An Assay for Growth Hormone and Prolactin-Releasing Activities Using a Bovine Pituitary Cell Culture System

Machlin, L. J.; Jacobs, Laurence S.; Cirulis, N.; Kimes, R. C.; Miller, Robert F.

doi:10.1210/endo-95-5-1350

Cited by 46 publications

(13 citation statements)

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“…Although hypothalamic control of prolactin (PRL)' secretion is now recognized to involve both stimulatory (1)(2)(3)(4)(5) and inhibitory (3,(6)(7)(8) components, the predominant influence appears to be inhibitory. A considerable amount of experimental data, using both animal and human models, now exists which indicates that this hypothalamic inhibitory-tone is controlled to a major extent by a dopaminergic mechanism.…”

Section: Introductionmentioning

confidence: 99%

“…In a separate experiment, four normal men, age 25-35 yr, four normal women, age 19-39 yr, and three of the patients with pituitary tumors were given an intravenous infusion of dopamine hydrochloride at the rate of 4 ,ug/kg per min for 180 min using an infusion pump. The dopamine solution was diluted in 5% dextrose in water immediately before use and protected from light during the period of infusion.…”

Section: Introductionmentioning

confidence: 99%

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Loss of Central Nervous System Component of Dopaminergic Inhibition of Prolactin Secretion in Patients with Prolactin-Secreting Pituitary Tumors

Fine¹,

Frohman²

1978

J. Clin. Invest.

137

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A B S T R A C T The administration of L-dopa suppresses prolactin (PRL) secretion in normal subjects and in patients with hyperprolactinemia, although it is not known whether this effect, which requires the conversion of dopa to dopamine, is mediated peripherally or through the central nervous system. To distinguish between these effects, 10 normal subjects (6 male, 4 female) and 8 patients with hyperprolactinemia associated with pituitary tumors were given L-dopa, 0.5 g alone, or 0.1 g after a 24-h pretreatment with carbidopa, 50 mg every 6 h, which produces peripheral dopa decarboxylase inhibition. Similar degrees of PRL suppression were observed in normal subjects (basal plasma PRL 13+2 ng/ml) after L-dopa alone (48±+4%) and after L-dopa plus carbidopa (58+6%). In patients with pituitary tumors and elevated plasma PRL (73+14 ng/ml), L-dopa alone led to PRL suppression comparable with that in normal subjects (47±+6%). However, L-dopa plus carbidopa resulted in only minimal suppression of plasma PRL (19+4%) which was significantly less than after L-dopa alone (P < 0.001). Urinary homovanillic acid excretion, which reflected peripheral dopa decarboxylation was similar in controls and tumor patients after L-dopa both alone and after carbidopa pretreatment.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Loss of Central Nervous System Component of Dopaminergic Inhibition of Prolactin Secretion in Patients with Prolactin-Secreting Pituitary Tumors

Fine¹,

Frohman²

1978

J. Clin. Invest.

137

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“…Since dopa con version to DA could not have occurred peripherally in the presence of MK-486, the results indicate that the residual dopa-decarboxylase activity within the central nervous system (CNS) was capable of permitting sufficient conversion of L-dopa to DA to inhibit Prl secretion. These results provide evidence that L-dopa is capable of exerting its suppressive action on Prl secretion when its decarboxylation to DA is restricted to CNS sites.The hypothalamic control of prolactin (Prl) secretion is now recognized to involve both stimulatory [Meites et al, 1960;Valverde et al, 1972; Dular et al, 1974;Machlin et al, …”

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confidence: 99%

Effect of the Dopa Decarboxylase Inhibitor MK-486 on L-dopa-Induced Inhibition of Prolactin Secretion: Evidence for CNS Participation in the L-dopa Effects

Szabó¹,

Nakawatase²,

Kovathana³

et al. 1977

Neuroendocrinology

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The present studies were performed in order to determine whether the inhibition of prolactin (Prl) secretion which follows the systemic administration of L-dopa and its conversion to dopamine (DA) is mediated by central or by peripheral mechanisms. The effects of pretreatment with the dopa-decarboxylase inhibitor MK-486 (L-α-methyldopa-hydrazide) on the L-dopa and DA inhibition of Prl secretion and on dopa-decarboxylase activity in anterior pituitary, hypothalamus, cerebral cortex and adrenal medulla were evaluated in rats using a dose reported to cause peripheral but not central dopa-decarboxylase inhibition. I.v. infusions of DA, 1 and 10 µg/kg/min, and of L-dopa, 0.1 and 1 mg/kg/min for 15 min, suppressed plasma Prl levels as well as the Prl release response to 0.2 porcine stalk median eminence equivalents (pSME). I.p. administration of MK-486, 50 mg/kg, 30 min before the infusion of L-dopa did not alter either basal or pSME-stimulated Prl secretion or the inhibitory effect of L-dopa. Dopa-decarboxylase activity in the anterior pituitary and the adrenal medulla was completely inhibited by MK-486, while hypothalamic and cerebral cortex dopa-decarboxylase activity was reduced 85 and 84%, respectively. Since dopa conversion to DA could not have occurred peripherally in the presence of MK-486, the results indicate that the residual dopa-decarboxylase activity within the central nervous system (CNS) was capable of permitting sufficient conversion of L-dopa to DA to inhibit Prl secretion. These results provide evidence that L-dopa is capable of exerting its suppressive action on Prl secretion when its decarboxylation to DA is restricted to CNS sites.

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“…Sephadex G-10 and G-25 columns, being separated from PIF (Dular et al 1974;Machlin et al 1974). Several authors reported that TRH has properties of PRF (Noel et al 1974;Rabello et al 1974;Refetoff et al 1974).…”

Section: Discussionmentioning

confidence: 99%

Relationship between prolactin secretion and hypothalamic prolactin releasing factor in pregnant and puerperium rats.

Takahashi¹,

Saito²,

Wakai³

et al. 1976

Tohoku J. Exp. Med.

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The present study attempted to elucidate stimulatory factor(s) in the rat hypothalamus which controls prolactin secretion from the anterior pituitary.Rat serum prolactin was elevated so much in late pregnancy that we prepared the hypothalamic extract of late pregnant rats. Prolactin levels in serum and pituitary were determined by radioimmunoassay. After injection of this extract into a lactating rat 43-60 hr after delivery, the serum prolactin level was elevated significantly one to four hr later and the pitui tary prolactin level declined two hr later. On the other hand, the hypothalamic extract of normal female rats prepared in a similar manner inhibited prolactin secretion from the anterior pituitary in the lactating rat as described by other authors.These data indicate that the prolactin releasing factor may consist in the hypothalamus of late pregnant rat, and be predominant over the prolactin inhibiting factor during late pregnancy. Prolactin secretion was also investigated in lactating and non-lactating puerperium rats. Prolactin in serum and pituitary declined with days after delivery in non-lactating rats, but not in lactating rats. The presumed factor for such prolactin release in lactating rats is considered to be the prolactin releasing factor. prolactin; prolactin releasing factor; hy pothalamus; lactation and pregnancyThe predominantly inhibitory influence of the hypothalamus on prolactin secretion from the pituitary has been well established.The stimulatory factor, however, was recently reported.The participation of serotonergic neurons appears to be important in the neuronal events leading to this hypothalamic stimulation of prolactin release (Lu and Meites 1973;Krulich 1975). In addition, oral admin istration of 5-hydroxytryptophan, a precursor of serotonin, significantly increases plasma prolactin (Kato et al. 1974).Although evidence of the hypothalamic regulation of prolactin secretion is generally accepted, there has been no establishment of hypothalamic control during pregnancy when prolactin secretion increases. In the present study, the prolactin releasing factor (PRF) in the hypothalamus was investigated using late pregnant

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An Assay for Growth Hormone and Prolactin-Releasing Activities Using a Bovine Pituitary Cell Culture System

Cited by 46 publications

References 0 publications

Loss of Central Nervous System Component of Dopaminergic Inhibition of Prolactin Secretion in Patients with Prolactin-Secreting Pituitary Tumors

Loss of Central Nervous System Component of Dopaminergic Inhibition of Prolactin Secretion in Patients with Prolactin-Secreting Pituitary Tumors

Effect of the Dopa Decarboxylase Inhibitor MK-486 on L-dopa-Induced Inhibition of Prolactin Secretion: Evidence for CNS Participation in the L-dopa Effects

Relationship between prolactin secretion and hypothalamic prolactin releasing factor in pregnant and puerperium rats.

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