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On the role of extracellular Ca2+ for prolactin release and adenosine 3′:5′-monophosphate formation induced by thyroliberin in cultured rat pituitary cells
Authors:Kaare M Gautvik  Jens-Gustav Iversen  Olav Sand
Institution:x. Institute of Physiology, University of Oslo, Karl Johansgt. 47, Oslo 1, Norway
Abstract:In cultured rat pituitary tumour cells (GH3 cells) the absence of extracellular Ca++ or addition of NaEGTA reduced spontaneous prolactin (PRL) release and abolished the stimulatory effect of thyroliberin (TRH). Readdition of CaCl2, but not of equimolar concentrations of MgCl2 increased spontaneous hormone release, and restored the effect of TRH. The calcium ionophore, A-23187, induced PRL release during normal calcium conditions, but not when an excess NaEGTA was present. TRH increased cyclic AMP accumulation in the presence and the absence of extracellular calcium. The effect of TRH on PRL release and cyclic AMP formation occured concomitantly with an increased efflux of 45Ca2+. Intracellular electrophysiological recordings from the same single cells before and after TRH activation showed increased frequency and duration of the Ca2+ dependent action potentials. We conclude that TRH elevates the Ca2+ influx which depends on the depolarizing action current, and this effect is probably linked to formation of cyclic AMP and PRL release.
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