Transport Across the Cell Membrane and the Resting Membrane Potential

The actions of grayanotoxin I, veratrine, and tetrodotoxin on the membrane potential of the Schwann cell were studied in the giant nerve fiber of the squid Sepioteuthis sepioidea. Schwann cells of intact nerve fibers and Schwann cells attached to axons cut lengthwise over several millimeters were utilized. The axon membrane potential in the intact nerve fibers was also monitored. The effects of grayanotoxin I and veratrine on the membrane potential of the Schwann cell were found to be similar to those they produce on the resting membrane potential of the giant axon. Thus, grayanotoxin I (1-30 muM) and veratrine (5-50 mug-jl-1), externally applied to the intact nerve fiber or to axon-free nerve fiber sheaths, produce a Schwann cell depolarization which can be reversed by decreasing the external sodium concentration or by external application of tetrodotoxin. The magnitude of these membrane potential changes is related to the concentrations of the drugs in the external medium. These results indicate the existence of sodium pathways in the electrically unexcitable Schwann cell membrane of S. sepioidea, which can be opened up by grayanotoxin I and veratrine, and afterwards are blocked by tetrodotoxin. The sodium pathways of the Schwann cell membrane appear to be different from those of the axolemma which show a voltage-dependent conductance.

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Water and electrolyte contents, cell pH and membrane potentials of cultured turtle thyroid cells

Journal of Endocrinology ◽

10.1677/joe.0.1040045 ◽

1985 ◽

Vol 104 (1) ◽

pp. 45-52 ◽

Cited By ~ 9

Author(s):

S. Y. Chow ◽

Y. C. Yen-Chow ◽

D. M. Woodbury

Keyword(s):

Membrane Potential ◽

Cell Membrane ◽

Culture Medium ◽

Resting Membrane Potential ◽

Follicular Cells ◽

Iodide Uptake ◽

Thyroid Cells ◽

Cell Ph ◽

Cells Cultured ◽

In Cells

ABSTRACT Water and electrolyte contents, cell pH, membrane potential and 125I− uptake were determined in cultured follicular cells of turtle thyroid. The Na+, K+ and Cl− concentrations in the cultured thyroid cells were 59·2, 119·0 and 50·9 mmol/l cell water respectively. Treatment with TSH (10 mu./ml for 24 h) increased the K+ and Cl− and decreased the Na+ concentrations in cells. The water and protein contents of these cells were 81·6 and 8·7 g/100 g cells respectively. The cell pH was 6·91. With glass microelectrodes, the resting membrane potential of thyroid cells cultured in Medium 199 averaged 33·9 ± 0·63 mV which is slightly higher than 29·8 ± 1·6 mV as calculated from the data on the uptakes of [14C]methyltriphenylphosphonium and 3H2O by the cells. The potential varied linearly with the log of external K + concentration (between 15 and 120 mmol/l) with a slope of about 24 mV per tenfold change in K+ concentration. Both TSH and cyclic AMP depolarized the cell membrane. Calculations based on the values for the electrolyte concentrations in cells and in culture medium indicated that Na+, K+ and Cl− were not distributed according to their electrochemical gradients across the cell membrane. Na+ was actively transported out of the cells and K+ and Cl− into the cells. Follicular cells of turtle thyroid cultured in the medium without addition of TSH formed a monolayer. Their iodide-concentrating ability was low and they did not respond to TSH with an increase in iodide uptake. In contrast, cells cultured in medium containing TSH tended to aggregate and organize to form follicles. They had higher ability to concentrate iodide and respond to TSH. J. Endocr. (1985) 104, 45–52

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Muscle water and electrolytes following varied levels of dehydration in man

Journal of Applied Physiology ◽

10.1152/jappl.1976.40.1.6 ◽

1976 ◽

Vol 40 (1) ◽

pp. 6-11 ◽

Cited By ~ 137

Author(s):

D. L. Costill ◽

R. Cote ◽

W. Fink

Keyword(s):

Body Weight ◽

Membrane Potential ◽

Cell Membrane ◽

Muscle Cell ◽

Muscle Tissue ◽

Muscle Biopsy ◽

Resting Membrane Potential ◽

Muscle Water ◽

Percent Decrease ◽

Muscle Cell Membrane

In an effort to assess the effects of dehydration on the content of water and electrolytes (Na+, K+, Cl-, and Mg2+) in plasma and muscle tissue, eight men exercised in the heat (39.5 degrees C, 25%). Blood urine, and muscle biopsy samples were obtained before exercise and after the subjects had reduced their body weight by 2.2, 4.1, and 5.8%. On the average, plasma and muscle water (H2Om) contents were found to decline 2.4 and 1.2% for each percent decrease in body weight. Muscle sodium (Na+m) and chloride (Cl-m) content remained unchanged with dehydration, while muscle magnesium (Mg2+m) declined 12% as a result of the 5.8% dehydration. In terms of intracellular concentrations, K+i increased 7.2 and 10.6% at the 2.2 and 4.1% dehydration levels, respectively. Calculations of the resting membrane potential suggest that the water and electrolyte losses observed in these studies do not significantly alter the excitability of the muscle cell membrane.

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Effect of low chloride on relaxation in hamster diaphragm muscle

Journal of Applied Physiology ◽

10.1152/jappl.1986.61.1.180 ◽

1986 ◽

Vol 61 (1) ◽

pp. 180-184 ◽

Cited By ~ 11

Author(s):

S. A. Esau ◽

N. Sperelakis

Keyword(s):

Membrane Potential ◽

Muscle Fatigue ◽

Time Constant ◽

Diaphragm Muscle ◽

Resting Membrane Potential ◽

Krebs Solution ◽

Sarcolemmal Membrane ◽

Cl Conductance

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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Calcium channels and excitation–contraction coupling in cardiac cells. I. Two components of contraction in guinea-pig papillary muscle

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-284 ◽

1987 ◽

Vol 65 (9) ◽

pp. 1821-1831 ◽

Cited By ~ 4

Author(s):

E. Honoré ◽

M. M. Adamantidis ◽

B. A. Dupuis ◽

C. E. Challice ◽

P. Guilbault

Keyword(s):

Membrane Potential ◽

Guinea Pig ◽

Papillary Muscle ◽

Cardiac Cells ◽

Resting Membrane Potential ◽

Tonic Component ◽

Contraction Coupling ◽

Rich Solution ◽

The Relationship ◽

Guinea Pig Atria

Biphasic contractions have been obtained in guinea-pig papillary muscle by inducing partial depolarization in K+-rich solution (17 mM) containing 0.3 μM isoproterenol; whereas in guinea-pig atria, the same conditions led to monophasic contractions corresponding to the first component of contraction in papillary muscle. The relationships between the amplitude of the two components of the biphasic contraction and the resting membrane potential were sigmoidal curves. The first component of contraction was inactivated for membrane potentials less positive than those for the second component. In Na+-low solution (25 mM), biphasic contraction became monophasic subsequent to the loss of the second component, but tetraethylammonium unmasked the second component of contraction. The relationship between the amplitude of the first component of contraction and the logarithm of extracellular Ca2+ concentration was complex, whereas for the second component it was linear. When Ca2+ ions were replaced by Sr2+ ions, only the second component of contraction was observed. It is suggested that the first component of contraction may be triggered by a Ca2+ release from sarcoplasmic reticulum, induced by the fast inward Ca2+ current and (or) by the depolarization. The second component of contraction may be due to a direct activation of contractile proteins by Ca2+ entering the cell along with the slow inward Ca2+ current and diffusing through the sarcoplasm. These results do not exclude the existence of a third "tonic" component, which could possibly be mixed with the second component of contraction.

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