Search PubMed⌕ Search

Biomedical subjects

F Labrie

Publications and source records attributed to F Labrie.

At least 559 records · Page 31Linked to original sources
PubMed1980

Changes of cell morphology and prolactin secretion induced by 2-Br-alpha-ergocryptine, estradiol, and thyrotropin-releasing hormone in rat anterior pituitary cells in culture.

The secretion of prolactin in cultured pituitary cells was studied in correlation with the cellular changes induced by stimulatory or inhibitory agents. The techniques used in this study were: radioimmunoassay, immunocytochemistry, scanning (SEM) as well as transmission (TEM) electron microscopy. Prolactin secretion was stimulated by 17 beta-estradiol (10 nM) as well as thyrotropin-releasing hormone (TRH) (3 nM) and inhibited by 2-Br-alpha-ergocryptine (CB-154) (1 muM). The total prolactin (release and cell content) increased between 2 and 8 d of estradiol treatment, indicating an increase of both synthesis and release of prolactin. This finding was in agreement with TEM observations because, in estradiol-treated prolactin cells, the Golgi saccules were distended and Golgi elements were increased, thus indicating increased synthetic activity of these cells. The addition of TRH over a 4-h period resulted in a significant degranulation of prolactin cells. In contrast, prolactin secretory granules became accumulated in the cells after CB-154 treatment for a period ranging from 4 to 24 h. In agreement, light microscope immunocytochemistry showed an increased reaction for prolactin after short-term (< 24 h) incubation with CB-154. Because prolactin cells represent approximately 70% of the glandular cell population as revealed by immunocytochemistry, it was then possible to observe the changes of cell surface by SEM. In most cells, estradiol and TRH led to an increase in the number and prominence of microvilli and blebs, whereas CB-154 treatment resulted in a slightly decreased number of microvilli and an increased occurrence of membrane foldings. This report thus provides morphological evidence for the stimulatory effects of estradiol and TRH, and the inhibitory effects of CB-154 on prolactin secretion in pituitary cells in primary culture. These data, moreover, show that acute changes in secretory activity of prolactin-secreting cells are accompanied by marked changes of their morphological characteristics.

Animals↗
PubMed1980

Luteolytic activity of LHRH and [D-Ser(TBU)6, des-Gly-NH2(10)]LHRH ethylamide: a new and physiological approach to contraception in women.

The administration of five subcutaneous 250-microgram doses of luteinizing hormone-releasing hormone (LHRH) at 4-hour intervals on 1 or 2 consecutive days between days 1 and 9 following the spontaneous LH surge in normal women shortened the luteal phase from 1 to 4 days in 16 out of 17 treatment cycles. Treatment appeared to be more efficient when LHRH was administered on days 6 to 9 after the LH surge as compared with days 1 to 5. In fact, the luteal phase was shortened from 3.3 +/- 0.2 versus 1.4 +/- 0.2 days (P < 0.01) and the serum progesterone level was decreased to 44 +/- 5 versus 71 +/- 6% of control levels (P < 0.01) when the neurohormone was injected late as compared with early in the luteal phase. A similar luteolytic effect has been obtained after intranasal administration of 500 microgram of [D-Ser(TBU)6, des-Gly-NH2(10)]LHRH ethylamide at 0800 and 1700 h on one day between days 4 and 9 following the LH peak. In six women treated with the LHRH analogue during two consecutive cycles, the luteal phase was shortened by 2.6 +/- 0.4 days (range 0.5-4.5 days) and plasma progesterone levels were reduced to 61.3 +/- 9.2% of control. As determined by daily blood sampling for LH, FSH, estradiol, and progesterone, normal cycles occurred immediately after treatment. The present data indicate the luteolytic effect of treatment with LHRH or a LHRH agonistic analogue in normal women and support the interest of such a new and physiological approach for the control of corpus luteum function and menstrual cycle in women.

Administration, Intranasal↗
PubMed1980

beta-Endorphin and met-enkephalins: their distribution, modulation by estrogens and haloperidol, and role in neuroendocrine control.

A single dose of 0.5 micrograms beta-endorphin injected intraventricularly in unanesthetized male rats bearing chronic intraventricular and intrajugular cannulas led to a sevenfold stimulation of plasma prolactin (PRL) levels 10 to 20 min after injection of the peptide, while a dose of 2 micrograms of beta-endorphin led to a comparable stimulation of plasma growth hormone (GH) concentration. Met-Enkephalin was much less potent than beta-endorphin in stimulating PRL and GH release. Naloxone, a specific opiate antagonist, completely blocked the stimulation of GH and PRL release at the doses of 0.5 and 12.5 mg/kg, respectively. beta-Endorphin and Met-enkephalin from 41 discrete brain nuclei were measured by radioimmunoassay (RIA). beta-Endorphin was found in the hypothalamus medial preoptic nucleus, nucleus interstitialis striae terminalis (NIST), nucleus medialis thalami, and periaqueductal gray. Met-Enkephalin was found predominantly in the globus pallidus, NIST, medial preoptic nucleus, nucleus amygdaloideus centralis, and nucleus lateralis hypothalami. Treatment with both estrogens and haloperidol led to differential effects on Met-enkephalin content in various brain nuclei. Estrogen treatment increased Met-enkephalin levels in globus pallidus, NIST, medial and lateral preoptic nuclei, and periaqueductal gray, while a decrease of the Met-enkephalin content in the nucleus amygdaloideus centralis was found. Haloperidol treatment led to a stimulatory effect in striatum, medial and lateral preoptic nuclei, and interpeduncular nucleus.

Animals↗
PubMed1980

Interactions between hypothalamic and peripheral hormones in the control of prolactin secretion.

The absence of nerve terminals in the anterior pituitary gland offers the possibility of studying a pure population of dopamine (DA) receptors. This study is facilitated by the use of anterior pituitary cells in primary culture, which permit the measurement of a precise parameter under typical dopaminergic control, namely prolactin secretion. On the other hand, since DA is the main hypothalamic factor controlling prolactin secretion, in vivo changes of plasma prolactin levels can be used as an index of DA release from the hypothalamus. Treatment with estrogens not only stimulates basal prolactin secretion but also can reverse the inhibitory effect of DA on prolactin secretion in vivo and in vitro. As assessed by the increased plasma prolactin levels following administration of a maximal dose of the DA antagonist thioproperazine, estrogens increase DA release from the hypothalamus. Progesterone, although inactive alone, can reverse the effect of estrogens on prolactin secretion both in vivo and in vitro. Under the same experimental conditions, dihydrotestosterone exerts inhibitory effects on spontaneous prolactin secretion and can reverse the stimulatory effects of estrogens.

Animals↗
PubMed1979

Effects of colchicine on the morphology and prolactin secretion of rat anterior pituitary cells in monolayer culture.

The effects of incubation of rat anterior pituitary cells in monolayer culture with 10(-6) M colchicine have been investigated during time-intervals extending from 1 to 96 hours. Prolactin release, as measured by radioimmunoassay, was rapidly inhibited by colchicine, this inhibition being accompanied by increased cellular prolactin content for up to 24 hours of treatment and followed by decreased values of cellular prolactin concentration at later time-intervals. Immunocytochemical localization showed an increased positive reaction for prolactin up to 24 hours after colchicine treatment, whereas transmission electron microscopy demonstrated, in parallel, an increased number of intracellular prolactin secretory granules during the same interval. Longer periods of treatment (24-96 hours) resulted in the appearance of more lysosomes, autophagic vacuoles and microfilaments in the cells, whereas the number of Golgi elements was decreased. Following four hours of colchicine treatment and at later stages, microtubules could no longer be observed in the sections. Scanning electron microscopic data showed that colchicine treatment induced dramatic changes in the cell surface morphology: at short time intervals (4 and 8 hours), the number of microvilli decreased and the cell surface became folded, whereas, later, "bleb"-like protrusions of variable dimensions partially covered the cell surface and seemed to be released from it. These data show a good correlation between secretory activity of prolactin-producing cells and morphological changes induced by colchicine treatment.

Animals↗