Abstract

Thyrotropin-releasing hormone (TRH) acts via a G-protein-coupled receptor on lactotrophs to increase the intracellular free calcium ion concentration, [Ca 2+] i. The [Ca 2+] i response depends on both TRH concentration and the duration of TRH exposure. An initial, short-lived [Ca 2+] i spike results from release of Ca 2+ from intracellular stores, whereas a later sustained [Ca 2+] i increase, often characterized by [Ca 2+] i oscillations, results from an influx of extracellular Ca 2+ through both voltage-gated and non-voltage-gated, store-operated Ca 2+ channels. The initial spike phase predominates at high doses of TRH, whereas the plateau phase predominates at low doses. The mechanisms underlying the complex [Ca 2+] i response to TRH are discussed.

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