Calcium Oscillations in Anterior Pituitary Cells

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Abstract
I. Introduction OVER the last two decades it has become evident that intracellular Ca2+ signals are critically important for the control of cellular activities including excitability, exocytosis, and contraction, as well as cell growth, differentiation, and division. Elevations of [Ca2+]i occur spontaneously or in response to agonist stimulation and are commonly expressed as prominent Ca2+ oscillations in single cell studies. Such oscillations are dependent on the entry of Ca2+ and/or its release from intracellular stores. In many cell types, both mechanisms are involved in the generation of Ca2+ oscillations. The cellular pathways involved in the regulation of Ca2+ entry include VSCC, receptor- and second messenger-operated Ca2+ channels, and mechanically operated Ca2+ channels. Ca2+ discharge from intracellular Ca2+ pools also occurs through calcium channels; one of these is the inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]-sensitive- and another is the ryanodine-sensitive Ca2+ release channel (1). In pituitary cells, spontaneous calcium oscillations are usually associated with Ca2+ entry through VSCC, and are typical of excitable endocrine cells. In addition to VSCC, sodium, potassium, calcium-activated potassium, and chloride channels are present in pituitary cells. The sum of the various currents flowing at any time point determines the pituitary cell membrane potential. In these cells, action potentials (APs) are triggered by a slow depolarization that reaches the threshold for opening VSCC. The inward calcium current then further depolarizes the plasma membrane, leading to Ca2+ influx which in turn is terminated indirectly by rapid activation of transient voltage-dependent K+ channels, and/or activation of Ca2+-sensitive K+ channels, which repolarize the membrane (2–5). This mechanism forms the basis of the plasma-membrane oscillator (6). Several agonists operate through facilitatory or inhibitory modulation of plasma membrane oscillatory activity (7, 8).

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