Neonatal testosterone potentiates stimulated prolactin secretion in adult oestrogen-primed rats

1986 ◽  
Vol 109 (1) ◽  
pp. 57-60 ◽  
Author(s):  
R. G. Dyer ◽  
S. Mansfield
Keyword(s):  
Testosterone Propionate ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Neonatal Exposure ◽  
Adult Rats ◽  
Blood Samples ◽  
Before And After ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

ABSTRACT Blood samples were collected from oestrogen-primed gonadectomized adult rats before and after electrical stimulation of the preoptic part of the hypothalamus. Six groups of rats were used for the experiments. These were (a) males castrated on the first day of life, (b) males castrated after puberty, (c) females ovariectomized after puberty and (d), (e) and (f) females given testosterone propionate at birth (1·25, 0·125 and 0·0125 mg/rat respectively). Neonatal exposure of the female rats to testosterone caused a dose-dependent increase in the amounts of prolactin released to levels significantly (P<0·01) higher than those observed in male animals and in untreated females. The results indicate that although neonatal testosterone inhibits oestrogen-stimulated prolactin secretion in adult rats, the neuroendocrine apparatus controlling secretion of the hormone is capable of being activated to greater effect after exposure to androgens at the time of birth. J. Endocr. (1986) 109, 57–60

LORDOSIS BEHAVIOUR IN MALE, FEMALE AND ANDROGENIZED FEMALE RATS

1976 ◽  
Vol 70 (3) ◽  
pp. 409-420 ◽  
Author(s):  
P. SÖDERSTEN
Keyword(s):  
Testosterone Propionate ◽  
Female Rats ◽  
Male Rats ◽  
High Dose ◽  
Normal Female ◽  
Adult Rats ◽  
Oestradiol Benzoate ◽  
Series Of Experiments ◽  
Lordosis Behaviour ◽  
Dose Dependent

SUMMARY Sex differences in the lordosis response of adult rats to ovarian hormones were studied in a series of experiments. Male rats were less sensitive to oestradiol benzoate (OB, a single injection of 10, 100 or 1000 μg/kg or seven daily injections of 2, 10 or 50 μg/kg) than were female rats. Oestradiol benzoate-primed (10 μg/kg) female, but not male, rats showed dose-dependent responses to progesterone (0·4, 2·0 or 10·0 mg/kg). Male rats responded clearly to progesterone (2 mg/rat) only when primed with a high dose of OB (100 μg/rat). Display of the whole pattern of female sexual behaviour was induced in male rats by treatment with 100 μg OB and 2 mg progesterone. Female rats treated with 1 mg testosterone propionate (TP) on day 4 of life, ovariectomized as adults and tested under the same endocrine conditions as the rats described above, retained behavioural OB sensitivity but responded poorly to progesterone. Evidence is presented that ovarian secretions during development significantly modify the response of neonatally TP-treated and normal female rats to OB in adulthood.

DISAPPEARANCE RATE OF BOVINE PROLACTIN FROM PLASMA OF FEMALE RATS STUDIED AT INTERVALS OF UP TO 160 MINUTES BY RADIOIMMUNOASSAY

1970 ◽  
Vol 64 (4) ◽  
pp. 718-725 ◽  
Author(s):  
A. A. van der Gugten ◽  
H. G. Kwa
Keyword(s):  
Intravenous Administration ◽  
Female Rats ◽  
Disappearance Rate ◽  
Blood Samples ◽  
Dose Dependent

ABSTRACT Plasma values resulting from the intravenous administration of 300, 100, 30 and 10 μ of bovine prolactin to rats on day 1 of pregnancy were followed by taking blood samples after 10, 20, 40, 80 and 160 minutes respectively. The rate of disappearance was found to be dose-dependent and to vary in time in the same rat. It is suggested that at least two processes of elimination take place: 1. a (possibly excretory) process, which can bring »unphysiologically high« prolactin levels down to approximately its treshold level of 1.7 μg/ml and 2. a process, which breaks down the hormone into »immunoreactive« polypeptides. This process can degrade 10 μg of bovine prolactin quantitatively within 10 minutes, but appears to become rapidly »saturated« by larger amounts of the hormone.

Gonadal hormones organize and modulate the circadian system of the rat

1981 ◽  
Vol 241 (1) ◽  
pp. R62-R66 ◽  
Author(s):  
H. E. Albers
Keyword(s):  
Testosterone Propionate ◽  
Wheel Running ◽  
Activity Rhythm ◽  
Gonadal Hormones ◽  
Circadian System ◽  
Female Rats ◽  
Constant Darkness ◽  
Before And After ◽  
Free Running ◽  
Free Running Period

The circadian wheel-running rhythms of gonadectomized adult male, female, and perinatally androgenized female rats, maintained in constant darkness, were examined before and after implantation of Silastic capsules containing cholesterol (C) or estradiol-17 beta (E). The free-running period of the activity rhythm (tau) before capsule implantation tended to be shorter in animals exposed to perinatal androgen. Administration of C did not reliably alter tau in any group. E significantly shortened tau in 100% of females injected with oil on day 3 of life. In females, injected with 3.5 micrograms testosterone propionate on day 3, and males, E shortened or lengthened tau, with the direction and magnitude of this change in tau inversely related to the length of the individual's pretreatment tau. These data indicate that the presence of perinatal androgen does not eliminate the sensitivity of the circadian system of the rat to estrogen, since estrogen alters tau in a manner that depends on its pretreatment length.

Stimulation of acetylcholine release in myenteric plexus by calcitonin gene-related peptide

1990 ◽  
Vol 259 (6) ◽  
pp. G934-G939 ◽  
Author(s):  
M. W. Mulholland ◽  
S. Jaffer
Keyword(s):  
Myenteric Plexus ◽  
Acetylcholine Release ◽  
Calcitonin Gene Related Peptide ◽  
Ach Release ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Dependent Mechanism ◽  
Stimulation Of

The effects of calcitonin gene-related peptide (CGRP) on acetylcholine (ACh) release from myenteric plexus neurons in primary culture were investigated. CGRP (10(-12) to 10(-6) M) produced a dose-dependent increase in [3H]ACh release. The ACh release caused by CGRP was significantly inhibited (74 +/- 24%) by preincubation with dideoxyadenosine but was increased more than threefold by preincubation with theophylline. Incubation of myenteric plexus neurons with CGRP (10(-8) M) in the presence of diltiazem (10(-5) M) or in a calcium-free medium markedly reduced [3H]ACh release. CGRP potentiated [3H]ACh release stimulated by potassium or substance P but not by cholecystokinin octapeptide or forskolin. The results demonstrate that CGRP cause release of ACh from guinea pig myenteric plexus neurons and suggest that the peptide acts through an adenosine 3',5'-cyclic monophosphate-dependent mechanism that involves neuronal calcium channels.

EFFECTS OF TESTOSTERONE MEDIATED OR MODULATED BY PITUITARY FACTORS

1975 ◽  
Vol 67 (1) ◽  
pp. 71-79 ◽  
Author(s):  
P. DE MOOR ◽  
M. ADAM-HEYLEN ◽  
H. VAN BAELEN ◽  
G. VERHOEVEN
Keyword(s):  
Body Weight ◽  
Testosterone Propionate ◽  
Total Body Weight ◽  
Seminal Vesicles ◽  
Female Rats ◽  
Male Rats ◽  
Intact Male ◽  
Adult Rats ◽  
Organ Weights ◽  
Total Body

SUMMARY Adult rats of both sexes were either gonadectomized or hypophysectomized and gonadectomized. Three to eight weeks later they were treated for 14 consecutive days with oil or with 75 or 200 μg testosterone propionate (TP) per 100 g body weight. The animals were killed and for each sex the gonadectomized animals were compared with the hypophysectomized-gonadectomized animals as far as their NADPH- and NADH-dependent 3α-hydroxysteroid dehydrogenases (3α-HSD) in renal microsomes, transcortin levels in serum and five organ weights relative to total body weight were concerned. For two of the latter, i.e. the relative kidney and prostatic weights, no significant differences were found. Transcortin levels, relative adrenal weights and renal NADPH-dependent 3α-HSD activities were higher in oil-treated gonadectomized animals than in oil-treated hypophysectomized-gonadectomized animals. The opposite was found for the relative weights of uterus and seminal vesicles and renal NADH-dependent 3α-HSD activities. These differences between gonadectomized and hypophysectomized-gonadectomized animals disappeared after TP treatment as far as transcortin levels were concerned but remained for the five other parameters. After gonadectomy sexual differences subsisted for all parameters studied. But whereas intact male rats had higher NADH-dependent 3α-HSD activities than female rats the opposite was found after gonadectomy. After gonadectomy plus hypophysectomy the between sex differences disappeared as far as transcortin levels were concerned but remained in the other parameters studied.

Cardiac effects of injections of epinephrine into the spinal intermediolateral column

1993 ◽  
Vol 265 (2) ◽  
pp. H633-H641 ◽  
Author(s):  
V. K. Malhotra ◽  
A. Kachroo ◽  
H. N. Sapru
Keyword(s):  
Adrenergic Receptors ◽  
Cardiovascular Responses ◽  
Spinal Level ◽  
Cardiac Effects ◽  
Alpha Adrenergic Receptors ◽  
Small Doses ◽  
The Right ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

Small doses of epinephrine (0.008, 0.05, and 0.1 pmol, i.e., 20-nl volumes of 0.40, 2.5, and 5 microM solutions) produced a dose-dependent increase in heart rate when micro-injected into the right intermediolateral column (IML) at T2 spinal level. These effects were mediated via alpha 1-adrenergic receptors because prazosin blocked them. The presence of alpha 1-adrenergic receptors at this site was confirmed by microinjections of phenylephrine (a specific agonist for these receptors); phenylephrine elicited tachycardia. Larger doses of epinephrine (320, 2,000, and 3,200 pmol, i.e., 20-nl volumes of 16, 100, and 160 mM solutions) caused bradycardia when microinjected into the IML. These effects were mediated via alpha 2-adrenergic receptors because idazoxan blocked them. The presence of alpha 2-adrenergic receptors at this site was confirmed by microinjections of clonidine (a specific agonist for these receptors); clonidine elicited bradycardia. Injections of the vehicle (20 nl of normal saline containing 0.3% ascorbic acid, pH 7.4) did not evoke a response. Epinephrine, prazosin, or idazoxan did not alter the responses to L-glutamate. None of the doses of epinephrine elicited any response when injected intravenously. The aforementioned results provide pharmacological evidence for the presence of alpha 1- and alpha 2-adrenergic receptors in the IML at T2. Thus a basis is provided for investigating the role, if any, of alpha-adrenergic receptors in the IML in mediating cardiovascular responses elicited by the stimulation of different brain stem areas.

Stimulation of HCO3- transport in isolated proximal bullfrog duodenum by prostaglandins

1980 ◽  
Vol 239 (3) ◽  
pp. G198-G203 ◽  
Author(s):  
G. Flemstrom
Keyword(s):  
Electrical Potential ◽  
Potential Difference ◽  
Electrical Potential Difference ◽  
Morphological Examination ◽  
Minimal Concentration ◽  
Dependent Transport ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

An in vitro preparation of proximal duodenum from the bullfrog transported alkali into the luminal solution (approximately 1 mueq x h-1 x cm-2) and generated a transepithelial electrical potential difference (5-10 mV, lumen negative). Transport was inhibited by 2,4-dinitrophenol (10(-5) M), CN- (5 X 10(-3) M), indomethacin (5 X 10(-5) M), and acetazolamide (5 X 10(-3) M) indicating that metabolism is required. Both alkali transport and the electrical potential difference showed a dose-dependent increase on administration of the prostaglandins E2, 16,16-dimethyl E2, and F2 alpha. The minimal concentration stimulating transport was lower with the E-type prostaglandins (10(-8) M than with F2 alpha (10(-6) M), and the former also produced greater maximal responses. In addition to metabolic-dependent transport of alkali, there was passive transmucosal migration of HCO3-, amounting to approximately 40% of basal (unstimulated) transport and sensitive to variation of the transmucosal hydrostatic pressure. Morphological examination showed that the preparation is devoid of Brunner glands. Stimulation of duodenal epithelial HCO3- transport by prostaglandins may contribute to their previously demonstrated ability to prevent duodenal ulceration.

SENSITIVITY OF ANTERIOR HYPOTHALAMIC AREAS TO GONADAL STEROID IMPLANTATION IN ANDROGENIZED FEMALE RATS

1977 ◽  
Vol 74 (2) ◽  
pp. 315-NP ◽  
Author(s):  
A. DANGUY ◽  
J. L. PASTEELS ◽  
F. ECTORS
Keyword(s):  
Single Injection ◽  
Mammary Glands ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Control Synthesis ◽  
Normal Female ◽  
Immunofluorescence Studies ◽  
Oestradiol Benzoate ◽  
Stimulation Of

A single injection of 1 mg of a complex of testosterone esters on day 5 of life was used to prepare constantly oestrous rats. Such androgenized female rats were then ovariectomized and submitted to stereotaxical implantation of 1 μg oestradiol benzoate, 5 μg testosterone isobutyrate or, as a control, 10 μg cholesterol in the anterior hypothalamic areas. The effects of the steroids on plasma and pituitary FSH and LH were assessed by radioimmunoassay. As reported previously by us in normal female and male rats, the preoptic–suprachiasmatic area (POA) was able to control synthesis and secretion of both gonadotrophins and did not lose its sensitivity to oestradiol and testosterone in androgenized rats. Evidence for enhanced prolactin secretion in androgenized rats was derived from immunofluorescence studies of the pituitary gland and from histology of the mammary glands. In this respect the condition of the androgenized females was opposite to that of the males. The present work demonstrated that stimulation of prolactin secretion in androgenized female rats resulted from oestrogen action due to permanent oestrus rather than from impairment of hypothalamo-hypophysial relationships. Indeed, prolactin stimulation was suppressed when the androgenized rats were ovariectomized and restored when they were subsequently implanted with oestradiol in the POA.

Effect of the anterior pituitary gland and gonads on enzyme components of the hepatic microsomal cytochrome P-450 system of male and female rats

1983 ◽  
Vol 96 (2) ◽  
pp. 259-267 ◽  
Author(s):  
B. Gillham ◽  
J. S. M. Hutchinson ◽  
M. B. Thorn
Keyword(s):  
Sex Difference ◽  
Anterior Pituitary ◽  
Testosterone Propionate ◽  
Specific Activity ◽  
Female Rats ◽  
Intact Male ◽  
Adult Rats ◽  
Microsomal Cytochrome ◽  
Male And Female Rats ◽  
Cytochrome P 450

The concentration of cytochrome P-450 in microsomes prepared from the livers of mature female Wistar-derived rats was significantly lower than in mature males. This sex difference was abolished after hypophysectomy, when the concentration of the cytochrome in males and females was not significantly different from that in the intact male. A concentration of cytochrome P-450 characteristic of females was restored by two anterior pituitary transplants under the kidney capsule of hypophysectomized females; a partial 'feminization' occurred in similarly treated hypophysectomized males. A partial 'feminization' was also achieved by the administration of rat or sheep prolactin to hypophysectomized females. Unexpectedly, the administration of l-dihydroxyphenylalanine to normal females was without effect on cytochrome P-450, whereas in intact males 'feminization' resulted. Castration of adult rats resulted in the 'feminization' of cytochrome P-450, whereas ovariectomy was without effect. Administration of testosterone propionate for 10 days, either immediately after the operation or 14 weeks later to rats castrated when adult failed, however, to reverse the fall in cytochrome P-450. The establishment of a higher concentration of cytochrome P-450 in the liver of female rats could not be brought about by the administration of testosterone propionate, whether given as a single dose on the second day after birth or as a 10-day course of treatment after puberty or both. It is concluded that the sex difference in hepatic microsomal cytochrome P-450 is maintained by the release in the female of an anterior pituitary factor(s) that serves to depress its concentration. The factor(s) shows some of the characteristics of prolactin but the findings are not consistent with that hormone being responsible for all of the effects observed. The release of the factor(s) in the male may be inhibited by a compound of gonadal origin other than testosterone. A sex difference could not be 'imprinted' in the female by either neonatal and/or postpubertal testosterone treatment. The concentration of hepatic microsomal cytochrome b5 and the specific activity of NADPH-cytochrome c reductase were found not to be sex-dependent in the rats used. However, anterior pituitary factor(s) other than prolactin and growth hormone act to suppress partially the concentration of the former and to promote the specific activity of the latter in the endoplasmic reticulum of rat hepatocytes.

Prolactin secretion by mixed ACTH-prolactin pituitary adenoma cells in culture

1985 ◽  
Vol 108 (4) ◽  
pp. 456-463 ◽  
Author(s):  
Tohru Yamaji ◽  
Miyuki Ishibashi ◽  
Akira Teramoto ◽  
Takanori Fukushima
Keyword(s):  
Pituitary Adenoma ◽  
Cultured Cells ◽  
Prolactin Secretion ◽  
Thyrotrophin Releasing Hormone ◽  
Cells In Culture ◽  
Corticotrophin Releasing Factor ◽  
Lysine Vasopressin ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Corticotroph Adenomas

Abstract. To characterize the functional aspect of prolactin (Prl) cells coexisting with corticotroph adenomas, pituitary adenoma cells obtained from a patient with Cushing's disease and a patient with Nelson's syndrome, who were associated with hyperprolactinaemia, were cultured in monolayer and their Prl responses to various secretagogues were compared with those of prolactinoma cells in culture. Immunohistochemistry performed in one of these two adenomas demonstrated the presence of Prl-containing cells in addition to ACTH cells. When ACTH-Prl adenoma cells were exposed to ovine corticotrophin-releasing factor (CRF), a dose-dependent increase in both ACTH and Prl secretion was observed, which was blocked by coincubation with hydrocortisone. In contrast, no stimulatory effect of CRF on Prl release was observed in all of the experiments using prolactinoma cells. Thyrotrophin-releasing hormone, which consistently stimulated Prl secretion in ACTH-Prl adenomas, was effective in triggering Prl release in only 25% of the prolactinomas. Exposure of the cultured cells to lysine vasopressin, growth hormone-releasing factor and vasoactive intestinal peptide resulted in an increase in ACTH and Prl secretion in one ACTH-Prl adenoma, however, none of the prolactinomas responded to these stimuli to secrete Prl. Dopamine and somatostatin, on the other hand, uniformly suppressed Prl secretion from ACTH-Prl adenomas as well as from prolactinoma cells. These results suggest that the mode of Prl secretion by mixed ACTH-Prl pituitary adenomas is not identical to that by pure prolactinomas and is, at least in part, common to that of ACTH secretion.

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