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Literature DB >> 7175747

Metabolism and transport of strontium in giant axons of Loligo.

Abstract

1. The strontium content of squid axons averages 2.9 mumol kg-1 axoplasm and squid blood contains 75 mumol Sr l-1. The bulk of the Sr inside axons is bound, possibly within mitochondria. Sr seems to be handled by squid axons in an essentially similar manner to Ca. 2. Sr uptake is increased by electrical activity, by lowering external Na, by depolarization with K and by poisoning with cyanide or FCCP. Uptake is unaffected by ouabain. 3. Sr efflux has a Q10 of 2.2. Efflux can be divided operationally into three components: one dependent on external Ca (or Sr), one dependent on external Na and a residual component that can be inhibited by external lanthanum or internal vanadate. 4. Poisoning an axon with cyanide or FCCP results in a large increase in Sr efflux which can be divided operationally into two components: one dependent on external Ca (or Sr) and one dependent on external Na.

Entities: Chemical Disease

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Year: 1982 PMID： 7175747 PMCID： PMC1225303 DOI： 10.1113/jphysiol.1982.sp014346

Source DB: PubMed Journal: J Physiol ISSN： 0022-3751 Impact factor: 5.182

24 in total

Metabolism and transport of strontium in giant axons of Loligo.

1. Movements of labelled calcium in squid giant axons.

2. Studies on the internal pH of large muscle and nerve fibres.

3. A comparison of the phosphorus metabolism of intact squid nerve with that of the isolated axoplasm and sheath.

4. Uptake and binding of calcium by axoplasm isolated from giant axons of Loligo and Myxicola.

5. The kinetics of influx of calcium and strontium into rat intestine in vitro.

6. Intracellular pH of snail neurones measured with a new pH-sensitive glass mirco-electrode.

7. Mobility and transport of magnesium in squid giant axons.

8. The effect of cyanide on the efflux of calcium from squid axons.

9. The effects of Ca2+ antagonists on Ca2+ accumulation by subcellular fractions of rat myometrium.

10. Intracellular pH transients in squid giant axons caused by CO2, NH3, and metabolic inhibitors.

1. Divalent cations differentially support transmitter release at the squid giant synapse.