Physiological Concentrations of Dopamine Decrease Adenosine 3′,5′-Monophosphate Levels in Cultured Rat Anterior Pituitary Cells and Enriched Populations of Lactotrophs: Evidence for a Causal Relationship to Inhibition of Prolactin Release*

Swennen, Luc; Denef, Carl

doi:10.1210/endo-111-2-398

Cited by 111 publications

(42 citation statements)

References 38 publications

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“…When an ergocryptine dose of 10 The inhibitory effects of haloperidol were dose-and time-dependent, being seen as early as 6 hr after treatment. This is in contrast to the studies described by Hoilt et al (9) (23). The lack of responsiveness of cAMP accumulation to dopamine in the corticotrophs of the AP may account for the lack of inhibition of POMC mRNA level and biosynthesis.…”

contrasting

confidence: 79%

Regulation of the pro-opiomelanocortin mRNA levels in rat pituitary by dopaminergic compounds.

Chen¹,

Dionne²,

Roberts³

1983

Proc. Natl. Acad. Sci. U.S.A.

135

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Dopamine-containing neurons directly innervate the intermediate lobe of the pituitary and dopaminergic compounds exert inhibitory effects on the secretion and the content of a-melanocyte-stimulating hormone and P-endorphin in this tis-sue. In this study, we have investigated the effects of dopamine receptor agonists and antagonists on the level of pro-opiomelanocortin (POMG) mRNA in rat pituitary. RNAs isolated from neurointermediate pituitary (NIP) or anterior pituitary were spotted on nitrocellulose filters and the levels of POMC mRNA were quantified by hybridization to a POMC-specific complementary DNA probe coupled with autoradiography and densitometry. Administration of a dopamine receptor antagonist, haloperidol (2 mg/kg per day), to adult female rats resulted in a 3-to 5-fold increase in POMC mRNA level in the NIP. Treatment with the dopamine agonist 2-Br-a-ergocryptine (1 mg/kg per day) decreased significantly the content of POMC mRNA in the NIP. These drugs had no apparent effect on the POMC mRNA levels in the anterior pituitary. The effect of haloperidol and ergocryptine on POMC mRNA in the NIP is time-and dose-dependent. The elevation of POMC mRNA content in the NIP by haloperidol can be observed as early as 6 hr after treatment. These effects of dopaminergic compounds can also be demonstrated in adult male and ovariectomized female rats. The (-endorphin content of the NIP, as measured by radioimmunoassay, and the de novo synthesis of POMC, as determined by radioactive amino acid labeling and two-dimensional gel electrophoresis analysis, also show negative regulation by dopaminergic compounds.The monoamine neurotransmitter dopamine and its agonists have been shown to inhibit the release of ca-melanocyte-stimulating hormone (a-MSH) and ,B-endorphin, two pro-opiomelanocortin (POMC)-derived peptides, from the intermediate lobe (IP) of the rat pituitary (1-3). Dopamine antagonists, such as haloperidol, stimulate the release of a-MSH and ,B-endorphin (3,4). These effects on POMC-derived peptide secretion from the IP appear to be mediated through a D2 dopamine receptor on the IP melanotroph (for a review, see ref. 5). Dopamine-containing synaptic endings had been identified directly in the rat IP, suggesting direct neural control of IP POMC secretion (6). In the rat pituitary anterior lobe (AP), a tissue that also synthesizes and secretes POMC-derived peptides, dopaminergic agonists and antagonists have not been shown to have similar effects on POMC peptide secretion (1,7,8).Recently, it has been shown that in addition to having effects on POMC peptide secretion, dopaminergic compounds can also change IP content of POMC peptides (3, 9). Chronic treatment of the rat with dopamine agonists or antagonists either decreases or increases, respectively, the amount of radioimmunoactive ,3endorphin or a-MSH in the IP. Such observations would suggest.that these drugs have effects on POMC synthesis parallel to their effects on secretion. Indeed, a very recent study by Hollt et al. showed that chronic (7 day) ...

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contrasting

confidence: 79%

Regulation of the pro-opiomelanocortin mRNA levels in rat pituitary by dopaminergic compounds.

Chen¹,

Dionne²,

Roberts³

1983

Proc. Natl. Acad. Sci. U.S.A.

135

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“…Elevation of cyclic AMIP does not modify the effects of apomorphine A well-known effect of dopamine receptor activation, for example in pituitary lactotrophs, is inhibition of adenylate cyclase, resulting in a marked decrease of cyclic AMP levels (De Camilli & Macconi, 1979;Swennen & Denef, 1982;Delbeke & Dannies, 1985;Enjalbert. Sladeezek, Guillon, Bertrand, Shu, Epelbaum, Garcia-DOPAMINE MODULLATION OF CATECHOLAMINE SECRETIONN 511 Sainz, Jard, Lombard, Kordon & Bockaert, 1986). In order to establish whether the effects of apomorphine on ionic currents and catecholamine release might involve a cyclic AMP-dependent mechanism, treatments that cause elevation of cyclic AMP were given to chromaffin cells prior to exposure to apomorphine and stimulation with nicotine or 59 mm-K+.…”

Section: Role Of G-proteins In Apomorphine Actionmentioning

confidence: 99%

Modulation of secretion by dopamine involves decreases in calcium and nicotinic currents in bovine chromaffin cells.

Sontag

Sanderson

Klepper

et al. 1990

The Journal of Physiology

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SUMMARY1. Catecholamine secretion from cultured bovine adrenal chromaffin cells was decreased in a dose-dependent manner by the D2 dopamine agonists apomorphine and LY 17 1555.2. 45Ca2+ uptake was similarly inhibited and whole-cell Ca2+ currents were reduced by apomorphine.3. These inhibitory effects of D2 agonists depended on the secretagogue used, being much more pronounced for nicotine-evoked responses compared to high K+ stimulation, indicating another possible site of action of apomorphine up-stream of Ca2+ entry.4. Inhibition by apomorphine of nicotine-evoked responses could not be explained by competitive antagonism against nicotine or DMPP (1,1-dimethyl-4-phenylpiperazinium iodide).5. Apomorphine caused reductions of inward whole-cell nicotinic current evoked by ACh and nicotine.6. Inhibition of nicotine-evoked secretion and 22Na+ influx by apomorphine were not affected by tetrodotoxin, and voltage-dependent, whole-cell Na+ currents were unaltered by apomorphine.7. No evidence was obtained for increases in K+ conductance by apomorphine. 8. Action potentials recorded in whole-cell current clamp were blocked by apomorphine when they were triggered by nicotinic depolarization but not when they were elicited by direct electrical stimulation.9. Inclusion ofGDP-,-S in the pipette internal solution did not affect apomorphinedependent inhibition of nicotinic-evoked responses, while the decrease in whole-cell Ca2`current induced by apomorphine was completely inhibited in the presence of GDP-fl-S.

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“…The actions of VIP are mediated by activation of adenylate cyclase and the increase in intracellular cAMP levels (Robberecht et al 1979, Wanke & Rorstad 1990. Previous studies have provided evidence of an important role for cAMP not only in the regulation of lactotroph functions, such as secretion, synthesis and transcriptional regulation of PRL (Maurer 1981, Swennen & Denef 1982, Liang et al 1992, Romano et al 2003, but also in the proliferation of lactotrophs (Suzuki et al 1999). Moreover, VIP activates MAPK cascade through the cAMP/protein kinase A (PKA) pathway in the GH4C1 rat pituitary cell line (Le Péchon-Vallée et al 2000).…”

Section: Introductionmentioning

confidence: 99%

IGF-I and vasoactive intestinal peptide (VIP) regulate cAMP-response element-binding protein (CREB)-dependent transcription via the mitogen-activated protein kinase (MAPK) pathway in pituitary cells: requirement of Rap1

Fernández¹,

Sánchez‐Franco²,

Palacios³

et al. 2005

Journal of Molecular Endocrinology

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In previous studies we demonstrated that vasoactive intestinal peptide (VIP) mediation, and interactions between mitogen-activated protein kinase (MAPK) and cAMP/protein kinase A (PKA) signaling pathways are implicated in insulin-like growth factor I (IGF-I)-and VIP-induced lactotroph proliferation. These facts led us to investigate the intracellular mechanisms involved in IGF-I-and VIP-induced lactotroph proliferation. Exposure of cultured male rat pituitary cells to IGF-I (10 −7 M) or VIP (10 −7 M) stimulated the MAPK cascade. Studies in GH4C1 cells, with an expression vector for Rap1 GTPase-activating protein (Rap1 GAP1), demonstrated reduced VIP-induced MAPK activation, indicating that VIP-dependent activation of the extracellular signal-regulated kinase (ERK) pathway requires PKA-Rap1 signaling. IGF-I induced cAMP-response element (CRE)-binding protein (CREB) phosphorylation through the Ras-MAPK pathway, whereas VIP phosphorylated CREB directly via PKA. The mechanisms that regulate IGF-Iand VIP-CREB-dependent gene transcription were examined using GH4C1 cells transiently transfected with a CRE reporter gene. IGF-I and VIP stimulation of CRE-mediated transcription required activation of both Ras-MAPK and cAMP/PKA signaling. This activation was blocked in the presence of Rap1 GAP1. In summary, we showed that IGF-I and VIP stimulated MAPK activity and the phosphorylation of CREB in pituitary cells. Furthermore, VIP-dependent activation of PKA-Rap1-ERK pathways mediated VIP and IGF-I effects on CREB-dependent transcription in GH4C1 cells. Thus, it is possible that VIP-and IGF-I-induced lactotroph proliferation may involve Rap1.

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Physiological Concentrations of Dopamine Decrease Adenosine 3′,5′-Monophosphate Levels in Cultured Rat Anterior Pituitary Cells and Enriched Populations of Lactotrophs: Evidence for a Causal Relationship to Inhibition of Prolactin Release*

Cited by 111 publications

References 38 publications

Regulation of the pro-opiomelanocortin mRNA levels in rat pituitary by dopaminergic compounds.

Regulation of the pro-opiomelanocortin mRNA levels in rat pituitary by dopaminergic compounds.

Modulation of secretion by dopamine involves decreases in calcium and nicotinic currents in bovine chromaffin cells.

IGF-I and vasoactive intestinal peptide (VIP) regulate cAMP-response element-binding protein (CREB)-dependent transcription via the mitogen-activated protein kinase (MAPK) pathway in pituitary cells: requirement of Rap1

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