Time-correlation between membrane depolarization and intracellular calcium in insulin secreting BRIN-BD11 cells: studies using FLIPR

Cell Calcium ◽  
2004 ◽  
Vol 36 (1) ◽  
pp. 43-50 ◽  
Author(s):  
João C Miguel ◽  
Steven Patterson ◽  
Yasser H.A Abdel-Wahab ◽  
Paulo C.F Mathias ◽  
Peter R Flatt
Keyword(s):  
Intracellular Calcium ◽  
Time Correlation ◽  
Membrane Depolarization

scholarly journals The Potassium Channel, Kir3.4 Participates in Angiotensin II-Stimulated Aldosterone Production by a Human Adrenocortical Cell Line

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4328-4335 ◽  
Author(s):  
Kenji Oki ◽  
Maria W. Plonczynski ◽  
Milay Luis Lam ◽  
Elise P. Gomez-Sanchez ◽  
Celso E. Gomez-Sanchez
Keyword(s):  
Cytochrome P450 ◽  
Angiotensin Ii ◽  
Potassium Channel ◽  
Intracellular Calcium ◽  
Regulatory Protein ◽  
Membrane Depolarization ◽  
Membrane Voltage ◽  
Aldosterone Secretion ◽  
Calmodulin Kinase ◽  
Kinase Cascade

Angiotensin II (A-II) regulation of aldosterone secretion is initiated by inducing cell membrane depolarization, thereby increasing intracellular calcium and activating the calcium calmodulin/calmodulin kinase cascade. Mutations in the selectivity filter of the KCNJ5 gene coding for inward rectifying potassium channel (Kir)3.4 has been found in about one third of aldosterone-producing adenomas. These mutations result in loss of selectivity of the inward rectifying current for potassium, which causes membrane depolarization and opening of calcium channels and activation of the calcium calmodulin/calmodulin kinase cascade and results in an increase in aldosterone secretion. In this study we show that A-II and a calcium ionophore down-regulate the expression of KCNJ5 mRNA and protein. Activation of Kir3.4 by naringin inhibits A-II-stimulated membrane voltage and aldosterone secretion. Overexpression of KCNJ5 in the HAC15 cells using a lentivirus resulted in a decrease in membrane voltage, intracellular calcium, expression of steroidogenic acute regulatory protein, 3-β-hydroxysteroid dehydrogenase 3B2, cytochrome P450 11B1 and cytochrome P450 11B2 mRNA, and aldosterone synthesis. In conclusion, A-II appears to stimulate aldosterone secretion by depolarizing the membrane acting in part through the regulation of the expression and activity of Kir3.4.

Olfactory neurons exhibit heterogeneity in depolarization-induced calcium changes

1990 ◽  
Vol 258 (6) ◽  
pp. C1051-C1061 ◽  
Author(s):  
D. Restrepo ◽  
J. H. Teeter
Keyword(s):  
Intracellular Calcium ◽  
Ictalurus Punctatus ◽  
Free Acid ◽  
Single Cells ◽  
Membrane Depolarization ◽  
Calcium Currents ◽  
Acetoxymethyl Ester ◽  
Olfactory Neurons ◽  
Fura 2 ◽  
Wide Range

Olfactory neurons from the channel catfish, Ictalurus punctatus, were isolated by a brief (15 min) treatment with papain. After incubation with fura-2 acetoxymethyl ester (fura-2/AM) for 1 h, the isolated olfactory receptor cells are found to hydrolyze fura-2/AM to fura-2 free acid without detectable traces of intermediate products of hydrolysis. Intracellular calcium measured with fura-2 in single cells covers a wide range (from less than 2 to 100 nM with a median of 17.6 nM, n = 140 cells). Twenty-one percent of the cells respond to potassium-induced depolarization with an increase in intracellular calcium mediated by influx of extracellular calcium. The L-type calcium channel antagonist nimodipine inhibits the increase in intracellular calcium triggered by membrane depolarization and blocks small unitary barium currents displaying the characteristics of L-type calcium currents (unitary conductance of 29 +/- 5 pS in 55 mM BaCl2 and high selectivity for Ba2+ over Na+ and K+) recorded from azolectin bilayers at the tip of patch pipettes into which isolated olfactory cilia membrane vesicles had been incorporated. Olfactory neurons are found to be functionally heterogeneous in their response to membrane depolarization and can be separated into three groups: one in which the increase in intracellular calcium is rapid and transient, another in which calcium increases slowly, and a third group of cells in which depolarization causes no change in intracellular calcium.

Ultra-Rapid Freezing of Isolated Skeletal Muscle Fibers

1977 ◽  
Vol 35 ◽  
pp. 576-577
Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Granular Material ◽  
Nuclear Envelope ◽  
Intracellular Calcium ◽  
Ruthenium Red ◽  
Threshold Concentration ◽  
Rapid Freezing ◽  
Frog Skeletal Muscle ◽  
Electrical Isolation

After Howell (1) had shown that ruthenium red treatment of fixed frog skeletal muscle caused collapse of the intermediate cisternae of the sarcoplasmic reticulum (SR), forming a pentalaminate structure by obi iterating the SR lumen, we demonstrated that the phenomenon involves the entire SR including the nuclear envelope and that it also occurs after treatment with other cations, including calcium (2,3,4).From these observations we have formulated a hypothesis which states that intracellular calcium taken up by the SR at the end of contraction causes the M rete to collapse at a certain threshold concentration as the first step in a subsequent centrifugal zippering of the free SR toward the junctional SR (JSR). This would cause a) bulk transport of SR contents, such as calcium and granular material (4) into the JSR and, b) electrical isolation of the free SR from the JSR.

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