ACTIVATION OF ANTERIOR PITUITARY. THYROID AND ADRENAL GLAND IN RATS AFTER DISTURBANCE STRESS

1977 ◽  
Vol 86 (3) ◽  
pp. 489-497 ◽  
Author(s):  
K.-D. Döhler ◽  
K. Gärtner ◽  
A. von zur Mühlen ◽  
U. Döhler
Keyword(s):  
Emotional Stress ◽  
Experimental Period ◽  
Serum Levels ◽  
Normal Serum ◽  
Male Rats ◽  
Serum Prolactin ◽  
Blood Collection ◽  
Pituitary Hormone ◽  
Serum Lh ◽  
Pituitary Thyroid Axis

ABSTRACT Groups of adult male rats were decapitated without anaesthesia 30 seconds or 5, 10, 15 and 60 min after disturbance stress (investigators entering the animal room and moving the cages). The serum concentrations of LH, FSH, TSH, prolactin, triiodothyronine (T3) and thyroxine (T4) were measured by radioimmunoassay and corticosterone by a fluorometric method. With regard to the hormone levels measured in serum obtained within 30 seconds after induction of disturbance stress to resemble most closely the actual unstressed levels of endogenous hormones in circulation, serum corticosterone levels increased within 5 min. indicating that the procedure was stressful to the animals. In addition the serum prolactin and TSH levels were significantly elevated within 5 min, T3 within 60 min. Whereas corticosterone reached peak levels after 15 min. the serum levels of prolactin, TSH and T3 were still rising after 60 min. The FSH levels remained rather stable during the first 10 min. but started to rise during the following 5 min. At 60 min FSH levels were back to normal. Serum LH and T4 showed only minor fluctuations during the experimental period. These results indicate, that not only is the pituitary-adrenal axis stimulated by emotional stress, but also the pituitary-thyroid axis. It also seems, that emotional stress leads to a general activation of pituitary hormone release. Hence, proper care should be taken with regard to animal keeping, handling and the method of blood collection when dealing with rats as experimental animals.

ANNUAL RHYTHMS OF LUTEINIZING HORMONE, FOLLICLE-STIMULATING HORMONE, PROLACTIN AND TESTOSTERONE IN THE SERUM OF MALE RHESUS MONKEYS

1979 ◽  
Vol 83 (2) ◽  
pp. 131-139 ◽  
Author(s):  
W. BECK ◽  
W. WUTTKE
Keyword(s):  
Rhesus Monkeys ◽  
Serum Testosterone ◽  
Serum Levels ◽  
Serum Prolactin ◽  
First Year ◽  
Thyrotrophin Releasing Hormone ◽  
Testosterone Levels ◽  
Serum Lh ◽  
June July ◽  
Male Rhesus

Six male rhesus monkeys were kept under rigidly controlled conditions for 1–2 years. During August of the first year a thyrotrophin releasing hormone (TRH) test was performed on each of the monkeys by giving 10 μg TRH as a bolus injection. Significantly increased serum prolactin levels occurred 15 min after the injection. After a training period of 2 months, during which blood samples were collected every other day by puncture of the saphenous vein, blood was collected three times a week for 14 months. Serum levels of prolactin, LH, FSH and testosterone were measured by radioimmunoassay. Mean serum prolactin levels increased significantly during June, July and August in all six animals. Peak levels were observed in August and September and then levels declined gradually to reach a minimum in April and May. Mean serum testosterone levels closely paralleled the annual pattern of prolactin. Mean serum LH levels significantly decreased during the time when mean serum prolactin and testosterone levels were increasing and they increased again at the time of decreasing mean prolactin levels, i.e. mean serum LH and prolactin were negatively correlated. In individual monkeys, however, a rigid negative correlation between serum prolactin and LH could not be demonstrated. Mean serum FSH levels did not change significantly.

THE SEQUENCE OF HORMONAL CHANGES DURING PROSTAGLANDIN INDUCED LUTEOLYSIS OF THE SUPERLUTEINIZED RAT OVARY

1978 ◽  
Vol 87 (3) ◽  
pp. 617-624 ◽  
Author(s):  
P. A. Torjesen ◽  
R. Dahlin ◽  
E. Haug ◽  
A. Aakvaag
Keyword(s):  
Binding Sites ◽  
Limit Of Detection ◽  
Serum Levels ◽  
Female Rats ◽  
Serum Prolactin ◽  
Hormonal Changes ◽  
Subsequent Increase ◽  
Serum Progesterone ◽  
Serum Lh ◽  
Prostaglandin F

ABSTRACT Immature female rats were pre-treated with pregnant mare's serum gonadotrophin (PMSG) and human chorionic gonadotrophin (HCG) to achieve superluteinization. Eight days after the HCG administration luteolysis was induced by sc injection of 5 μg of the prostaglandin F2α (PGF2α) analogue cloprostenol (Estrumate®). The serum levels of progesterone, 20α-dihydroprogesterone (20α-DHP), prolactin (PRL) and luteinizing hormone (LH) as well as the number of ovarian LH binding sites were measured during the first 23 h after cloprostenol injection. The serum levels of progesterone decreased from 500 to 200 ng/ml within 25 min after cloprostenol administration. A further decrease to 20 ng/ml occurred during the next 4 h, and serum progesterone remained low for the rest of the period. An increase in serum prolactin (PRL) to values between 28 and 44 ng/ml was observed after 3 h and the values remained elevated for the next 7 h. Although the serum levels of progesterone declined immediately, the serum 20α-dihydroprogesterone (20α-DHP) levels remained at 60 to 140 ng/ml for the first 5 h and then gradually increased to values corresponding to the initial progesterone levels 14 to 23 h after treatment. The number of ovarian LH binding sites was between 1.2 and 1.4 × 10−12 mol/mg protein during the first 9 h after prostaglandin (PG) injection, and then decrreased to 0.8 and 0.5 × 10−12 mol/mg protein at 14 and 23 h, respectively. The serum LH levels remained below the limit of detection for the assay (10 ng/ml) throughout the observation period. PGF2α injection induced the same basic changes in the serum levels of progesterone and 20α-DHP as cloprostenol treatment. Thus, the first effect of PG treatment measured was an immediate decline in the serum levels of progesterone, and this decline probably initiated the subsequent increase in pituitay PRL and ovarian 20α-DHP secretion. Therefore, the decrease in the number of ovarian LH binding sites appeared to be a consequence rather than a mediator of luteolytic effects of the prostaglandins.

EFFECT OF SYNTHETIC THYROTROPHIN RELEASING FACTOR ON PROLACTIN AND LUTEINIZING HORMONE SECRETION IN MALE AND FEMALE RATS DURING VARIOUS REPRODUCTIVE STATES

1975 ◽  
Vol 67 (3) ◽  
pp. 425-430 ◽  
Author(s):  
R. P. DEIS ◽  
NIA ALONSO
Keyword(s):  
Hormone Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Serum Prolactin ◽  
Serum Prolactin Level ◽  
Luteinizing Hormone Secretion ◽  
Male And Female Rats ◽  
Serum Lh ◽  
The Mean ◽  
Lh Secretion

SUMMARY The effect of synthetic thyrotrophin releasing factor (TRF) on serum prolactin and LH concentrations was determined by radioimmunoassay in male, cyclic and pseudopregnant female rats. A solution of TRF (0·1, 0·25, 0·5 and 1 μg/rat) was injected i.v. at 17.00 h into rats pretreated with sodium pentobarbitone at 13.00 h. A group of male rats was also treated with TRF at 11.00 h after pretreatment with sodium pentobarbitone at 07.00 h. Fifteen minutes after TRF administration, blood samples were obtained by heart puncture. Doses of 0·25, 0·5 and 1 μg TRF significantly increased the serum prolactin concentration in pro-oestrous rats. The mean serum prolactin level after the injection of 0·5 and 1 μg into oestrous rats and 0·5 μg TRF into dioestrous day 2 rats, was significantly greater than the control values. Injection of TRF on day 1 of dioestrus had no effect. Serum LH concentration was not significantly modified by the various doses of TRF administered. On day 3 of pseudopregnancy a significant increase of serum prolactin values was obtained with 0·5 and 1 μg TRF. On day 7 of pseudopregnancy a dose of 0·5 μg produced the same effect, but on day 10 of pseudopregnancy only 1 μg TRF significantly increased serum prolactin levels when compared with the control rats. In male rats serum prolactin concentration was significantly greater than the control values after TRF treatment either in the morning or the afternoon. The response was similar to that obtained in pro-oestrous rats. The results suggest that the ability of synthetic TRF to stimulate prolactin release exists in both female and male rats and that TRF does not affect LH secretion.

GONADOTROPHIN SUPPRESSION BY STEROIDS IN NORMAL, ADULT MALE RATS

1977 ◽  
Vol 84 (4) ◽  
pp. 842-849 ◽  
Author(s):  
H. L. Verjans ◽  
K. B. Eik-Nes
Keyword(s):  
Body Weight ◽  
High Activity ◽  
Adult Male ◽  
Subcutaneous Administration ◽  
Serum Levels ◽  
Steroid Treatment ◽  
Male Rats ◽  
Normal Adult ◽  
Serum Lh ◽  
Testosterone Metabolites

ABSTRACT Effects of subcutaneous administration of various doses of different steroids on serum levels of LH and FSH in normal, adult male rats were investigated. Each steroid was injected daily during 7 days in doses of 50, 25, 12.5 or 6.25 μg per 100 g body weight. Ring A 5α-reduced testosterone metabolites exerted high activity in suppressing serum LH and FSH levels. 5α-Androstane-3β,17β-diol had in the doses tested, however, no such effects on serum gonadotrophins. Serum LH concentrations in normal rats appeared more sensitive to steroid treatment than serum FSH concentrations.

EFFECTS OF NALOXONE ON LUTEINIZING HORMONE AND PROLACTIN IN SERUM OF RATS

1980 ◽  
Vol 85 (2) ◽  
pp. 307-315 ◽  
Author(s):  
M. S. BLANK ◽  
A. E. PANERAI ◽  
H. G. FRIESEN
Keyword(s):  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Immature Female ◽  
Subcutaneous Injections ◽  
Serum Lh ◽  
Opiate Peptides ◽  
Lh Release ◽  
Lh Secretion

The effects of subcutaneous injections of the opiate antagonist naloxone on the tonic and phasic secretion of prolactin and LH were studied in rats. During development, resting levels of prolactin in serum were decreased by naloxone (2·5 mg/kg body wt) on days 24,45 and 50 in female rats and on days 28,45 and 50 in male rats. In the adult, naloxone (2·5 mg/kg body wt) decreased basal levels of serum prolactin in male rats and levels during oestrus in female rats. In 25-day-old female rats, serum LH rose from resting levels within 7·5 min of naloxone administration (2·5 mg/kg body wt) and returned to pretreatment levels by 30 min, while prolactin fell by 7·5 min and remained low for as long as 60 min after treatment. Furthermore, a tenfold lower dose of naloxone (0·25 mg/kg body wt) did not raise basal levels of serum LH but still decreased resting levels of serum prolactin in immature female rats (24 days old). The effect of naloxone (2·5 mg/kg body wt) on phasic LH release was studied in 29-day-old immature female rats primed on day 27 with pregnant mare serum gonadotrophin (PMSG). In these PMSG-treated rats the onset of the prolactin surge was blunted by naloxone while it had no effect on phasic LH release. Naloxone (5 mg/kg body wt) also induced a rise in levels of serum LH in ovariectomized rats and, if administered with morphine, it reversed the short-term inhibition of LH secretion caused by morphine. However, naloxone was ineffective after pretreatment with oestradiol benzoate. These findings suggest that the responses of serum LH and prolactin to naloxone were dissociated and that oestrogens and opiate peptides may have interacted to regulate secretion of LH.

Hyperprolactinaemia attenuates the gonadotrophin releasing hormone receptor response to gonadectomy in rats

1982 ◽  
Vol 95 (2) ◽  
pp. 267-274 ◽  
Author(s):  
R. N. Clayton ◽  
L. C. Bailey
Keyword(s):  
Female Rats ◽  
Male Rats ◽  
Serum Prolactin ◽  
Intact Male ◽  
Adult Rats ◽  
Releasing Hormone ◽  
Receptor Response ◽  
Serum Lh ◽  
Gonadotrophin Releasing Hormone ◽  
Qualitative Index

Measurement of pituitary gonadotrophin releasing hormone (Gn-RH) receptor content provides a qualitative index of prior exposure of the pituitary gland to endogenous Gn-RH. The effect of moderate hyperprolactinaemia (serum prolactin = 95–250 μg/l), achieved with three pituitary grafts beneath the renal capsule, on the pituitary Gn-RH receptor content and serum LH responses to gonadectomy of adult rats has been studied. In males the presence of hyperprolactinaemia for 7 days completely prevented the increase in Gn-RH receptor content 3 days after castration and inhibited the serum LH rise by 45%. By 6 days after castration, Gn-RH receptors had increased in the hyperprolactinaemic castrated animals but values were 33% lower than in sham-grafted controls, while the serum LH increase was attenuated by 30%. Pituitary LH content was also lower in grafted castrated animals 6 days after castration. Hyperprolactinaemia for 3 weeks had no effect on Gn-RH receptors or pituitary LH content of intact male rats, although basal serum LH was decreased by 50%. Hyperprolactinaemia also attenuated the increases in Gn-RH receptors, serum LH and pituitary LH which occurred 6 days after ovariectomy in female rats. In all experiments the pituitary content of prolactin was reduced by 80–90% in animals bearing pituitary grafts. These results suggest that hyperprolactinaemia restricts the Gn-RH receptor response to gonadectomy by decreasing endogenous hypothalamic Gn-RH secretion.

The contribution of corticosterone and testosterone to the suppression of serum LH in hyperprolactinaemic adult male rats with pituitary transplants

1987 ◽  
Vol 113 (1) ◽  
pp. 111-116 ◽  
Author(s):  
R. F. A. Weber ◽  
M. P. Ooms ◽  
J. T. M. Vreeburg
Keyword(s):  
Adult Male ◽  
Serum Testosterone ◽  
Serum Levels ◽  
Male Rats ◽  
Male Rat ◽  
Serum Concentrations ◽  
Testosterone Secretion ◽  
Accessory Sex Glands ◽  
Serum Lh ◽  
Stimulation Of

ABSTRACT The effects of hyperprolactinaemia on serum levels of LH were investigated in adult male rats of the R × U strain. Hyperprolactinaemia was induced by three pituitary grafts under the kidney capsule, transplanted on day 0 of each experiment. Special attention was paid to the contribution of prolactin-stimulated testes, adrenals and corticosterone. In experiment 1, hyperprolactinaemia significantly reduced the serum concentrations of LH in intact rats. In spite of a significant increase in the serum levels of corticosterone, serum testosterone was not significantly affected by hyperprolactinaemia. The weights of both the adrenals and accessory sex glands were significantly increased at autopsy. In experiment 2, treatment with 10 mg corticosterone s.c. daily from day 14 to day 28 after pituitary grafting significantly reduced serum levels of both LH and testosterone. The suppression of testosterone in the hyperprolactinaemic corticosterone-treated animals was significantly less than in the corticosterone-treated control animals. The weights of the accessory sex glands were significantly increased in the hyperprolactinaemic animals. In experiment 3, rats were adrenalectomized and half of them were substituted with corticosterone. Serum testosterone levels significantly increased in both hyperprolactinaemic adrenalectomized rats and in adrenalectomized corticosterone-treated animals without any significant effect on serum LH. Again the weights of the accessory sex glands were significantly increased in the hyperprolactinaemic animals. In experiment 4, rats were adrenalectomized, gonadectomized and corticosterone treated on day 0 and then implanted with a 2, 1·5 or 1 cm silicone elastomer capsule containing testosterone. On day 28 after pituitary grafting, LH levels were significantly suppressed in animals with a 2 or 1·5 cm testosterone implant. The weights of the accessory sex glands were not increased in the hyperprolactinaemic animals. These results show that in the male rat the inhibitory effects of hyperprolactinaemia on serum LH levels may be due to (1) increased sensitivity of the hypothalamic-pituitary axis to the negative feedback action of testosterone by prolactin and by the prolactin-stimulated corticosterone secretion and (2) stimulation of testicular testosterone secretion by prolactin, which can also explain the increased weights of the accessory sex glands. Even in the presence of high serum concentrations of corticosterone, stimulation of testicular testosterone secretion by prolactin was observed. J. Endocr. (1987) 113,111–116

Oestrogenic regulation of testicular androgen production during development in the rat

1985 ◽  
Vol 105 (2) ◽  
pp. 211-218 ◽  
Author(s):  
B. A. Keel ◽  
T. O. Abney
Keyword(s):  
Serum Testosterone ◽  
Male Rats ◽  
Serum Prolactin ◽  
Testicular Function ◽  
Intact Male ◽  
Oestrogen Treatment ◽  
Testosterone Production ◽  
Age Related ◽  
Serum Lh

ABSTRACT The influence of age on the sensitivity of the testis to oestrogens was investigated. Intact male rats at 10, 25, 40 and 53 days of age were injected s.c. with vehicle, 5 or 50 μg oestradiol or diethylstilboestrol (DES)/100 g body wt twice daily for 2 days; the animals were killed 12 h after the last injection. Subsequently, the concentrations of testicular androgens and serum LH, prolactin, testosterone and androstanediol (5α-androstane-3α, 17β-diol) were measured. Testicular androgen production was determined in vitro in the presence or absence of human chorionic gonadotrophin (hCG) or dibutyryl cyclic AMP (dbcAMP). Androgens in the serum and testes displayed an age-related alternating pattern with androstanediol being the major androgen produced at 27 days of age. As a result of oestrogen treatment, serum LH concentrations were decreased while serum prolactin was increased. Serum testosterone was decreased by 36–55% in the 12-day-old group and further reduced by 95% of control values by day 55; serum androstanediol was less sensitive to oestrogen suppression. Testicular concentrations of both testosterone and androstanediol exhibited a marked reduction in 12-day-old animals as a result of oestrogen administration. These values were reduced by 85–95% at day 27 and remained suppressed even at 55 days. Basal production of testosterone was unaffected by oestrogen treatment in 12- and 27-day-old animals but was markedly decreased by day 42. Significant suppression of basal production of androstanediol was observed as early as day 12. Oestradiol treatment caused a significant reduction in hCG responsiveness of both androgens at days 12, 42 and 55. Oestrogen administration resulted in a significant (32–59%) decline in dbcAMP-responsive testosterone production in the 42-day group and a further suppression in the 55-day group. A marked inhibition of dbcAMP-stimulated androstanediol production was also observed in the 42- and 55-day groups. Testosterone production in response to dbcAMP was not significantly altered in the 12- and 27-day groups. With few exceptions the effects of oestradiol and DES on testicular function were similar. The data presented here suggest that the inhibitory effects of oestrogens become more pronounced as the animal approaches adulthood, that oestradiol and DES are similarly effective in regulating testicular function at all ages studied and that the production of both testosterone and androstanediol are suppressed by oestrogen administration. J. Endocr. (1985) 105, 211–218

Effect of modified brain histamine contents on prolactin and thyrotropin secretion in male rats

1996 ◽  
Vol 134 (2) ◽  
pp. 209-214 ◽  
Author(s):  
Raimo K Tuominen ◽  
Leena Tuomisto ◽  
Pekka T Männistö
Keyword(s):  
Histidine Decarboxylase ◽  
Inhibitory Effect ◽  
Prolactin Secretion ◽  
Histamine Content ◽  
Male Rats ◽  
Serum Prolactin ◽  
Pituitary Hormone ◽  
Brain Histamine ◽  
Endogenous Histamine ◽  
The Brain

Tuominen RK, Tuomisto L, Männistö PT. Effect of modified brain histamine contents on prolactin and thyrotropin secretion in male rats. Eur J Endocrinol 1996;134:209–14. ISSN 0804–4643 Effects of modified brain histamine contents on thyrotropin and prolactin secretion were studied in male rats. Under basal conditions the histamine content in the hypothalamus was approximately 8–10-fold higher than that in the striatum and the rest of the brain. l-Histidine (1000 mg/kg, ip), a histamine precursor, and metoprine (20 mg/kg, ip), an inhibitor of histamine methyltransferase, elevated histamine content in the brain by 65% and 167%, respectively. When the treatments were given together an additive effect (119–250% increase) on brain histamine was observed. Metoprine significantly decreased serum prolactin levels, while l-histidine had no effect. This effect of metoprine was not modified by treatment with l-histidine. Thus, metoprine has an inhibitory effect on prolactin secretion that is not related to elevated brain histamine contents. The increased brain histamine content after l-histidine treatment had no effect on prolactin secretion. Basal levels of serum thyrotropin were decreased by both l-histidine and metoprine, l-histidine being more potent. In rats treated with α-fluoromethylhistidine, an inhibitor of l-histidine decarboxylase, the cold-induced (rats kept for 60 min at +4°C) thyrotropin secretion was increased while the stress-induced prolactin secretion was decreased. In these rats, metoprine did not affect thyrotropin release but blunted the prolactin response. In conclusion, endogenous histamine inhibits thyrotropin secretion but does not affect prolactin release. Owing to its other effects, metoprine is not suitable as a tool to elevate endogenous histamine contents in the brain, at least when the regulation of anterior pituitary hormone release is being studied. Raimo K Tuominen, Institute of Biomedicine, Department of Pharmacology and Toxicology, PO Box 8, FIN-00014 University of Helsinki, Finland

The effect of d-fenfluramine on anterior pituitary hormone release in the rat: in vivo and in vitro studies

1987 ◽  
Vol 65 (12) ◽  
pp. 2449-2453 ◽  
Author(s):  
O. Serri ◽  
E. Rasio
Keyword(s):  
Growth Hormone ◽  
Male Rats ◽  
Serum Prolactin ◽  
Pituitary Hormone ◽  
Pituitary Cells ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Serum Growth Hormone

Administration of d-fenfluramine, a serotonin-releasing drug, to male rats induced a dose-dependent increase in both serum prolactin and corticosterone concentrations. Serum growth hormone levels increased, but not significantly, at a dose of 1.25 mg/kg i.p. and decreased significantly at higher doses. When rats were pretreated with the serotonin uptake inhibitor fluoxetine (10 mg/kg i.p.) 30 min prior to injection of d-fenfluramine (5 mg/kg i.p.), the serum prolactin response to d-fenfluramine was partially inhibited, whereas the growth hormone response was not significantly modified. Fluoxetine pretreatment increased the serum corticosterone to the same level as did d-fenfluramine. d-Fenfluramine's effect on prolactin and growth hormone release was further tested in a hypothalamic–pituitary in vitro system. The addition of d-fenfluramine (5–500 ng/mL) for 30 min to rat hypothalami resulted in an enhancement of prolactin and growth hormone-releasing activities. These were expressed as the ability of the media in which the hypothalami had been incubated to stimulate prolactin and growth hormone release by cultured pituitary cells. The data suggest that the effect of d-fenfluramine on prolactin secretion is exerted through the hypothalamus and is probably mediated, at least partially, by a serotoninergic mechanism. The mechanism of d-fenfluramine's effect on corticosterone and growth hormone release needs further evaluation.

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