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Endocrinology, Vol 127, 1948-1955, Copyright © 1990 by Endocrine Society
ARTICLES |
IS Login, SI Kuan, AM Judd and RM MacLeod
Department of Neurology, University of Virginia Health Sciences Center, Charlottesville 22908.
We studied the role of calcium in dopaminergic control of the neuroendocrine effects of neurotensin. In primary cultures of dispersed normal female rat anterior pituitary cells the interactions of dopamine and neurotensin were examined with reference to the rate of PRL release, the magnitude of 45Ca2+ uptake, the rate of fractional 45Ca2+ efflux, and the dynamic response of the intracellular calcium concentration (Cai) monitored with the fluorescent dye, Indo-1. Neurotensin stimulated calcium uptake and also mobilized a pool of intracellular calcium to increase Cai in a sustained plateau-like pattern. The response of PRL release and fractional efflux to neurotensin, however, each displayed typical spike and plateau profiles. In the presence of dopamine the stimulation of PRL release and calcium uptake due to neurotensin were abolished, and the rise in Cai was barely detectable, but neurotensin-stimulated fractional efflux persisted almost unchanged. These data suggest that dopamine may modulate Cai by inhibiting calcium uptake and possibly also by enhancing cellular calcium extrusion under stimulated conditions. Further, the increased inositol trisphosphate production reportedly stimulated by neurotensin apparently does not generate a spike-like response of intracellular calcium, and stimulated hormone release may display a spike and plateau pattern solely with a plateau Cai profile.
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