Calcium content and net fluxes in squid giant axons.

Requena, Jaime; Mullins, L. J.; Brinley, F. J.

doi:10.1085/jgp.73.3.327

Cited by 29 publications

(18 citation statements)

References 31 publications

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“…+ . These findings agree qualitatively first with flux measurements showing that Ca efflux is virtually fully activated by a Na 0 of 180 mM (Blaustein, 1977) and that Ca influx is virtually unaltered at this value for Na 0 (Baker et al 1969) and, second, with analytical Ca measurements (Requena et al 1979). In Table 5 below, flux values from analytical measurement of Cai and aequorin glow data are compared for several experimental variables known to alter intracellular Ca regulation.…”

Section: (D) the Effect Of External Monovalent Cations On Ca\ +supporting

confidence: 79%

Calcium movement in nerve fibres

Requena

Mullins

1979

Quart. Rev. Biophys.

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Given the existence of a difference in electrical potential between the interior of a nerve cell and the media surrounding it, where the cytoplasm is some 70 mV negative (Hodgkin, 1958), it must be expected that any positively charged ion to which the cell membrane is permeable is more concentrated in the cell interior. For monovalent cations such as Na and divalent cations such as Ca and Mg this is not the case in the majority of the cells such as the squid giant axon. In other words, nerve cells maintain a lower intracellular concentration of these ions, as compared with their concentration in the extracellular fluid. For Mg, Ca and Na ions, this lower internal concentration must, in the steady state, be effected by some membrane based mechanism which consumes energy.

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Section: (D) the Effect Of External Monovalent Cations On Ca\ +supporting

confidence: 79%

Calcium movement in nerve fibres

Requena

Mullins

1979

Quart. Rev. Biophys.

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“…It has been suggested that the transmembrane Na and Ca gradients are electrochemically coupled so that the downhill movement of Na ions provides sufficient energy for the uphill movement of Ca. This hypothesis is supported by the recent work of Requena, Mullins & Brinley (1979). In the absence of ATP, net extrusion of Ca from previously loaded squid axons can occur only in the presence of an electrochemical gradient for Na.…”

Section: Introductionsupporting

confidence: 58%

Sodium efflux in rabbit myocardium: relationship to sodium—calcium exchange

Bridge

Cabeen

Langer

et al. 1981

The Journal of Physiology

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SUMMARY1. The washout of 22Na, 45Ca and 58CoEDTA-has been observed in arterially perfused rabbit interventricular septa both in the presence and absence ofintoxicating doses of the aglycone, 3 acetylstrophanthidin (ACS).2. The washout of 22Na from paced septa (21P0/min) was rapid with approximately 99 % of the exchange occurring in 30 min.3. Septa labelled with 22Na and washed out in the presence of 10-5 M-ACS were quiescent, exhibited marked contracture and a slowed 22Na exchange with 99 % of the initial 22Na leaving the tissue in approximately 200 min.4. Comparison of the washout of the extracellular marker 58CoEDTA-from paced and intoxicated septa revealed no differences, suggesting that regions of the extracellular space had not become inexchangeable as a result of the contracture that these septa exhibited.5. Simultaneous measurements of the distribution of 22Na and 58CoEDTA-in the presence of 10-5 M-ACS revealed an apparent cellular Na concentration of 54-8 + 10-4 (S.E.). This was considerably in excess of the maximum amount of Na contributing to the slowest component of Na efflux from intoxicated septa. Origins of this discrepancy are considered.6. The slowest component of 22Na efflux from intoxicated septa could be markedly stimulated by increasing the external Ca concentration from a nominal 1-5 to 16 mM.The magnitude of stimulation was 44-3 + 7-8 % (S.E.). Increases in the concentration of Mg from 1-0 to 16-0 mm were without effect on the 22Na efflux.7. Application of 10-5 M-ACS produced marked depolarization of the membrane to new stable levels that lay between -10 and -20 mV.8. Washout of ACS after several hours of intoxication resulted in a partial decline in contracture tension, an acceleration of Ca efflux, little change in 22Na efflux and a repolarization of the cell membrane.

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“…This small apparent alkalinization, occurring together with the increase in resting Ca, is to be compared to observations in the absence of alcohols where a large Ca entry acidifies axoplasm (see Mullins et al, 1983 for related references and discussion). The Ca release is a negligible fraction of the total analytical Ca (68 gmol/kg axoplasm) (Requena et al, 1979). It is also known that in fresh axons (those not exposed to high Ca sea water) the mitochondria have a negligible fraction of the total analytical Ca stored (Brinley et al, 1977) so that it has usually been assumed that it is the smooth endoplasmic reticulum of the axon that stores the bulk of the Ca.…”

Section: Discussionmentioning

confidence: 99%

Increases in internal Ca2+ and decreases in internal H+ are induced by general anesthetics in squid axons

Vassort¹,

Whittembury²,

Mullins³

1986

Biophysical Journal

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Squid axons were injected with arsenazo III and treated with sea water containing compounds usually classified as general anesthetics, (pentanol-decanol and a variety of hydrocarbons and their derivatives). Such treatment led to an increase in absorbance by arsenazo III at wavelengths sensitive to [Ca]i. The effect was independent of the presence or absence of Ca++ in sea water and it was not modified by substances that release Ca from internal stores. The effect was easily reversible. In axons injected with phenol red or impaled with a glass electrode sensitive to H+, a similar treatment led to an alkalinization that was also readily reversible. Both Ca release and the change to an alkaline pH had identical time courses. The dose required for action by all of the chemical agents studied could be predicted from a knowledge of their fractional saturation in sea water, i.e. from their thermodynamic activity. For compounds with 8-10 carbon atoms, Ca-release effects can occur at concentration less than those necessary to block either conduction or Na/Ca exchange. A special chemical agent was octylamine, which induced a marked rise in pHi and in addition its nonionic form produced the typical Ca release associated with general anesthetics.

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Calcium content and net fluxes in squid giant axons.

Cited by 29 publications

References 31 publications

Calcium movement in nerve fibres

Calcium movement in nerve fibres

Sodium efflux in rabbit myocardium: relationship to sodium—calcium exchange

Increases in internal Ca2+ and decreases in internal H+ are induced by general anesthetics in squid axons

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