ArticleBiophysical journal1994
Relationships between amplitudes and kinetics of rapid cytosolic free calcium fluctuations in GH4C1 rat pituitary cells: roles for diffusion and calcium-induced calcium release.
Article in Biophysical journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Impairment of CFTR activity in cultured epithelial cells upregulates the expression and activity of LDH resulting in lactic acid hypersecretion.Cellular and molecular life sciences : CMLS · 2019Article
- Caffeine-induced oscillations of cytosolic Ca2+ in GH3 pituitary cells are not due to Ca2+ release from intracellular stores but to enhanced Ca2+ influx through voltage-gated Ca2+ channels.Pflugers Archiv : European journal of physiology · 1996Article
- Alterations in the frequency and shape of Ca2+ fluctuations in GH4C1 cells induced by thyrotropin-releasing hormone and Bay K 8644.The Biochemical journal · 1995Article
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4 authors.
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Abstract
We have examined statistical relationships between the amplitudes and the kinetics (rise times, fall times, and decay constants) of cytosolic free calcium fluctuations (spikes) in a population of 353 individual GH4C1 rat pituitary cells. The fast falling phase was approximated by a single exponential decay, and the decay time constant, tau, increased linearly with spike amplitude in 80% of the cells studied. The slope of the tau versus amplitude plot for each cell was inversely related to the cell's mean spike amplitude. Thus, some process responsible for prolonging the decay phase of spikes appeared to operate strongly in cells with spikes of low amplitude, but to become less prominent in cells with high amplitude spikes. Mean tau correlated more strongly with mean rise and fall times than with mean spike amplitude, indicating that the kinetic properties of spikes were not tightly coupled to spike amplitude. These findings are consistent with a model wherein the rise phase corresponds to entry of extracellular calcium via L-type calcium channels into localized sub-plasmalemmal domains, followed by diffusion of subplasmalemmal calcium into the cell interior; and the falling phase corresponds to further calcium diffusion combined with activation of cytoplasmic calcium-induced calcium release, which prolongs the falling phase.
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