. Thus TPP+ accumulation in Rh. glutinis reflected actual electrical potential difference across the plasma membrane.


1985 ◽  
Vol 249 (1) ◽  
pp. E17-E25
Author(s):  
K. Zierler ◽  
E. M. Rogus ◽  
R. W. Scherer ◽  
F. S. Wu

These experiments were designed to test the hypothesis that insulin-induced hyperpolarization is a link in the chain of events leading to stimulation of glucose transport. External potassium concentration, [K+]o, was increased by equimolar substitution of KCl for NaCl, a method known to cause cell swelling, and by substitution of [K+]o for [Na+]o with maintenance of constant [K+]o X [Cl-]o product, a method that does not cause cell swelling. When there was constant KCl product, even at 76.8 meq [K+]o insulin continued to hyperpolarize, although by only approximately 44% as much as in normal [K+]o, and insulin-stimulated 2-deoxyglucose uptake was only approximately 60% of that at normal [K+]o. With equimolar substitution of KCl for NaCl: electrical potential difference across cell membranes of surface fibers of rat caudofemoralis muscle decreased with logarithm [K+]o, in the presence or absence of insulin. Insulin-induced hyperpolarization decreased as [K+]o increased and disappeared at 36 mM [K+]o. The amount of insulin bound to its receptors in 1 h was not affected by [K+]o over the range studied. Insulin effects on membrane potential and on 2-deoxyglucose uptake, as both were altered by [K+]o, correlated well. As the probe moved in depth through the first six fibers there was stepwise decrease in depolarization in high [K+]o in the absence of insulin. Insulin hyperpolarized the deepest of these fibers, even when it did not hyperpolarize the outermost. The decrease in insulin-induced hyperpolarization as [K+]o increases is consistent with the hypothesis that insulin hyperpolarizes by decreasing the ratio PNa/PK.


1975 ◽  
Vol 67 (1) ◽  
pp. 119-125
Author(s):  
P. J. BENTLEY

SUMMARY The electrical potential difference and short-circuit current (scc, reflecting active transmural sodium transport) across the toad urinary bladder in vitro was unaffected by the presence of hypo-osmotic solutions bathing the mucosal (urinary) surface, providing that the transmural flow of water was small. Vasopressin increased the scc across the toad bladder (the natriferic response), but this stimulation was considerably reduced in the presence of a hypo-osmotic solution on the mucosal side, conditions under which water transfer across the membrane was also increased. This inhibition of the natriferic response did not depend on the direction of the water movement, for if the osmotic gradient was the opposite way to that which normally occurs, the response to vasopressin was still reduced. The natriferic response to cyclic AMP was also inhibited in the presence of an osmotic gradient. Aldosterone increased the scc and Na+ transport across the toad bladder but this response was not changed when an osmotic gradient was present. The physiological implications of these observations and the possible mechanisms involved are discussed.


1986 ◽  
Vol 61 (1) ◽  
pp. 180-184 ◽  
Author(s):  
S. A. Esau ◽  
N. Sperelakis

With muscle fatigue the chloride (Cl-) conductance of the sarcolemmal membrane decreases. The role of lowered Cl- conductance in the prolongation of relaxation seen with fatigue was studied in isolated hamster diaphragm strips. The muscles were studied in either a Krebs solution or a low Cl- solution in which half of the NaCl was replaced by Na-gluconate. Short tetanic contractions were produced by a 160-ms train of 0.2-ms pulses at 60 Hz from which tension (T) and the time constant of relaxation were measured. Resting membrane potential (Em) was measured using KCl-filled microelectrodes with resistances of 15–20 M omega. Mild fatigue (20% fall in tension) was induced by 24–25 tetanic contractions at the rate of 2/s. There was no difference in Em or T in the two solutions, either initially or with fatigue. The time constant of relaxation was greater in low Cl- solution, both initially (22 +/- 3 vs. 18 +/- 5 ms, mean +/- SD, P less than 0.05) and with fatigue (51 +/- 18 vs. 26 +/- 7 ms, P less than 0.005). Lowering of sarcolemmal membrane Cl- conductance appears to play a role in the slowing of relaxation of hamster diaphragm muscle seen with fatigue.


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