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Department of Physiology, Abramsky Hall, Queen's University, Kingston, Ontario, Canada, K7L 3N6
(Received 17 July 1978)
It is well established that the stress of ether anaesthesia raises the level of prolactin in the circulation of the rat (Wakabayashi, Arimura & Schally, 1971; Krulich, Hefco, Illner & Read, 1974). Morphine or the endogenous morphine-like peptides, endorphins and enkephalins, can stimulate the secretion of prolactin in vivo (Ojeda, Harms & McCann, 1974; Martin, Audet & Saunders, 1975; Bruni, Van Vugt, Marshall & Meites, 1977; Rivier, Vale, Ling, Brown & Guillemin, 1977; Chihara, Arimura, Coy & Schally, 1978); naloxone, however, blocks the stimulatory effects of these substances (Bruni et al. 1977; Rivier et al. 1977). It was recently demonstrated that naloxone inhibits the secretion of prolactin induced by stress due to heat or immobilization (Van Vugt, Bruni & Meites, 1978). The restraintinduced stress produced an immediate increase in the concentration of prolactin
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Abstract
The effects of somatostatin (SRIF) on prolactin (PRL) synthesis and release were examined in primary cultured pituitary cells derived from normal and estradiol (E2)-primed male rat pituitaries. The cells were continuously incubated in a pulse medium containing [3H]leucine with or without 10−6 mol/l SRIF for a period of 15, 30, 60, 180 or 360 min. Following incubation, the medium was recovered and the cells were fractionated into cytosolic and granular fractions. PRL was isolated by SDS-PAGE and newly synthesized PRL ([3H]PRL) was identified by coincident peaks of tritium activities and PRL contents. The specific activity (SA, c.p.m./ng), a ratio of [3H]PRL to total PRL, was determined for the granular, cytosolic and medium fractions.
In control and SRIF-treated groups of non-primed pituitary cells, SAs of all three fractions significantly increased during the 6-h incubation. Cytosolic and granular SAs showed similar profiles of increasing rate in comparison to control. Medium SAs showed a significantly higher value in the SRIF-treated group than in the control group only at 180 min. These observations indicate that, in the non-primed condition, PRL synthesis is not inhibited by SRIF. Medium SAs in the E2-primed group were significantly higher than SAs in the non-primed control cells during the initial 3 h of incubation, and cytosolic and granular SAs were significantly higher than those of the non-primed control during the 3- to 6-h incubation period. These observations demonstrate that E2 enhances PRL synthesis and secretion of newly synthesized PRL. SRIF treatment of E2-primed lactotrophs resulted in a significant decrease in SAs of all three fractions as compared with those of the E2-primed control. Our results indicate that in normal male rat pituitary cells SRIF does not inhibit PRL synthesis but effectively inhibits PRL synthesis in E-primed lactotrophs. This suggests that the inhibitory action of SRIF on PRL synthesis is estrogen dependent.
Journal of Endocrinology (1996) 148, 69–76
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ABSTRACT
The chemical structure of dopamine includes an ortho-catechol group which is labile to oxidizing agents. Ascorbic acid, a reducing agent, has in the past been added to the incubation medium in order to protect dopamine against oxidation. However, there has been no thorough examination of the biological effect of ascorbic acid on prolactin release. In this present study we have shown that ascorbic acid has neither a stimulatory nor an inhibitory effect on prolactin release but reduces by approximately two orders of magnitude the concentration of dopamine necessary to inhibit prolactin release from cultured anterior pituitary cells. The strong potentiation effect of ascorbic acid was reproduced using apomorphine. We compared the effect of ascorbic acid and isoascorbic acid on dopamine inhibition of prolactin release. Isoascorbic acid is an epimer of ascorbic acid, having the same reduction–oxidation potential as ascorbic acid, but is less biologically active. Isoascorbic acid was less effective in potentiating the dopaminergic effect than was ascorbic acid, which supports the notion that potentiation by ascorbic acid is not entirely due to its reducing property.
In order to dissociate further the chemical protection of dopamine from the biological potentiation, the inhibitory effects of freshly made and 3-h-old dopamine solutions were compared. Neither one of the two solutions contained any ascorbic acid, yet the two solutions did not show any difference in their ability to inhibit prolactin release during the 3-h incubation period, indicating that no significant amount of dopamine was oxidized. The minimum effective concentration of ascorbic acid necessary to demonstrate potentiation was between 0·001 and 0·01 mmol/l. The potentiation effect was shown after 1, 2, or 3 h of exposure to dopamine, and was evident in both 2- and 6-day-old cultured cells.
The effect of ascorbic acid can either be a pharmacological potentiation or a physiological effect on the primary cultured pituitary cells. However, it is quite clear that ascorbic acid is not a simple anti-oxidant but produces a strong potentiating effect on the dopaminergic inhibition of prolactin release by some other means.
J. Endocr. (1988) 118, 287–294
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Department of Physiology, Queen's University, Kingston, Ontario, Canada
(Received 11 November 1974)
Gonadal steroids in the circulation are thought to act on adenohypophysial luteinizing hormone (LH) and hypothalamic LH releasing hormone (LH-RH) to reduce their secretion. The data on which this concept is based were obtained with relatively insensitive bioassay methods (Piacsek & Meites, 1966). Contrary to expectation, we found that both serum and hypothalamic LH-RH had fallen 3 weeks after castration (Shin, Howitt & Milligan, 1974). This is not consistent with the conventional feedback concept of hypothalamic LH-RH, but has recently received confirmation (Eskay, Oliver, Grollman & Porter, 1974; Ferland, Coté & Labrie, 1974).
To clarify better our understanding of the factors that influence LH-RH secretion, the time course of changes in LH and LH-RH after castration have been examined in more detail.
Male Sprague–Dawley rats were handled as described previously (Shin et al. 1974). Hypothalami were extracted according
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Abstract
The neurohypophysial hormones, oxytocin and vasopressin, are present as non-covalently bound complexes with their designated neurophysin in the secretory granules of the posterior pituitary. The neurophysins are generally considered to be biologically inert carrier proteins for oxytocin and vasopressin. We have examined the actions of bovine neurophysin-I (bNP-I), bovine neurophysin-II (bNP-II), rat neurophysin (rat NP) and oxytocin on prolactin release using primary cultured rat pituitary cells. A dynamic perifusion system was chosen to test their stimulatory actions. The rat NP and bNP-II stimulated prolactin release. It is a new observation that rat NP and bNP-II stimulate prolactin release from primary cultured rat pituitary cells. The maximum sensitivities, the lowest concentration which stimulate prolactin release, of rat NP, bNP-II, bNP-I and oxytocin in primary cultured cells were 1 nmol/l, 1 nmol/l, 1000 nmol/l and 1 nmol/l respectively. The maximum sensitivities of rat NP and bNP-II were within the physiologically relevant concentrations.
Journal of Endocrinology (1995) 144, 225–231
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ABSTRACT
Patterns of prolactin release were examined using stimulating and inhibiting agents. Primary cultured pituitary cells primed with oestrogens were used for perifusion experiments. TRH (100 nmol/l) increased the peak prolactin concentration to 360% of the basal concentration, while TRH, under inhibition by 1 nmol somatostatin/l, raised the peak prolactin concentration to 185% of the basal levels. When the somatostatin concentration was increased to 10, 100 and 1000 nmol/l, TRH still stimulated prolactin release to 128%, 121% and 140% respectively, indicating that concentrations of somatostatin of 10 nmol/l or higher did not further suppress the stimulatory effect of TRH. TRH (1 μmol/l) stimulated prolactin release under the influence of 0 (control), 1, 10, 100 and 1000 nmol dopamine/l (plus 0·1 mmol ascorbic acid/l) to 394, 394, 241, 73 and 68% of the basal concentration respectively, showing that the dopamine concentrations and peak prolactin concentrations induced by TRH have an inverse linear relationship in the range 1–100 nmol dopamine/l. The stimulatory effect of dibutyryl cyclic AMP (dbcAMP) on prolactin release was also tested. The relationship between dbcAMP and somatostatin was similar to that between TRH and somatostatin. When adenohypophyses of male rats were used for perifusion experiments, somatostatin (100 nmol/l) did not inhibit basal prolactin release from the fresh male pituitary in contrast with the primary cultured pituitary cells, but dopamine (1 μmol/l) effectively inhibited prolactin release.
In conclusion, (1) oestrogen converts the somatostatin-insensitive route into a somatostatin-sensitive route for basal prolactin release, (2) TRH-induced prolactin release passes through both somatostatin-sensitive and -insensitive routes, (3) dopamine blocks both somatostatin-sensitive and -insensitive routes and (4) cAMP activates both somatostatin-sensitive and -insensitive routes.
Journal of Endocrinology (1991) 130, 79–86
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Department of Physiology, Queen's University, Kingston, Ontario, Canada K7L 3N6
(Received 20 May 1974)
It is well established that gonadal steroid hormones stimulate prolactin secretion and increase the level of prolactin in the blood (Meites, Lu, Wuttke, Welsch, Nagasawa & Quadri, 1972). Many studies of the factors affecting the level of prolactin in the blood have been performed with anaesthetized rats (Chen & Meites, 1970; Wuttke & Meites, 1970; Kalra, Fawcett, Krulich & McCann, 1973). However, since it is now reasonably well established that anaesthetic agents can change levels of prolactin in the circulation (Wakabayashi, Arimura & Schally, 1971; Ajika, Kalra, Fawcett, Krulich & McCann, 1972; Terkel, Blake & Sawyer, 1972), we decided to re-examine the effect of gonadal steroids upon plasma levels of prolactin in the unanaesthetized rat. Animals were castrated and prolactin levels were determined at three intervals with and without the administration of testosterone.
Young male rats
