Modulation of the kinetics of inositol 1,4,5-trisphosphate-induced [Ca2+](i) oscillations by calcium entry in pituitary gonadotrophs
Author
dc.contributor.author
Kukuljan Padilla, Manuel
Author
dc.contributor.author
Vergara, Leoncio
Author
dc.contributor.author
Stojilkovic, Stanko S.
Admission date
dc.date.accessioned
2019-01-29T15:55:05Z
Available date
dc.date.available
2019-01-29T15:55:05Z
Publication date
dc.date.issued
1997
Cita de ítem
dc.identifier.citation
Biophysical Journal, Volumen 72, Issue 2 I, 2018, Pages 698-707
Identifier
dc.identifier.issn
00063495
Identifier
dc.identifier.other
10.1016/S0006-3495(97)78706-X
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/162780
Abstract
dc.description.abstract
Inositol 1,4,5-trisphosphate (InsP3) binds to its receptor channels and causes liberation of Ca2+ from intracellular stores, frequently in an oscillatory manner. In addition to InsP3, the activation and inactivation properties of these intracellular channels are controlled by Ca2+. We studied the influence of Ca2+ entry on the kinetics of InsP3-triggered oscillations in cytosolic calcium ([Ca2+](i)) in gonadotrophs stimulated with gonadotropin-releasing hormone, an agonist that activates InsP3 production. The natural expression of voltage-gated Ca2+ channels (VGCC) in these cells was employed to manipulate Ca2+ entry by voltage clamping the cells at different membrane potentials (V(m)). Under physiological conditions, the frequency of the GnRH-induced oscillations increased with time, while the amplitude decreased, until both reached stable values. However, in cells with V(m) held at -50 mV or lower, both parameters progressively decreased until the signal was abolished. These effects