Actions of pertussis toxin on the inhibitory effects of dopamine and somatostatin on prolactin and growth hormone release from ovine anterior pituitary cells

Boyd, Robert S.; Ray, Keith P.; Wallis, Michael

doi:10.1677/jme.0.0010179

Cited by 13 publications

(7 citation statements)

References 36 publications

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“…TPA pretreatment had no significant effect on basal CAMP levels, but led to significantly enhanced stimulation of CAMP concentration by GHRH (table 1). Somatostatin had no effect on CAMP levels, irrespective of TPA pretreatment, in accordance with previous results in ovine pituitary cells [12,13].…”

Section: Resultssupporting

confidence: 92%

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Effects of pretreatment with tetradecanoyl phorbol acetate on regulation of growth hormone and prolactin secretion from ovine anterior pituitary cells

Boyd

Wallis

1989

FEBS Letters

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Tetradecanoyl phorbol acetate (TPA) stimulates growth hormone (GH) and prolactin secretion from ovine anterior pituitary cells. Pretreatment of the cells with TPA abolishes this effect, presumably due to down-regulation of protein kinase C. Such pretreatment did not alter effects of thyrotropin-releasing hormone or dopamine on prolaction secretion, suggesting no involvement of protein kinase C. Pretreatment with TPA attenuated actions of GH-releasing hormone on GH release (but not actions on cyclic AMP levels), possibly due to depletion of cellular stores of GH. Such pretreatment also attenuated inhibition of GH release by somatostatin, possibly due to phosphorylation of receptors or associated proteins by protein kinase C.

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Section: Resultssupporting

confidence: 92%

“…TPA (100 ng/ml) stimulated secretion of GH and prolactin from ovine anterior pituitary cells as shown previously [5,12]. Pretreatment of the cells with 0.1-1000 ng/ml TPA for 5 h resulted in a dose-dependent inhibition of this stimulatory effect ( fig.1).…”

Section: Resultssupporting

confidence: 85%

Effects of pretreatment with tetradecanoyl phorbol acetate on regulation of growth hormone and prolactin secretion from ovine anterior pituitary cells

Boyd

Wallis

1989

FEBS Letters

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“…Early studies suggested that inhibition of cAMP production contributes to inhibition of PRL release (578,580). However, the relevance of cAMP in dopamine actions on PRL release was questioned by the finding that dopamine inhibits PRL secretion in cells with activated ACs by forskolin (582). We also observed that the dopamine agonist-induced inhibition of basal release of prestored PRL was preserved when cAMP levels were elevated by forskolin treatment (583).…”

Section: Dopamine Modulation Of Calcium Influx In Lactotrophs and Melmentioning

confidence: 73%

Ion Channels and Signaling in the Pituitary Gland

2010

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Endocrine pituitary cells are neuronlike; they express numerous voltage-gated sodium, calcium, potassium, and chloride channels and fire action potentials spontaneously, accompanied by a rise in intracellular calcium. In some cells, spontaneous electrical activity is sufficient to drive the intracellular calcium concentration above the threshold for stimulus-secretion and stimulus-transcription coupling. In others, the function of these action potentials is to maintain the cells in a responsive state with cytosolic calcium near, but below, the threshold level. Some pituitary cells also express gap junction channels, which could be used for intercellular Ca(2+) signaling in these cells. Endocrine cells also express extracellular ligand-gated ion channels, and their activation by hypothalamic and intrapituitary hormones leads to amplification of the pacemaking activity and facilitation of calcium influx and hormone release. These cells also express numerous G protein-coupled receptors, which can stimulate or silence electrical activity and action potential-dependent calcium influx and hormone release. Other members of this receptor family can activate calcium channels in the endoplasmic reticulum, leading to a cell type-specific modulation of electrical activity. This review summarizes recent findings in this field and our current understanding of the complex relationship between voltage-gated ion channels, ligand-gated ion channels, gap junction channels, and G protein-coupled receptors in pituitary cells.

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“…Such an action could be coupled to the effects of cAMP and its kinase on the exocytotic pathway (23) and/or inhibition of Ca 2ϩ signaling pathway (24). However, the relevance of cAMP in dopamine actions on PRL release was questioned by the finding that dopamine inhibits PRL secretion in cells with activated ACs by forskolin (25).…”

mentioning

confidence: 99%

Dopamine Inhibits Basal Prolactin Release in Pituitary Lactotrophs through Pertussis Toxin-Sensitive and -Insensitive Signaling Pathways

González-Iglesias

Murano

et al. 2007

Endocrinology

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Dopamine D2 receptors signal through the pertussis toxin (PTX)-sensitive G(i/o) and PTX-insensitive G(z) proteins, as well as through a G protein-independent, beta-arrestin/glycogen synthase kinase-3-dependent pathway. Activation of these receptors in pituitary lactotrophs leads to inhibition of prolactin (PRL) release. It has been suggested that this inhibition occurs through the G(i/o)-alpha protein-mediated inhibition of cAMP production and/or G(i/o)-betagamma dimer-mediated activation of inward rectifier K(+) channels and inhibition of voltage-gated Ca(2+) channels. Here we show that the dopamine agonist-induced inhibition of spontaneous Ca(2+) influx and release of prestored PRL was preserved when cAMP levels were elevated by forskolin treatment. We further observed that dopamine agonists inhibited both spontaneous and depolarization-induced Ca(2+) influx in untreated but not in PTX-treated cells. This inhibition was also observed in cells with blocked inward rectifier K(+) channels, suggesting that the dopamine effect on voltage-gated Ca(2+) channel gating is sufficient to inhibit spontaneous Ca(2+) influx. However, agonist-induced inhibition of PRL release was only partially relieved in PTX-treated cells, indicating that dopamine receptors also inhibit exocytosis downstream of voltage-gated Ca(2+) influx. The PTX-insensitive step in agonist-induced inhibition of PRL release was not affected by the addition of wortmannin, an inhibitor of phosphatidylinositol 3-kinase, and lithium, an inhibitor of glycogen synthase kinase-3, but was attenuated in the presence of phorbol 12-myristate 13-acetate, which inhibits G(z) signaling pathway in a protein kinase C-dependent manner. Thus, dopamine inhibits basal PRL release by blocking voltage-gated Ca(2+) influx through the PTX-sensitive signaling pathway and by desensitizing Ca(2+) secretion coupling through the PTX-insensitive and protein kinase C-sensitive signaling pathway.

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Actions of pertussis toxin on the inhibitory effects of dopamine and somatostatin on prolactin and growth hormone release from ovine anterior pituitary cells

Cited by 13 publications

References 36 publications

Effects of pretreatment with tetradecanoyl phorbol acetate on regulation of growth hormone and prolactin secretion from ovine anterior pituitary cells

Effects of pretreatment with tetradecanoyl phorbol acetate on regulation of growth hormone and prolactin secretion from ovine anterior pituitary cells

Ion Channels and Signaling in the Pituitary Gland

Dopamine Inhibits Basal Prolactin Release in Pituitary Lactotrophs through Pertussis Toxin-Sensitive and -Insensitive Signaling Pathways

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