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

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 mu M) 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.