Effects of amphotericin B on the electrical properties and electrolyte content of frog sartorius muscle

1980 ◽  
Vol 58 (9) ◽  
pp. 1138-1141 ◽  
Author(s):  
A. Coulombe ◽  
O. F. Schanne ◽  
I. Reisin ◽  
E. Ruiz-Ceretti

We studied the effect of amphotericin B (52 μM) on the membrane potential, membrane resistance, and intracellular Na+ and K+ concentrations in isolated frog sartorius muscles to characterize further the nature of the ionic conductance induced by the antibiotic. After 5 h of exposure to amphotericin B, the membrane depolarized from −89.9 to −51.0 mV, the membrane resistance decreased from 4537 to 907 Ωcm2, [K]i decreased from 122 to 31.2 mmol/L fiber H2O, and [Na]i increased from 30.9 to 88.7 mmol/L fiber H2O. The relative sodium permeability, PNa/PK, calculated with the Goldman equation remained apparently constant at a value of 0.01 in treated and untreated muscles. We hypothesize that amphotericin B creates either a nonselective cation channel or a completely nonselective ionic leak channel whose equilibrium potential is equal or close to the membrane potential.

1972 ◽  
Vol 60 (2) ◽  
pp. 221-236 ◽  
Author(s):  
Carlos Sevcik ◽  
Toshio Narahashi

The contractility of the frog sartorius muscle was suppressed after treatment with a Ringer solution added with ethylene glycol (EGR). No contraction was elicited by nerve stimulation when the muscle was brought back to normal Ringer solution after having been soaked in 876 mM EGR for 4 hr or in 1095 mM EGR for 2 hr. However, the action potential of normal amplitude was generated and followed by a depolarizing afterpotential. The resting membrane potential was slightly decreased from the mean normal value of –91.1 mv to –78.8 mv when 1095 mM EGR was used, and to –82.3 mv when 876 mM EGR was used, but remained almost constant for as long as 2 hr. The afterpotential that follows a train of impulses and a slow change in membrane potential produced by a step hyperpolarizing current (so-called "creep") were suppressed after treatment with ethylene glycol. The specific membrane capacity decreased to about 50% of the control values while the specific membrane resistance increased to about twice the control values Therefore, the membrane time constant remained essentially unchanged. The water content of the muscle decreased by about 30% during a 2 hr immersion in 1095 mM EGR, and increased by about 30% beyond the original control level after bringing the muscle back to normal Ringer. The intracellular potassium content did not change significantly during these procedures. Some differences between the present results and those obtained with glycerol are discussed.


1984 ◽  
Vol 51 (4) ◽  
pp. 689-704 ◽  
Author(s):  
W. R. Schlue ◽  
J. W. Deitmer

The intracellular K activity (aKi) and membrane potential of sensory neurons in the leech central nervous system were measured in normal and altered external K+ concentrations, [K+]o, using double-barreled, liquid ion-exchanger microelectrodes. In control experiments membrane potential measurements were made using potassium chloride-filled single-barreled microelectrodes. All values are means +/- SD. At the normal [K+]o (4 mM) the mean aKi of all cells tested was 72.6 +/- 10.6 mM (n = 40) and the average membrane potential was -47.3 +/- 5.2 mM (n = 40). When measured with single-barreled microelectrodes, the membrane potential averaged -45.3 +/- 2.9 mV (n = 12). Assuming an intracellular K+ activity coefficient of 0.75, the intracellular K+ concentration of sensory neurons would be 96.8 +/- 14.1 mM). With an extracellular K+ concentration of 5.8 mM in the intact ganglion compared to the K+ concentration of 4 mM in the bath, the K+ equilibrium potential was -71.5 mV. When the ganglion capsule was opened, the extracellular K+ concentrations in the ganglion were similar to that of the bathing medium and the calculated K+ equilibrium potential was -81 mV. The membrane of sensory neurons depolarized following the changes to elevated [K+]o (greater than or equal to 10-100 mM), whereas aKi changed only little or not at all. At very low [K+]o (0.2, 0 mM) aKi and membrane potential showed little short-term (less than 3 min) effect but began to change after longer exposure (greater than 3 min). Reduction of [K+]o from 4 to 0.2 mM (or 0 mM) produced first a slow, and then a more rapid decrease of aKi and membrane resistance, accompanied by a slow membrane hyperpolarization. Following readdition of normal [K+]o, the membrane first depolarized and then transiently hyperpolarized, eventually returning slowly to the normal membrane potential.(ABSTRACT TRUNCATED AT 400 WORDS)


1959 ◽  
Vol 196 (6) ◽  
pp. 1191-1196 ◽  
Author(s):  
S. Ochs ◽  
A. K. Mukherjee

Resting potentials of frog sartorius muscle fibers were taken with microelectrodes at different distances along the length of muscles before and after adding acetylcholine or choline. The mean membrane potential drop and scatter of the potentials recorded in the relatively nerve-free, and in the more densely innervated parts of the muscle, were similar. The loss of direct excitability to electrical and mechanical stimulation was correlated with the concentration of choline or acetylcholine presented. d-tubocurarine added beforehand protected against the depolarizing effect of acetylcholine and choline everywhere along the length of the muscle. A generalized action of acetylcholine and choline and also of d-tubocurarine all along the muscle fibers was inferred. This generalized action at higher concentrations of acetylcholine and choline is believed to be additional to a more specific end plate action.


1959 ◽  
Vol 42 (5) ◽  
pp. 983-1003 ◽  
Author(s):  
Raymond A. Sjodin

The reduction of membrane potential in frog sartorius muscle produced by rubidium and cesium ions has been studied over a wide concentration range and compared with depolarization occasioned by potassium ions. The constant field theory of passive flux has been used to predict the potential changes observed. The potential data suggest certain permeability coefficient ratios and these are compared with ratios obtained from flux data using radioactive tracers. The agreement of the flux with the potential data is good if account is taken of the inhibition of potassium flux which occurs in the presence of rubidium and cesium ions. A high temperature dependence has been observed for cesium influx (Q10 = 2.5) which is correlated with the observation that cesium ions depolarize very little at low temperatures. The observations suggest that cesium ions behave more like sodium ions at low temperatures and more like potassium ions at room temperature with respect to their effect on the muscle cell resting potential. The constant field theory of passive ion flux appears to be in general agreement with the experimental results observed if account is taken of the dependence of permeability coefficients on the concentrations of ions used and of possible interactions between the permeabilities of ions.


1963 ◽  
Vol 47 (1) ◽  
pp. 117-132 ◽  
Author(s):  
L. J. Mullins ◽  
K. Noda

The membrane potential of frog sartorius muscle fibers in a Cl- and Na-free Ringer's solution when sucrose replaces NaCl is about the same as that in normal Ringer's solution. The K+ efflux is also about the same in the two solutions but muscles lose K and PO4 in sucrose Ringer's solutions. The membrane potential in sucrose Ringer's solution is equal to that given by the Nernst equation for a K+ electrode, when corrections are made for the activity coefficients for K+ inside and outside the fiber. For a muscle in normal Ringer's solution, the measured membrane potential is within a few millivolts of EK. This finding is incompatible with a 1:1 coupled Na-K pump. It is consistent with either no coupling of Na efflux to K influx, or a coupling ratio of 3 or greater.


1985 ◽  
Vol 248 (3) ◽  
pp. C217-C227 ◽  
Author(s):  
Roque A. Venosa ◽  
Basilio A. Kotsias

The movement of42K+across the sarcolemma and the resting membrane potential ( VM) of normal and denervated frog sartorius muscle were studied under several experimental conditions in preparations initially equilibrated in 100 mM K+and 219 mM Cl-. The results can be summarized as follows. 1) In the absence of any driving force on K+, i.e., when the difference between VMand the K+equilibrium potential ( EK) is zero ( VM- EK= 0), the K+conductance ( gK) was 368 ΜS·cm-2in control and 282 ΜS·cm-2in denervated muscle. 2) The reduced gK of denervated muscles results from the addition of the opposite changes in the conductances of a Rb+-sensitive inward rectifying pathway ( gIR), which decreases, and a Rb+-insensitive linear channel ( gL), which increases. Thus in control muscles gK(368 ΜS·cm-2) equals gIR(359 ΜS·cm-2) plus gL(9 ΜS·cm-2), while in denervated muscles gK(282 ΜS·cm-2) equals gIR(198 ΜS·cm-2) plus gL(84 ΜS·cm-2). 3) Denervation significantly reduces the inward rectifying properties of the resting K+permeability system. In the presence of outward driving forces on K+( VM- EK> 0) of 35-50 mV, the Rb+-sensitive inward rectifier channel appears to close completely in both control and denervated muscles. In the latter, however, the effect was not as well maintained as in the former, suggesting that its closing mechanism might be altered by denervation. 4) No changes were observed during the first 2 wk after denervation.sarcolemma; resting potential; K+equilibrium potential; K+conductanceSubmitted on July 25, 1983Accepted on July 11, 1984


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