Thyrotropin-Releasing Hormone: Role of Polyphosphoinositides in Stimulation of Prolactin Secretion

Proximal events after thyrotropin-releasing hormone (TRH)-receptor interaction have helped establish a biochemical basis for the transduction of the hormonal signal at the cell surface into prolactin secretion from rat mammotropic (GH)' pituitary cells. However, the observation that the removal of medium calcium prevented TRH-stimulated secretion was not sufficient to ascribe a role for enhanced influx of extracellular calcium as mediator of stimulates secretion, as it became evident that such manipulation dramatically depressed cellular calcium levels in GH cells. Thus, it was possible that the depletion of extracellular calcium led to loss of Ca 2+ from critical intracellular pools. The association of TRH-induced Ca 2+ -dependent action potentials and stimulation of secretion only suggested but did not prove a cause and effect relationship between these events. Further evidence to support the hypothesis that acute alterations in calcium metabolism were involved in stimulated prolactin secretion was derived from experiments in which the intracellular calcium pools of GH cells were labeled with radiocalcium ( 45 Ca).