In situ chelation of Ca(2+) in intracellular stores induces capacitative Ca(2+) entry in bovine adrenal chromaffin cells.
Reduction of intracellular Ca(2+) stores (by chelation with the EDTA structural analogue, TPEN) is itself a sufficient trigger of capacitative Ca(2+) entry. TPEN may be a useful tool in studies to investigate the mechanism of capacitative Ca(2+) entry, since potential confounders, such as changes in cytosolic Ca(2+) and second messenger levels, are obviated and the use of pharmacological modifiers of SERCA pumps and Ca(2+) release channels is avoided.
Powis
David A
DA
Neuroscience Group, School of Biomedical Sciences, The University of Newcastle, Callaghan, NSW 2308, Australia. davis.powis@newcastle.edu.au
Zerbes
Mariann
M
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D002417:Cattle; D002614:Chelating Agents / Q000494:pharmacology*; D019439:Chromaffin Cells / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005029:Ethylenediamines / Q000494:pharmacology*; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases
D002614:Chelating Agents; D005029:Ethylenediamines; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D000252:Calcium-Transporting ATPases; C044387:N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine; D002118:Calcium