Activation of the Adrenergic β-Receptor Stimulates Prolactin Release from Primary Cultured Pituitary Cells

Shin, Seon H.; Barton, Ruth E.

doi:10.1159/000126424

Cited by 6 publications

(6 citation statements)

References 23 publications

(28 reference statements)

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“…24] and/or receptor-coupled activation of different G proteins [9,25,26]. These, in turn, could determine the direction of change in cytosolic calcium controlling PRL secretion [27], It is also possible that the steroid background may determine shifts in receptor specificity [28,29] or post receptor transduction coupling efficiency [30]. The data of the present study suggest that the steroid hormonal environment may dictate which receptors, signalling sys tems or ion channels are activated to transduce the differ ential response to DA.…”

Section: Discussionmentioning

confidence: 99%

Effects of Ovarian Steroid Hormones on Dopamine-Controlled Prolactin Secretory Responses in vitro

Freeman²

1997

Neuroendocrinology

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Dopamine (DA), a well-established inhibitor of prolactin (PRL) secretion, has also been shown to stimulate PRL secretion from the anterior lobe of the pituitary gland of the rat. It has been reported that low doses of DA stimulate PRL whereas high doses inhibit PRL secretion. Our laboratory has previously reported that these PRL secretory responses are dependent upon the stages of the estrous cycle of the rat. The objective of the present study was to determine the steroid requirements for the differing PRL secretory responses to low and high doses of DA in perifusion. Animals were ovariectomized (OVX) and immediately given Silastic implants containing estradiol (E₂) which has previously been shown in our laboratory to produce blood levels of 70–100 pg/ml, progesterone which has previously been shown in our laboratory to produce blood levels of 30–40 ng/ml, or the combination. OVX rats served as controls. Ten days later, the anterior lobes of the pituitary glands were harvested and enzymatically dissociated. Cells were mixed with Sephadex G-10 and placed in six 0.5-ml perifusion chambers (1 × 10⁶ cells/chamber). Cells were perifused for 24 h with Dulbecco’s modified Eagle’s medium containing 0.2% bovine serum albumin and 0.1 mM ascorbic acid. The PRL secretory pattern was characterized in response to the following treatment sequence: (1) 30 min media alone (maximally uninhibited); (2) 24 min 100 pM DA; (3) 30 min media alone (DA withdrawal); (4) 24 min 1 µM DA, and (5) 30 min media alone (DA withdrawal). PRL secretion in the presence of 100 pM DA was unchanged in cells obtained from OVX animals, but exposure to 1 µMDA inhibited PRL release in these cells. Subsequent withdrawal stimulated PRL secretion relative to that of the initial exposure to media alone. The responses of cells from OVX rats implanted with progesterone alone was indistinguishable from those of the OVX controls. In cells obtained from animals implanted with E₂ alone, 100 pM DA and its subsequent withdrawal neither stimulated nor inhibited PRL secretion. In contrast, 1 µM DA exposure initially stimulated and then inhibited PRL secretion in cells from E₂-treated animals. Here, subsequent withdrawal of DA enhanced PRL secretion. In cells obtained from E₂+progesterone-treated animals, 100 pM DA exposure robustly enhanced PRL secretory responses. Withdrawal of this dose of DA had no further effect on PRL secretion. However, exposure of E₂+progesterone-treated cells to 1 µM DA robustly stimulated and subsequently only slightly inhibited PRL secretion. The results of these studies suggest that inhibition of PRL secretion by DA is independent of ovarian steroids while E₂ and progesterone in combination favors stimulation of PRL secretion in response to DA. Taken together, these data suggest that PRL secretory responses in this system are determined by the ovarian steroid milieu.

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Section: Discussionmentioning

confidence: 99%

Effects of Ovarian Steroid Hormones on Dopamine-Controlled Prolactin Secretory Responses in vitro

Freeman²

1997

Neuroendocrinology

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“…dopamine, epinephrine, norepinephrine) or adrenergic agents directly alter anterior pituitary functions (Denef and Baes, 1982;Swartz and Moberg, 1986;Li, 1989;Shin and Barton, 1993;Colthorpe et al, 2000). In this research, we have observed small (up to approx.…”

Section: The Effect Of Gnrh α-And β-Adrenergic Agents On Prl Secretimentioning

confidence: 60%

“…Studies performed with pituitary cells derived from male rats have yielded discrepant results. Perkins et al (1985) did not observe any influence of β-adrenergic agonist (ISOP) on PRL release from pituitary cells, whereas Denef and Baes (1982) and Shin and Barton (1993) have demonstrated a stimulatory effect of the agonist on PRL secretion. Moreover, on the basis of pharmacological studies, Shin and Bar-ton (1993) concluded that β 2 -adrenergic receptors are implicated in the stimulation of PRL secretion and then suggested their presence within lactotrophs.…”

Section: The Effect Of Gnrh α-And β-Adrenergic Agents On Prl Secretimentioning

confidence: 84%

“…In turn, release of β-END -proopiomelanocortin (POMC) processing product, co-released with ACTH -is mainly enhanced by corticotropin-releasing hormone (CRH), as well as by substance P, cholecystokinine (CCK), vasopressin, oxytocin (OT) and vasoactive intestinal peptide (VIP) (Matsumura et al, 1982(Matsumura et al, , 1983Sweep and Wiegant, 1989;Bogacka et al, 2002a). Catecholamines and gonadotrophinreleasing hormone (GnRH) are other candidates, which may influence pituitary PRL and β-END secretion (Denef and Baes, 1982;Gambacciani et al, 1988;Kerdelhue et al, 1988;Shin and Barton, 1993;Denef, 1994;Colthorpe et al, 2000). Studies primarily performed on laboratory rodents have established that catecholamines are involved in the regulation of prolactin secretion (Vijayan and McCann, 1978;Weiner and Ganong, 1978;Deaver and Dailey, 1982) and β-END secretion (Vermes et al, 1980;Berkenbosch et al, 1981;Pettibone and Mueller, 1982).…”

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confidence: 99%

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The effects of GnRH and adrenergic agents on PRL and ß-endorphin secretion by porcine pituitary cells in vitro

Siawrys

Bogacka

Okrasa

et al. 2003

Acta Veterinaria Hungarica

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The direct effects of α-and β-adrenergic agents on PRL and β-endorphin (β-END) secretion in vitro by porcine pituitary cells have been investigated. Pituitary glands were obtained from mature gilts, which were ovariectomised (OVX) one month before slaughter. Ovariectomised gilts, assigned to four groups, were primed with: (1) vehicle (OVX); (2) and (3) oestradiol benzoate (EB; 2.5 mg/100 kg b.w.) at 30-36 h (OVX+EB I) and 60-66 h (OVX+EB II) before slaughter, respectively; and (4) progesterone (P 4 ; 120 mg/100 kg b.w.) for 5 consecutive days before slaughter (OVX+P 4 ). Isolated anterior pituitary cells were submitted to 3.5 h incubation in the presence of GnRH, α-and β-adrenergic agonists [phenylephrine (PHEN) and isoproterenol (ISOP), respectively], or α-and β-adrenergic blockers [phentolamine (PHENT) and propranolol (PROP), respectively]. The culture media were assayed for PRL (exp. I) and β-endorphin-like immunoreactivity (β-END-LI) (experiment II). In experiment I, GnRH did not influence PRL release by pituitary cells in all experimental groups. Some of tested doses of adrenergic agonists, PHEN and ISOP, increased PRL release from pituitary cells of OVX gilts, but not from those of OVX+EB I animals. In the OVX+EB II group, PHEN alone, but ISOP with PROP, potentiated PRL secretion by the cells. In OVX+P 4 animals, PHEN alone or in combination with PHENT and also ISOP alone or with PROP enhanced PRL output from the cells. In experiment II, addition of GnRH increased β-END-LI release from pituitary cells only in the OVX+EB II group. PHEN and PHENT potentiated β-END-LI secretion by pituitary cells in OVX+EB II and OVX+P 4 groups, while ISOP and PROP increased β-END-LI secretion by the cells of OVX and OVX+EB II animals. In turn, in the OVX+EB I group, effect of PHENT and PROP on PRL secretion by pituitary cells was inhibitory. In conclusion, our results suggest that adrenergic agents can modulate PRL and β-END secretion by porcine pituitary cells in a manner dependent on the hormonal status of gilts.

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“…However, when dopamine stimulates or inhibits proiactin release in GH4ZR7 cells, it is clear that the dopamine should act on the short form of dopamine receptors since there is no other dopamine (or catecholamine) receptor in the GH4ZR7. A high concentration of dopamine can stimulate adrenergic P-receptors which transduct stimulatory action on proiactin release (Shin and Barton, 1993). Therefore, if other catecholamine receptors than dopamine are expressed in GH4ZR7 cells, there is a possibility that dopamine might activate other catecholamine receptors to stimulate proiactin release.…”

Section: Transduction Systemmentioning

confidence: 99%

Regulation of prolactin secretion: Dopamine is the prolactin‐release inhibiting factor (PIF), but also plays a role as a releasing factor (PRF)

Shin

Song

Ross

1999

Korean Journal of Biological Sciences

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Many in-depth reviews related to regulations of prolactin secretion are available. We will, therefore, focus on controversial aspects using personal opinion in this review. The neuroendocrine control of prolactin secretion from the anterior pituitary gland involves multiple factors including prolactin-release inhibiting factor (PIF) and prolactin releasing factor (PRF). The PIF exerts a tonic inhibitory control in the physiological conditions. The PIF should be able to effectively inhibit prolactin release for a lifetime, but the inhibitory action of dopamine cannot be sustained for a long period of time. Perifusion of a high concentration of dopamine (1,000 nM) could not sustain inhibitory action on prolactin release but when a small amount of ascorbic acid (0.1 mM) is added in a low concentration of dopamine (3 nM) solution, prolactin release was inhibited for a long period. Ascorbate is essential for dopamine action to inhibit prolactin release. We have, therefore, concluded that the PIF is dopamine plus ascorbate. The major transduction system for dopamine to inhibit prolactin release is the adenylyl cyclase system. Dopamine decreases cyclic AMP concentration by inhibiting adenylyl cyclase, and cyclic AMP stimulates prolactin release. However, the inhibitory mechanism of dopamine on prolactin release is much more complex than simple inhibition of cAMP production. The dopamine not only inhibits cyclic AMP synthesis but also inhibits prolactin release by acting on a link(s) after the cAMP event in a chain reaction for inhibiting prolactin release. Low concentrations of dopamine stimulate prolactin release. Lactotropes are made of several different subtypes of cells and several different dopamine receptors are found in pituitary. The inhibitory and stimulatory actions induced by dopamine can be generated by different subtype of receptors. The GH 4 ZR 7 cells express only the short isoform (D 2s ) of the dopamine receptor, as a result of transfecting the D 2s receptors into GH4C1 cells which do not express any dopamine receptors. When dopamine stimulates or inhibits prolactin release in GH 4 ZR 7 cells, it is clear that the dopamine should act on dopamine D 2s receptors since there is no other dopamine receptor in the GH 4 ZR 7 . Dopamine is able to stimulate prolactin release in a relatively low concentration while it inhibits in a high concentration in GH 4 ZR 7 . These observations indicate that the dopamine D 2 receptor can activate stimulatory and/or inhibitory transduction system depending upon dopamine concentrations.

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Activation of the Adrenergic β-Receptor Stimulates Prolactin Release from Primary Cultured Pituitary Cells

Cited by 6 publications

References 23 publications

Effects of Ovarian Steroid Hormones on Dopamine-Controlled Prolactin Secretory Responses in vitro

Effects of Ovarian Steroid Hormones on Dopamine-Controlled Prolactin Secretory Responses in vitro

The effects of GnRH and adrenergic agents on PRL and ß-endorphin secretion by porcine pituitary cells in vitro

Regulation of prolactin secretion: Dopamine is the prolactin‐release inhibiting factor (PIF), but also plays a role as a releasing factor (PRF)

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