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  • Title: Spontaneous transients of [Ca2+]i depend on external calcium and the activation of L-type voltage-gated calcium channels in a clonal pituitary cell line (AtT-20) of cultured mouse corticotropes.
    Author: Fiekers JF, Konopka LM.
    Journal: Cell Calcium; 1996 Apr; 19(4):327-36. PubMed ID: 8983853.
    Abstract:
    Spontaneous transients of [Ca2+]i were recorded from single nonstimulated cells of a clonal pituitary cell line of corticotropes, AtT-20/D16v. The spontaneous [Ca2+]i transients were dependent on calcium entry from the extracellular solution because they were abolished both in the absence of extracellular calcium and with the addition of cobalt to the calcium-containing extracellular solution. Calcium entry occurred through voltage-gated (VGCC) L-type calcium channels because the [Ca2+]i transients were blocked by L-type calcium channel antagonists, e.g. nifedipine, and were unaffected by the addition of tetrodotoxin. Bay K 8644 (1 microM) induced transient increases in [Ca2+]i which were also blocked reversibly by either the absence of extracellular calcium or the addition of an L-type calcium channel antagonist (e.g. nifedipine). The resting levels of [Ca2+]i and the frequency, but not the amplitude or duration, of the spontaneous [Ca2+]i transients increased as the concentration of extracellular calcium was elevated in concentrations ranging from 1.8-7.2 mM. Potassium depolarization reversibly elevated resting levels of [Ca2+]i and initiated the spontaneous calcium transients. These results indicate that extracellular calcium modulates the frequency of spontaneous [Ca2+]i transients in AtT-20 cells which are caused by the activation of L-type calcium channels by a spontaneous increase in the permeability of the cell membrane to calcium.
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