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

Further evidence that brain histamine H2 receptors are stimulatory in the control of prolactin in the rat

1988 ◽  
Vol 119 (4) ◽  
pp. 488-492 ◽  
Author(s):  
Carmela Netti ◽  
Valeria Sibilia ◽  
Francesca Guidobono ◽  
Isabella Villa ◽  
Paola Franco ◽  
...  
Keyword(s):  
Prolactin Secretion ◽  
Male Rats ◽  
Normal Male ◽  
Brain Histamine ◽  
H2 Receptors ◽  
The Central Nervous System ◽  
Brain Ventricle ◽  
The Brain ◽  
Chemical Analogue ◽  
Stimulation Of

Abstract. The effects of administration into the brain ventricle of H2 receptor agonists (4-methylhistamine, 0.8 μmol/rat; dimaprit, 0.4–0.8 μmol/rat), H2 antagonists (cimetidine, 0.8 μmol/rat; ranitidine, 0.4–0.8 μmol/rat; famotidine, 0.03 μmol/rat) and of the dimaprit chemical analogue SK&F 91487 (0.4 μmol/rat) on unstimulated and histamine-stimulated prolactin secretion in normal male rats were studied. The H2 agonist 4-methylhistamine caused a significant increase in unstimulated blood PRL, whereas dimaprit, SK&F 91487, and the H2 antagonists tested did not change PRL levels. 4-Methylhistamine significantly enhanced the stimulatory effects of histamine on prolactin, whereas all the H2 antagonists inhibited histamine-induced prolactin release. The inhibition of histamine-induced prolactin secretion by the H2 agonist dimaprit is nonspecific, since its chemical analogue SK&F 91487, which has no H2 agonist activity, also inhibits it. These results indicate that stimulation of the H2 receptors in the central nervous system is facilitatory for PRL secretion, suggesting that the activation of H2 receptors may contribute to the PRL-releasing effects of histamine.

Effect of α-Fluoromethylhistidine on the Histamine Content of the Brain ofW/WvMice Devoid of Mast Cells: Turnover of Brain Histamine

1983 ◽  
Vol 41 (1) ◽  
pp. 128-134 ◽  
Author(s):  
Kazutaka Maeyama ◽  
Takehiko Watanabe ◽  
Atsushi Yamatodani ◽  
Yoshitaka Taguchi ◽  
Hiroshi Kambe ◽  
...  
Keyword(s):  
Mast Cells ◽  
Histamine Content ◽  
Brain Histamine ◽  
The Brain

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.

EARLY EFFECTS OF STILBOESTROL ON GROWTH HORMONE AND PROLACTIN SECRETION AND ON PITUITARY MITOTIC ACTIVITY IN THE MALE RAT

1973 ◽  
Vol 58 (2) ◽  
pp. 227-231 ◽  
Author(s):  
H. M. LLOYD ◽  
J. D. MEARES ◽  
JOAN JACOBI
Keyword(s):  
Growth Hormone ◽  
Mitotic Activity ◽  
Single Injection ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Male Rat ◽  
Serum Prolactin ◽  
Serum Growth Hormone ◽  
Total Period ◽  
Early Effects

SUMMARY The effects of a single injection of 1 mg diethylstilboestrol dipropionate on pituitary mitotic activity and on secretion of growth hormone and prolactin were investigated in male rats on each of the first 15 days following the single dose and then at intervals for a total period of 63 days. Mitotic activity increased to a maximum on day 4 and then gradually diminished. Serum growth hormone was moderately increased during the 2nd week and serum prolactin showed a gradual rise with a return to normal on day 63. In the pituitary gland, growth hormone concentration diminished until day 28, whereas prolactin rose quickly at first, maintained a raised level and increased further on day 43. During the first 12 days, pituitary weight was significantly correlated with serum growth hormone and prolactin concentration. During days 13–28, serum prolactin, but not growth hormone, was significantly correlated with the pituitary mitotic index.

PERPHENAZINE-INDUCED PROLACTIN SECRETION IN ACROMEGALY

1977 ◽  
Vol 86 (4) ◽  
pp. 673-682 ◽  
Author(s):  
Maire T. Buckman ◽  
Glenn T. Peake
Keyword(s):  
Anterior Pituitary ◽  
Sella Turcica ◽  
Prolactin Secretion ◽  
Pituitary Function ◽  
Serum Prolactin ◽  
Pituitary Hormone ◽  
Radiographic Evidence ◽  
The Status ◽  
Anterior Pituitary Function ◽  
Tsh Deficiency

ABSTRACT Phenothiazine-induced prolactin secretion was studied in 6 untreated acromegalic patients with radiographic evidence of enlarged sella turcica and responses correlated with other parameters of anterior pituitary function. Five patients had normal basal serum prolactin levels and in one it was elevated. In patients with normal basal prolactin concentrations, prolactin responsiveness to perphenazine (Trilafon®) ingestion was normal in 3 and blunted in 2. The single patient with hyperprolactinaemia also demonstrated perphenazine unresponsiveness. Evaluation of the pituitary-adrenal, pituitary-thyroidal and pituitary-gonadal axes revealed a spectrum of hormonal deficiencies. Of the 3 patients with normal perphenazine-induced prolactin secretion, one had gonadotrophin deficiency, another TSH deficiency, and the remaining patient had no other demonstrable abnormality in pituitary function. In 2 patients prolactin unresponsiveness was not associated with other pituitary hormonal deficiencies. The sole patient with hyperprolactinaemia also had hypogonadotrophic hypogonadism. Thus, in acromegalic patients with radiographic evidence of enlarged sella turcicas, prolactin unresponsiveness was the commonest other abnormality observed in anterior pituitary function. In 2 patients normal prolactin responses, however, were associated with additional deficiencies. To establish pituitary functional capacity in acromegaly, the status of each pituitary hormone must be evaluated separately.

Role of the adrenal cortex in chronic stress-induced inhibition of prolactin secretion in male rats

1989 ◽  
Vol 120 (2) ◽  
pp. 269-273 ◽  
Author(s):  
A. López-Calderón ◽  
C. Ariznavarreta ◽  
M. D. Calderón ◽  
J. A. F. Tresguerres ◽  
M. I. Gonzalez-Quijano
Keyword(s):  
Adrenal Cortex ◽  
Chronic Stress ◽  
Immobilization Stress ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Prolonged Release ◽  
Plasma Prolactin

ABSTRACT The response of prolactin to chronic stress in intact, adrenalectomized and adrenomedullectomized male rats was studied. Immobilization stress in intact animals induced a significant increase in plasma concentrations of prolactin after 20 and 45 min and a significant decrease when the rats were submitted to chronic restraint (6 h daily for 4 days). Five weeks after adrenomedullectomy, plasma prolactin and corticosterone responses to chronic stress were not modified. In contrast, the inhibitory effect of chronic stress on prolactin secretion was totally suppressed by adrenalectomy. When treated with dexamethasone during the 4 days of restraint, adrenalectomized stressed rats showed similar plasma concentrations of prolactin to the intact stressed rats. These data indicate that the adrenal cortex is able to play an inhibitory role on prolactin secretion during stress only through a prolonged release of glucocorticoids. Journal of Endocrinology (1989) 120, 269–273

DNA SYNTHESIS AND DEPLETION OF PROLACTIN IN THE PITUITARY GLAND OF THE MALE RAT

1978 ◽  
Vol 77 (1) ◽  
pp. 129-136 ◽  
Author(s):  
H. M. LLOYD ◽  
J. M. JACOBI ◽  
J. D. MEARES
Keyword(s):  
Growth Hormone ◽  
Dna Synthesis ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Male Rat ◽  
Serum Prolactin ◽  
Inhibitory Effects ◽  
Pituitary Prolactin

Haloperidol, bromocriptine and diethylstilboestrol dipropionate were given in various régimes to male rats to determine their effects on pituitary DNA synthesis, prolactin secretion and growth hormone secretion. Haloperidol increased serum prolactin but did not stimulate pituitary DNA synthesis or reduce pituitary prolactin concentrations. Haloperidol potentiated the effects of oestrogen on serum prolactin and on pituitary DNA synthesis; pituitary prolactin concentrations were greatly reduced, and growth hormone secretion was slightly inhibited. The inhibitory effects of bromocriptine in oestrogen-stimulated rats were demonstrated by smaller pituitary weights and decreased DNA synthesis; serum prolactin levels were lowered and pituitary prolactin concentrations were increased. Haloperidol, given to rats treated with oestrogen and bromocriptine, reversed the inhibitory effects of bromocriptine on DNA synthesis and serum prolactin; pituitary prolactin concentrations fell to well below normal. The results suggest that the haloperidol potentiation of oestrogeninduced pituitary DNA synthesis may depend upon stimulation of prolactin secretion together with reduction of intracellular prolactin levels.

scholarly journals The Effect of Dopamine Secreted by the Brain into the Systemic Circulation on Prolactin Synthesis by the Pituitary gland in Ontogenesis

Acta Naturae ◽  
2016 ◽  
Vol 8 (3) ◽  
pp. 111-117 ◽  
Author(s):  
Yu O Nikishina ◽  
A. Ya. Sapronova ◽  
M. V. Ugrumov
Keyword(s):  
Pituitary Gland ◽  
Systemic Circulation ◽  
Inhibitory Effect ◽  
Prolactin Secretion ◽  
Endocrine Function ◽  
Pituitary Cells ◽  
Target Organs ◽  
Prolactin Synthesis ◽  
And Function ◽  
The Brain

This research was aimed at studying the brains endocrine function in ontogenesis. It has been previously shown in our laboratory that the brain serves as the source of dopamine in the systemic circulation of rats prior to the formation of the blood-brain barrier. This paper provides direct evidence that dopamine secreted by the brain directly into the systemic circulation in this period of ontogenesis has an inhibitory effect on prolactin secretion by pituitary cells. These results provide the basis for a fundamentally new understanding of the brains role in the neuroendocrine regulation of the development and function of peripheral target organs and, particularly in this study, the pituitary gland.

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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