Effects of divalent cations on acetylcholine-evoked membrane potential in the ionophore A23187 treated mouse pancreas

1984 ◽  
Vol 402 (4) ◽  
pp. 465-472 ◽  
Author(s):  
Noriyuki Iwatsuki
2019 ◽  
Vol 573 ◽  
pp. 579-587 ◽  
Author(s):  
Patricio Ramirez ◽  
Javier Cervera ◽  
Vicente Gomez ◽  
Mubarak Ali ◽  
Saima Nasir ◽  
...  

1979 ◽  
Vol 57 (9) ◽  
pp. 944-956 ◽  
Author(s):  
K. Krnjević ◽  
Y. Lamour ◽  
J. F. MacDonald ◽  
A. Nistri

In cats under Dial, Co, Mn, La, and Sr were injected extracellularly near lumbosacral motoneurones. All tended to improve intracellular recording, but when the membrane potential was initially stable, Mn, and especially Co, had a moderate and reproducible depolarizing action. Both Mn and Co depressed excitatory postsynaptic potentials evoked by dorsal root stimulation. The prominent after-hyperpolarization (a.h.p.), which normally follows the motoneuronal action potential, was consistently and reversibly depressed by Mn and Co (as well as La), the underlying conductance increase being also diminished, but there was no significant reduction in the after-depolarization. By contrast, Sr tended to potentiate the a.h.p., especially when this was depressed by a previous injection of Co or Mn. Unlike the other cations, Co had a marked depressant effect on the action potential, particularly its rate of rise. Since the action potential could be immediately restored by hyperpolarization or by an injection of Sr (in the absence of depolarization), Co may enhance Na inactivation.


Nature ◽  
1977 ◽  
Vol 270 (5636) ◽  
pp. 444-445 ◽  
Author(s):  
PETER FLATMAN ◽  
VIRGILIO L. LEW

1976 ◽  
Vol 70 (3) ◽  
pp. 527-540 ◽  
Author(s):  
M Schliwa

Low concentrations of calcium and magnesium ions have been shown to influence microtubule assembly in vitro. To test whether these cations also have an effect on microtubules in vivo, specimens of Actinosphaerium eichhorni were exposed to different concentrations of Ca++ and Mg++ and the divalent cation ionophore A23187. Experimental degradation and reformation of axopodia were studied by light and electron microscopy. In the presence of Ca++ and the ionophore axopodia gradually shorten, the rate of shortening depending on the concentrations of Ca++ and the ionophore used. Retraction of axopodia was observed with a concentration of Ca++ as low as 0.01 mM. After transfer to a Ca++-free solution containing EGTA, axopodia re-extend; the initial length is reached after about 2 h. Likewise, reformation of axopodia of cold-treated organisms is observed only in solutions of EGTA or Mg++, whereas it is completely inhibited in a Ca++ solution. Electron microscope studies demonstrate degradation of the axonemal microtubular array in organisms treated with Ca++ and A23187. No alteration was observed in organisms treated with Mg++ or EGTA plus ionophore. The results suggest that, in the presence of the ionophore, formation of axonemal microtubules can be regulated by varying the Ca++ concentration in the medium. Since A23187 tends to equilibrate the concentrations of divalent cations between external medium and cell interior, it is likely that microtubule formation invivo is influenced by micromolar concentrations of Ca++. These concentrations are low enough to be of physiological significance for a role in the regulation of microtubule assembly in vivo.


1975 ◽  
Vol 34 (01) ◽  
pp. 072-082 ◽  
Author(s):  
Erik H Mürer ◽  
Gwendolyn J Stewart ◽  
Michael A Rausch ◽  
H. James Day

SummaryThe addition of 0.1 μM ionophore A23187 to washed platelets incubated in citrated saline caused massive release of stored serotonin accompanied by intracellular accumulation of inosine monophosphate, but produced no detectable influx of externally added calcium or abnormal structural alterations. With increasing ionophore concentration there was a significant influx of calcium and a drastic alteration in the platelet ultrastructure. The increase in ionophore concentration was accompanied by the conversion of the major part of metabolic adenine nucleotides to inosine monophosphate and an almost complete blockage of further conversion to inosine and hypoxanthine. The metabolic changes were accentuated by the addition of calcium at concentrations less than 1/10 of the citrate concentration. In the presence of Ca++, or when citrate was omitted, there was a substantial leakage of cytoplasmic material, which at times suggested complete exchangeability between cytoplasm and extracellular medium. Our findings are consistent with the hypothesis that the platelet release reaction is triggered by intracellularly bound calcium. They also suggest that the application of high ionophore concentration has a toxicologic rather than a physiologic effect on platelets, and that a weak chelator added during incubation with the ionophore can in the absence of divalent cations prevent cell destruction, but not the toxic effect on cell metabolism.


Blood ◽  
1987 ◽  
Vol 70 (6) ◽  
pp. 1810-1815 ◽  
Author(s):  
C Brugnara ◽  
DC Tosteson

Abstract We report experiments on the effect of intracellular divalent cations (Mg, Ca, Mn) on K transport and cell volume in erythrocytes from patients with homozygous hemoglobin S disease (SS cells). When CO- treated SS erythrocytes are exposed to the ionophore A23187, removal of cell Mg markedly stimulates K efflux, whereas increasing cell Mg inhibits K efflux. The Ki for the inhibition by internal free Mg is 0.38 +/- 0.10 mmol/L, a value comparable to the concentration of free Mg in normal cells (0.3 to 0.4 mmol/L). When swollen SS cells with increased Mg content were incubated in plasma-like medium, they shrunk much less than swollen SS cells with normal Mg content. Thus, elevation of cell Mg produces inhibition of swelling-induced K movement from SS cells. Internal Ca and Mn also inhibit K movement from SS cells. The inhibition of volume regulation by divalent cations suggests that increases in intracellular divalent ions, especially Mg, could induce a persistent degree of cell swelling in SS RBCs and thereby inhibit intracellular polymerization.


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