PubMed Health⌕ Search

Biomedical subjects

C Libertun

Publications and source records attributed to C Libertun.

At least 91 records · Page 5Linked to original sources
PubMed1980

[Neurotransmitters, neurohormones and prolactin].

After pointing out the reasons for undertaking the study of the regulation of prolactin secretion, the neuroendocrine mechanisms implicated in such secretion are discussed. Special attention is dedicated to the participation of chemical agents. Thus, the principal effects dealt with are: the net inhibition produced by dopamine and the less generalized inhibition effects of nicotine and somatostatin; the facilitatory action of serotoninergic pathways, TRH, histamine and endorphins. The dual effect described for GABA and noradrenaline, as well as some paradoxical actions, e.g., the antiserotoninergic and antihistaminergic H2 drugs which liberate prolactin in basal conditions but abolish the prolactin releasing effect of the respective agonist, or the immediate blocking effect of muscarinic agonists and antagonists are discussed. Finally, the possibility of a new mechanism of control at anterior pituitary receptors level is postulated.

Catecholamines↗
PubMed1978

Biochemical and ultrastructural studies on estrogen-induced pituitary tumors in F344 rats.

The hormone function, the metabolism of nucleic acids, and the ultrastructure of estrogen-induced pituitary tumors and of normal glands were examined in male F344 rats. The tumors had a high capacity for prolactin (PRL) synthesis, and the plasma levels of PRL were elevated 65-fold to 100-fold in the tumor-bearing animals. Uridine uptake and phosphorylation to nucleotides, as well as uridine incorporation into total RNA, were similar in tumors and normal glands, whereas [3H]thymidine incorporation into DNA was double in the former group as compared to the latter. After a [3H]uridine pulse, labeled RNA turnover was different in tumors and normal glands. Electron microscopy of the tumors revealed hypertrophy, degranulation, and hyperplasia of cells producing PRL with proliferation of their ergastoplasm in whorls. Other pituitary cell types were reduced in number. It is suggested that the whorl configuration caused the high rate of protein and PRL synthesis as well as the changes in RNA metabolism displayed by the tumors.

Animals↗
PubMed1977

H1 and H2 histamine receptor participation in the brain control of prolactin secretion in lactating rats.

The aim of the present research was to evaluate the histaminergic regulation of prolactin secretion in the lactating rat and the possible involvement of H1 and H2 histamine receptors in this control. Prolactin was measured by radioimmunoassay in blood samples withdrawn through an intrajugular silastic catheter from undisturbed lactating mothers 10 to 15 days after delivery. In some of those rats a stainless steel cannula was placed in the third ventricle. The tested drugs, H1 and H2 receptor agonists and antagonists, were injected either by the intrasilastic route or intraventricularly immediately before the onset of suckling and after a basal sample was taken. New samples were withdrawn 10, 20, 30 and 60 min thereafter. Suckling caused a 12- to 18-fold increase in serum prolactin by 10 min in control saline-injected mothers. In non-suckled mothers (NSM) injected with saline, prolactin levels were low at all times. Systemic or intraventricular diphenhydramine and mepyramine, H1 receptor antagonists, suppressed the increment in prolactin observed in suckled mothers (SM). Intraventricular metiamide, an H2 receptor antagonist, did not modify prolactin secretion in SM but drastically increased serum prolactin in NSM. A small but significant increase in prolactin titers was observed in NSM injected intraventricularly with histamine. 4-Methylhistamine, an H2 agonist, was ineffective when used intraventricularly in NSM, but clearly suppressed prolactin enhancement in SM. It is postulated that in lactating mothers, brain histamine has a dual control on prolactin secretion. H2 receptors mediate events related to inhibition of prolactin release, since the agonist 4-methylhistamine blocked the prolactin rise in SM, while the antagonist metiamide promoted release of the hormone in NSM. H1 receptors seem to be related to a facilitatory mechanism since classical antihistamines suppress the serum prolactin increase that follows the onset of suckling, while histamine itself is able to release prolactin in NSM.

Animals↗
PubMed1976

The possible role of histamine in the control of prolactin and gonadotropin release.

To evaluate a possible role of histamine in the CNS control of prolactin and gonadotropin release, adult ovariectomized rats, with stainless steel cannulae implanted in the 3rd ventricle, were given s.c. injections of 10 mug of estradiol benzoate. 48 h later, 2 mul of 0.9% NaCl alone or of saline containing 1, 5, 25 or 125 mug of histamine dihydrochloride was microinjected into the ventricle. Immediately before and then 15, 30 and 60 min after, blood samples were withdrawn from etherized rats for radioimmunoassay (RIA) of serum prolactin, LH and FSH. In the histamine-injected rats, an increase in prolactin titers was observed and was highly significant in groups receiving the higher doses. A small yet significant release of LH, but not of FSH, was also observed. When 25 mug of histamine was injected directly into the pituitary or into the jugular vein, no elevations were observed, indicating a site of action in the brain. Restraint stress elevated serum prolactin and lowered serum LH and FSH in ovariectomized rats. These responses were blocked by the intrajugular injection of diphenhydramine (5 mg/kg). It is suggested that histamine may be involved in the hypothalamic control of prolactin release and possibly of gonadotropin release.

Animals↗
PubMed1976

Blockade of the postorchidectomy increase in gonadotropins by implants of atropine into the hypothalamus.

Bilateral implants of atropine sulphate were placed in various loci in the brain or into the anterior pituitary in male rats and the effects of the implants on the postcastration rise in plasma FSH and LH was determined. The increase in both gonadotropins at 16 hr after castration still occurred in animals with implants in the cerebral cortex. The postcastration rise of both FSH and LH was blocked by atropine implants in the anterior, middle, or posterior hypothalamus but was not interfered with by control implants of cholesterol. Bilateral implants of either cholesterol or atropine into the anterior pituitary failed to alter the increase in plasma LH following castration but both types of implants interfered with the postcastration rise in FSH, possibly because of trauma to the pituitary from the cannulae. It is suggested that hypothalamic cholinergic synapses may play a role in stimulating the increased LHRH release which induces the postcastration rise in gonadotropins.

Animals↗