Lack of coupling of D-2 receptors to adenylate cyclase in GH-3 cells exposed to epidermal growth factor: Possible role of a differential expression of Gi protein subtypes

Cristina Missale, Flora Boroni, Laura Castelletti, Roberto Dal Toso, Nadia Gabellini, Sandra Sigala, PierFranco Spano

Research output: Contribution to journalArticlepeer-review

Abstract

Exposure of GH-3 cells to epidermal growth factor for 4 consecutive days induced the expression of both D-2(415) and D-2(444) dopamine-receptor isoforms. Epidermal growth factor also promoted a remarkable increase in the content of Gi3 protein, which is responsible for receptor-induced activation of potassium channels in GH-3 cells. D-2 receptors in this model apparently activate a specific transducing pathway, leading to opening of potassium channels and inhibition of prolactin release by cAMP-independent mechanisms. This is shown by: 1) the selective D-2 agonist quinpirole, while inactive on vasoactive intestinal peptide-induced prolactin release, strongly inhibited the hormone secretion induced by neurotensin; 2) quinpi-role, up to 100 μM, did not inhibit cAMP production evoked by vasoactive intestinal peptide both in intact cells and in broken cell membrane preparations; and 3) quinpirole and other D-2 agonists strongly potentiated Rb+ efflux when measured in a nominally calcium-free reaction solution containing 100 mM potassium (voltage-dependent component), but did not modify Rb+ efflux if measured in a reaction solution containing 1 mM calcium and 5 mM potassium (calcium-activated, cAMP-dependent component).

Original languageEnglish
Pages (from-to)23392-23398
Number of pages7
JournalJournal of Biological Chemistry
Volume266
Issue number34
Publication statusPublished - Dec 5 1991

ASJC Scopus subject areas

  • Biochemistry

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