Role of [Ca2+](i) in 'Ca2+ stores depletion-Ca2+ entry coupling' in fibroblasts expressing the rat neurotensin receptor
(1996) The Journal of Physiology — Vol. 491, n° 3, p. 635-646 (1996)
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- 1. Transfected Chinese hamster ovary fibroblasts expressing the rat neurotensin receptor were used to study the 'Ca2+ stores depletion-Ca2+ entry coupling' which follows stimulation with neurotensin and liberation of InsP(3). 2. This coupling could be dissociated in time. Firstly, stores depletion was produced by neurotensin or thapsigargin which caused a first [Ca2+](i) transient in a Ca2+-free external medium. Secondly, readmission of external Ca2+ produced an influx of Ca2+ and a second [Ca2+](i) transient. 3. Various concentrations of thapsigargin (20 nM to 1 mu M) were used to produce complete stores depletion with small or large first peaks of [Ca2+](i). Upon return to external Ca2+ small or large second [Ca2+](i) peaks were observed. The amplitudes of both peaks were positively correlated. 4. The Ca2+ entry which followed stores depletion could occur at very low basal values of [Ca2+](i), was accelerated by okadaic acid and inhibited by staurosporine and the calmodulin antagonist W-7. 5. It is concluded that the rise in [Ca2+](i) during Ca2+ stores depletion is an essential parameter which determines the size of the subsequent Ca2+ entry.
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Gailly, P., Hermans, E., & Gillis, J.-M. (1996). Role of [Ca2+](i) in ‘Ca2+ stores depletion-Ca2+ entry coupling’ in fibroblasts expressing the rat neurotensin receptor. The Journal of Physiology, 491(3), 635-646. https://hdl.handle.net/2078.5/144134 (Original work published 1996)