Dopamine does not attenuate phosphoinositide hydrolysis in rat anterior pituitary cells

Canonico, Pier Luigi; Jarvis, W. D.; Judd, Allan M.; MacLeod, Robert M.

doi:10.1677/joe.0.1100389

Cited by 50 publications

(9 citation statements)

References 12 publications

(13 reference statements)

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“…The lack of effect of acute DA administration on the basal accumulation of inositol phosphates has been previously reported [3.6, 16]. Although the inhibition of stimulated ac cumulation is controversial [3,6,16], under our experimen tal conditions, the administration of DA did not affect ei ther basal ( fig. I ) or TRH-induced accumulation of inositol phosphates.…”

Section: Discussionsupporting

confidence: 62%

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Phosphoinositide Hydrolysis in Response to the Withdrawal of Dopamine Inhibition in Enriched Lactotrophs in Culture

1987

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The formation of inositol phosphates and hydrolysis of polyphosphoinositides in response to DA addition or removal was studied in cultured anterior pituitary cells from E2-treated rats. The cells were incubated for 24 h with [³H]inositol to label the polyphosphoinositides either with or without DA (500 nM) in the medium. [³H]inositol phosphate and [³H]polyphosphoinositide levels were determined by anion-exchange chromatography after KOH deacylation of the latter. Acute (5 min) administration of DA to cells cultured without DA resulted in no change in the levels of [³H]inositol phosphates but a significant increase (50 ± 10%) in the levels of [³H]polyphosphoinositides. Similarly, tonic exposure to DA for 40 h resulted in an increase (127 ± 9%) of [³H]polyphosphoinositide levels. Acute withdrawal of DA from the medium for 5 min induced a 77 ± 9% increase in the levels of [³H]inositol phosphate and a 27 ± 3% decrease in [³H]polyphosphoinositide levels. These results suggest that the inositol phosphate messenger system of lactotrophs is negatively coupled to DA receptors. The efficiency of dopamine removal to activate this pathway is consistent with the kinetics of DA binding to its receptor and observations that DA removal is an important physiological signal for PRL release.

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Section: Discussionsupporting

confidence: 62%

“…Acute administration of DA was reported to have no effect on the basal or stimu lated production of inositol phosphates (IPx) [3]. However, others reported that DA inhibited angiotensin I I-stimulated [6] orTRH-stimulated [16] production of IPx.…”

mentioning

confidence: 99%

Phosphoinositide Hydrolysis in Response to the Withdrawal of Dopamine Inhibition in Enriched Lactotrophs in Culture

1987

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“…PKC activated by phorbol esters enhances adenylate cyclase activity by inhibiting the inhibitory activity of GTP-binding Gj-protein. TRH also stimulates the cyclase activity by stimulat ing GTP-binding Gs-protein [16], It was also suggested that dopaminergic D2 receptors may be linked to the phospholipase C system by demonstrating that a brief ex posure to dopamine enhanced phosphatidyl inositol bi phosphate [17], Another group of workers proposed that the D2 receptors may be negatively coupled to the phos pholipase C system [18][19][20], but it has been difficult to demonstrate an inhibitory effect of dopamine on total inositol phosphate production [21].…”

Section: Inmentioning

confidence: 99%

Differential Inhibition of Dopamine and Bromocriptine on Induced Prolactin Release: Multiple Sites for the Inhibition of Dopamine

Hanna

Shin²

1992

Neuroendocrinology

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Effects of dopamine and bromocriptine on TRH- or dibutyryladenosine 3’,5’-cyclic monophosphate (dbcAMP)-induced prolactin release from primary cultured rat pituitary cells were studied using a perifusion system. TRH (100 nmol/l) stimulated prolactin release from basal concentrations of 33.8 ± 0.5 to 151.2 ± 28.0 ng/ml (net increase) or 447% increase. Dopamine inhibited the basal release of prolactin throughout the experiment, but TRH (100 nmol/l) was still able to stimulate prolactin release under the influence of dopamine. The increment in prolactin release was inversely proportional to the dopamine concentration. When TRH (100 nmol/l) was introduced during a perifusion period with bromocriptine 1 nmol/l, the prolactin concentration was increased to 110.9% of basal levels. The stimulatory effect of TRH under the influence of bromocriptine (1 nmol/l) was significantly lower than that without bromocriptine (control), although the higher concentrations of bromocriptine (10 and 100 nmol/l) did not further reduce the peak concentration of TRH-induced prolactin release. During a perifusion period with a low concentration of dopamine (1 nmol/l plus 0.1 mmol/l ascorbic acid), introduction of dbcAMP (3 mmol/l) stimulated prolactin release to 48% of basal concentration. A higher concentration of dopamine further reduced the stimulatory effect of prolactin release. Bromocriptine impeded the stimulatory effect of dbcAMP (3 mmol/l) on prolactin release in a similar manner as dopamine. Since a higher concentration of bromocriptine (10 and 100 nmol/ 1) did not further inhibit the TRH-induced prolactin release whereas a higher concentration of dopamine did, it is concluded that dopamine acts through additional mechanism(s) other than the D₂ receptor transduction system.

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“…Acute administration of DA has been shown to have no effect on either the basal or stimulated IP production in rat anterior pituitary cells [24]. However, while levels of DA (500 n M ) sufficient to elicit inhibition of prolactin release have been shown not to lower TRH-stimulated increases in intracellular IPs, higher levels such as those we have used (10 µ M ) were effective in reducing the magnitude of stimulated IP production [25]. Some laboratories have suggested that DA inhibits IP production by way of decreasing phosphoinositide-specific phospholipase C (PLC) activity [26, 27].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Hormonally Induced Inositol Trisphosphate Production in Transfected GH4C1 Cells: A Novel Role for the D5 Subtype of the Dopamine Receptor

White

Kimura²,

Sidhu³

1999

Neuroendocrinology

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We have previously found that the D₅ dopamine receptor couples to a G-protein other than G_sα, and could be involved in signaling pathways other than regulation of adenylyl cyclase. To describe interactions of the D₅ receptor with cellular effectors, we used GH₄C₁ cells transfected with cDNA for the human D₅ receptor. Thyrotropin-releasing hormone (TRH, 100 nM) stimulated accumulation of inositol phosphates (IPs) fivefold in D₅GH₄C₁ cells. Dopamine (DA, 10 µM) inhibited TRH-stimulated IP values by 29%; at higher concentrations (100 µM), maximal inhibition of 61% was observed. The D₅ agonist SKF R-38393 (10 µM) mimicked this effect (28% inhibition). SCH 23390, a D₅ antagonist, blocked the inhibition caused by both DA and SKF R-38393. Spiperone, a D₂ receptor antagonist, did not block the inhibition. The D₂ agonist (±)-2-(N-phenylethyl-N-propyl)amino-5-hydroxytetralin (PPHT) did not inhibit TRH-stimulated IP production, nor did it augment the effect of D₅ agonists. The DA-mediated suppression of IP levels was not sensitive to pertussis toxin; cholera toxin blocked both TRH stimulation and DA suppression of IP accumulation in response to 100 nM TRH. Neither dibutyryl cAMP nor forskolin lowered IP formation in response to TRH. Phorbol ester decreased TRH-stimulated IP accumulation in D₅GH₄C₁ cells; however, an inhibitor of protein kinase C (PKC) did not block the effect of DA.

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Dopamine does not attenuate phosphoinositide hydrolysis in rat anterior pituitary cells

Cited by 50 publications

References 12 publications

Phosphoinositide Hydrolysis in Response to the Withdrawal of Dopamine Inhibition in Enriched Lactotrophs in Culture

Phosphoinositide Hydrolysis in Response to the Withdrawal of Dopamine Inhibition in Enriched Lactotrophs in Culture

Differential Inhibition of Dopamine and Bromocriptine on Induced Prolactin Release: Multiple Sites for the Inhibition of Dopamine

Inhibition of Hormonally Induced Inositol Trisphosphate Production in Transfected GH<sub>4</sub>C<sub>1</sub> Cells: A Novel Role for the D<sub>5</sub> Subtype of the Dopamine Receptor

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