Transport and metabolism of calcium ions in nerve

Baker, P. F.

doi:10.1016/0079-6107(72)90007-7

Cited by 719 publications

(193 citation statements)

References 108 publications

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“…Indeed, the possible Ca" releasing action of veraparnil has also been noticed in frog sartorius muscle (13). It has been suggested that Ca" ions enter the nerve terminals through the opened voltage-gated channels, by translocation with an ionophore or by leaking through the resting membrane, and Ca" always stimulates transmitter release (14). In the present experiments, the sustained effect of verapamil was dependent on the presence of external Ca", suggesting the possibility that the sustained effect is supported by an influx of Ca++ into nerve terminals at the rat neuro muscular junction.…”

Section: Discussionsupporting

confidence: 44%

Verapamil-induced transmitter release in rat diaphragm muscle.

1982

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Abstract-Verapamilwas examined for its effect on the frequency of miniature end-date potential (m.e.p.p.) in rat diaphragm muscles. Verapamil (5x10-5 M) raised the m.e.p.p. frequency. This effect was reversible, reproducible, and concentration dependent.The rise in the frequency was maintained in the presence of external Ca" but was transient in the absence of external Ca".Lowering the temperature to 20°C slightly decreased the average frequency of m.e.p.p. in the normal medium.The effect of verapamil was also present at a low temperature but was delayed in its onset. The resting membrane potential of the muscle fiber was not affected by the agent.These results suggest the possibility that verapamil increases the transmitter release from motor nerve terminals, and the effect is possibly due to a release of Ca++ for its initiation, but is dependent on external Ca" for its maintenance.

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Section: Discussionsupporting

confidence: 44%

Verapamil-induced transmitter release in rat diaphragm muscle.

1982

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“…Therefore, we set the ionic conditions to induce only an outward exchange current by loading [Na] only inside and [Ca] outside. [Ca] i cannot be eliminated because it is necessary for the exchange to operate (Baker, 1972;Baker and McNaughton, 1976;Allen and Baker, 1985;Kimura et al, 1986), so a minimum amount of 100 nM free [Ca]i was added in all the internal solutions. Although it has been reported that the Na-Ca exchange also operates as a Ca-Ca exchange (Blaustein, 1977;Philipson and Nishimoto, 1981;Ledvora and Hegyvary, 1983;Slaughter et al, 1983) and that [Ca]i may inhibit the binding of [Na]i , we assumed that the fraction of Ca-Ca exchange was small enough and that [Ca]i would not compete effectively with [Na] i at 100 nM [Ca] i and 20 mM or higher [Na]i.…”

Section: Resultsmentioning

confidence: 99%

Translocation mechanism of Na-Ca exchange in single cardiac cells of guinea pig.

Kimura

1990

The Journal of General Physiology

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We have studied in single cardiac ventricular cells of guinea pig the ionic translocation mechanism of the electrogenic Na-Ca exchange, i.e., whether Na and Ca ions countercross the membrane simultaneously or consecutively with "ping pong" kinetics. The dose-response relation between the external Ca concentrations ([Ca]o) and the current density of the outward Na-Ca exchange current were measured at three different intracellular Na concentrations ([Nail) in the absence of external Na. Nonlinear regression curves of the dose-response relation obtained by computer revealed Michaelis-Menten type hyperbola from which the [Ca]o giving a half-maximal response (apparent K, Ca o or K'Cao) and the apparent maximum current magnitude (I~x) were estimated at each [Na]i. As [Na]i increased, the K'Cao increased progressively and the value of K'Cao/l'r~ tended to decrease. These results are consistent with the simultaneous mechanism. The K'Cao/l'm~ values, however, were small and close to each other, so it was not possible to completely preclude a consecutive mechanism.

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“…On the other hand, the Na+/K ÷ ATPase plays a complementary role by maintaining a gradient of Na ÷ and K ÷ ions across the plasma membrane. This gradient energizes the Na+/Ca 2+ exchange which plays an important function in excitable cells (Baker, 1972). Furthermore, the role of the Na+/K + pump in the regulation of membrane potential and cell volume is well known (Glynn, 1985).…”

Section: Discussionmentioning

confidence: 99%

Tacaribe Virus Infection May Induce Inhibition of the Activity of the Host Cell Ca2+ and Na+/K+ Pumps

Rey

Rossi²,

López³

et al. 1988

Journal of General Virology

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SUMMARYInfection of Vero cells with Tacaribe virus stocks containing a high ratio of standard (plaque-forming) viruses to defective interfering particles (DIP) induced inhibition of the host cell Ca 2+ ATPase (Ca 2+ pump) and the ouabain-sensitive Na+/K + ATPase (Na+/K + pump). The Mg 2+ ATPase which is not involved in cation transport was not affected. The presence of DIP in the inocula protected the cells from alteration of the transport-associated ATPases induced by standard viruses.

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Transport and metabolism of calcium ions in nerve

Cited by 719 publications

References 108 publications

Verapamil-induced transmitter release in rat diaphragm muscle.

Verapamil-induced transmitter release in rat diaphragm muscle.

Translocation mechanism of Na-Ca exchange in single cardiac cells of guinea pig.

Tacaribe Virus Infection May Induce Inhibition of the Activity of the Host Cell Ca2+ and Na+/K+ Pumps

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