Intraventricular administration of thyrotrophin-releasing hormone (TRH) suppresses prolactin secretion and synthesis: a possible involvement of dopamine release by TRH from rat hypothalamus

1992 ◽  
Vol 133 (1) ◽  
pp. 59-66 ◽  
Author(s):  
H. Ikegami ◽  
H. Jikihara ◽  
K. Koike ◽  
K. Morishige ◽  
H. Kurachi ◽  
...  
Keyword(s):  
Dopamine Release ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Serum Prolactin ◽  
Dependent Manner ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Prolactin Gene ◽  
Gene Transcripts

ABSTRACT The administration of thyrotrophin-releasing hormone (TRH) causes a variety of dopamine-related biological events. To understand the specific role of TRH on rat hypothalamic dopamine neurones, we examined the in-vivo effects of intraventricular (i.c.v.) infusion of TRH on the release and synthesis of prolactin in the rat pituitary gland and on the changes in binding of [3H]MeTRH and dopamine turnover rates in rat hypothalamus. We have also examined the in-vitro effects of TRH on the release of [3H]dopamine from dispersed tuberoinfundibular dopamine neurones. Female rats were treated with i.c.v. infusions of 1 μmol TRH/l daily for 1, 3 and 7 days using Alzet osmotic pumps. Following 7 days of treatment the serum prolactin concentrations were significantly decreased. A reduction in hypothalamic TRH-binding sites (Bmax) was also apparent but the dissociation constant (Kd) was unaffected. Northern blot analysis of total RNA isolated from the pituitary glands of control animals using 32P-labelled prolactin cDNA as a probe indicated the presence of three species of prolactin gene transcripts of approximately 3·7, 2·0 and 1·0 kb in size, and these were decreased by TRH treatment. We examined the turnover rate of dopamine in the rat hypothalamus when TRH was administered i.c.v. for 7 days. There was a significant increase in 3,4-dihydroxyphenylacetic acid/dopamine ratio with TRH treatment. Moreover, exposure to TRH stimulated [3H]dopamine release from rat tuberoinfundibular neurones in a time- and dose-dependent manner. Dopamine receptor antagonists such as SCH23390 and (−)sulpiride, and other neuropeptides such as vasoactive intestinal peptide and oxytocin did not affect TRH-stimulated [3H]dopamine release. These data suggest that i.c.v. administration of TRH might decrease both prolactin secretion and accumulation of prolactin gene transcripts in the pituitary by stimulating dopamine release from tuberoinfundibular neurones. Journal of Endocrinology (1992) 133, 59–66

Physiological roles of thyrotrophin-releasing hormone and vasoactive intestinal peptide on the pulsatile secretory patterns of prolactin in pituitary-grafted female rats

1994 ◽  
Vol 142 (3) ◽  
pp. 581-586 ◽  
Author(s):  
A Lafuente ◽  
J Marcó ◽  
A I Esquifino
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Thyrotrophin Releasing Hormone ◽  
Mean Values ◽  
Pulsatile Secretion ◽  
Releasing Hormone ◽  
Absolute Amplitude ◽  
The Mean ◽  
The Absolute

Abstract Much is known about the fact that thyrotrophin-releasing hormone (TRH) and vasoactive intestinal peptide (VIP) stimulate prolactin secretion but areas of uncertainty remain. This work was undertaken to describe the effects of TRH and VIP on the pulsatile secretion pattern of prolactin, in adult sham-operated and pituitary-grafted hyperprolactinaemic female rats. Two pulses of TRH (1 μg/rat) or one pulse of VIP (20 μg/rat) were given 60 or 120 min after the period of blood sampling. Pituitary grafting increased the mean values of prolactin, absolute amplitude and duration of the peaks and decreased their frequency, compared with control animals. In sham-operated rats, TRH elevated prolactin levels by increasing the absolute and relative amplitudes and duration of the pulses, along with a decrease in their frequency. No priming effects of TRH were observed in this study. Hyperprolactinaemia blunted TRH effects on the pulsatile secretion pattern of prolactin. In sham-operated rats, VIP administration increased the absolute and relative amplitudes of the prolactin peaks. None of the other parameters studied were changed. In pituitary-grafted animals, VIP administration increased the absolute and relative amplitudes of the prolactin peaks but to a lesser extent compared with controls. These data suggest that TRH and VIP affect prolactin pulsatility differentially. The effects of TRH and VIP were blunted to some extent by exposure to previously elevated circulating prolactin levels. Journal of Endocrinology (1994) 142, 581–586

Effects of orphanin FQ on central dopaminergic neuronal activities and prolactin secretion

2001 ◽  
Vol 280 (3) ◽  
pp. R705-R712 ◽  
Author(s):  
Kun-Ruey Shieh ◽  
Jenn-Tser Pan
Keyword(s):  
Receptor Gene ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Serum Prolactin ◽  
Antisense Oligodeoxynucleotide ◽  
Dependent Manner ◽  
Orphanin Fq ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
The Brain

Effects of orphanin FQ (OFQ) on central dopaminergic (DA) neurons and serum prolactin (PRL) were examined in ovariectomized, estrogen-primed Sprague-Dawley rats. The activities of central DA neurons, including the tuberoinfundibular (TI), nigrostriatal, mesolimbic, and incertohypothalamic ones, were determined by measuring the levels of 3,4-dihydroxyphenylacetic acid (DOPAC), the major metabolite of dopamine, in their projection regions in the brain by HPLC plus electrochemical detection. Intracerebroventricular administration of OFQ lowered DOPAC levels in the median eminence (ME), striatum, nucleus accumbens, and hypothalamic paraventricular nucleus in a dose (0.01–10 μg)- and time (30–90 min)-dependent manner. In contrast, OFQ increased DOPAC in the suprachiasmatic nucleus and had no effect in the periventricular nucleus. Serum PRL levels exhibited a typical inverse relationship with the activity of TIDA neurons, as determined by DOPAC levels in the ME. In the afternoon, we observed an endogenous decrease of ME DOPAC level accompanied by a PRL surge in estrogen-primed female rats. Although OFQ caused further decrease of ME DOPAC in the afternoon, it failed to augment the PRL surge level. Although pretreatment of an antisense oligodeoxynucleotide against the opioid receptor-like receptor gene had no effect on basal ME DOPAC levels in the morning or afternoon, it attenuated the afternoon PRL surge. Furthermore, it blocked the effects of exogenous OFQ on ME DOPAC and serum PRL levels, whereas the sense or missense oligodeoxynucleotide had no effect. These results indicate that OFQ and its receptors may be involved in the regulation of central DA neuronal activity and PRL secretion.

PEPTIDASES IN THE RAT HYPOTHALAMUS INACTIVATING THYROTROPHIN-RELEASING HORMONE (TRH)

1975 ◽  
Vol 79 (1) ◽  
pp. 209-216 ◽  
Author(s):  
E. C. Griffiths ◽  
K. C. Hooper ◽  
S. L. Jeffcoate ◽  
N. White
Keyword(s):  
Anterior Pituitary ◽  
Female Rats ◽  
Peptidase Activity ◽  
Thyrotrophin Releasing Hormone ◽  
Male And Female ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Male And Female Rats ◽  
Specific Radioimmunoassay ◽  
The Brain

ABSTRACT Peptidases capable of inactivating thyrotrophin-releasing hormone (TRH) have been demonstrated in the hypothalamus. With the development of a specific radioimmunoassay for TRH, this method was used to further study the enzymes acting on the releasing hormone. Whole hypothalamic homogenates from male and female rats inactivated TRH, with greater peptidase activity being found in the female animals. Separation of the homogenates into particulate (microsomal and mitochondrial) and supernatant (soluble/cytoplasmic) fractions showed approximately the same amounts of enzyme activity in both fractions, while dialysis of the fractions slightly reduced the TRH peptidase activity present, suggesting that a diffusible co-factor might be partially involved in the releasing hormone's degradation. These results confirm the presence of TRH-inactivating peptidases in the rat hypothalamus and suggest that the enzymes may be involved in some way in the mechanisms by which the brain controls thyrotrophin release by the anterior pituitary.

Stimulation of prolactin secretion by oestradiol in the rat is associated with increased hypothalamic release of thyrotrophin-releasing hormone

1984 ◽  
Vol 103 (2) ◽  
pp. 257-261 ◽  
Author(s):  
S. Franks ◽  
H. D. Mason ◽  
K. I. J. Shennan ◽  
M. C. Sheppard
Keyword(s):  
Incubation Medium ◽  
Prolactin Secretion ◽  
Serum Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Threefold Increase ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Pituitary Prolactin ◽  
Stimulation Of

ABSTRACT We have studied the effect of oestradiol (OE2) on secretion of prolactin and TSH by rat pituitary glands and correlated this with changes in hypothalamic content and release of thyrotrophin-releasing hormone (TRH). Ovariectomized Wistar rats received s.c. silicone elastomer implants of OE2 at a dose known to give pro-oestrous OE2 levels. After 1 week rats were decapitated, blood was collected for assay of prolactin and TSH, blocks of hypothalamus were dissected out and pituitary glands were removed and bisected. Medium bathing hemipituitary glands was collected for measurement of prolactin and TSH after a 30-min incubation. Immunoreactive TRH was measured in medium removed from hypothalami and in extracts of homogenized hypothalami. Serum prolactin was higher in OE2-treated than in control animals (59·3 ± 19·5 (s.e.m.) vs 9·4 ± 1·5 μg/l; P<0·05) and this was associated with a threefold increase in pituitary prolactin in the medium. By contrast, TSH concentrations in serum and pituitary incubation medium were not significantly different in the two groups. There was no difference between the groups in hypothalamic content of TRH but TRH release in the incubation medium was increased by OE2 (30·2 ± 6·5 vs 10·0 ± 1·3 pg/mg protein per 30 min; P<0·01). In summary, physiological levels of OE2 stimulated prolactin secretion without change in TSH and this was associated with a threefold increase in hypothalamic release of TRH. These findings suggest that the stimulating effect of OE2 on prolactin secretion may, in part, be mediated by hypothalamic TRH. J. Endocr. (1984) 103, 257–261

Indomethacin treatment prevents prolactin-induced luteolysis in the rat

1987 ◽  
Vol 112 (2) ◽  
pp. 317-322 ◽  
Author(s):  
J. E. Sánchez-Criado ◽  
K. Ochiai ◽  
I. Rothchild
Keyword(s):  
Corpus Luteum ◽  
Left Kidney ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Silicone Elastomer ◽  
Serum Prolactin ◽  
Corpora Lutea ◽  
Synthesis Inhibitor ◽  
Significant Difference ◽  
Indomethacin Treatment

ABSTRACT Adult female rats were hypophysectomized and their pituitary glands autotransplanted beneath the left kidney capsule on day 2 (day 1 was the day of ovulation). In such rats the pituitary secretes prolactin fairly constantly and the corpora lutea secrete progesterone for several months. To induce the luteolytic effect of prolactin the rats were first injected s.c. with 2-bromo-α-ergocryptine (CB-154) on cycle days 12, 13 and 14 (i.e. 10, 11 and 12 days after operation) to depress prolactin secretion, and then with CB-154 vehicle (70% ethanol) daily until cycle day 21, to allow prolactin secretion to resume. One ovary was removed from each rat on day 15 and the remaining one on day 22. The mean (± s.e.m.) weight of the corpora lutea on day 15 was 1·46±0·06 mg and 0·98±0·07 mg on day 22 (n = 17). In contrast, rats in which the CB-154 treatment was maintained to day 21 had corpora lutea which weighed 1·31 ±0·09 on day 15 and 1·47 ±0·08 mg on day 22 (n = 15). To investigate whether indomethacin, a prostaglandin synthesis inhibitor, affected the luteolytic action of prolactin, the experiment was repeated, but on day 15 (after the removal of one ovary) the groups in which CB-154 treatment was stopped, as well as the group in which CB-154 treatment was maintained, were each divided into two groups. In one, indomethacin-containing silicone elastomer wafers and, in the other, blank silicone elastomer wafers, were placed within the bursa of the remaining ovary. There were no differences in corpus luteum weight on day 15 among any of these groups and the two groups of the first experiment. There was no significant difference in corpus luteum weight between day 15 and day 22 in any of the six groups except for the two groups treated with the CB-154 vehicle and not with indomethacin. Thus, treatment with indomethacin prevented the fall in corpus luteum weight associated with the discontinuation of CB-154 treatment. Serum prolactin levels fell until day 15 in all rats and remained low in those in which the CB-154 treatment was maintained to day 21, but returned to control values in those treated with vehicle after day 14. Serum progesterone levels fell and remained low in all groups. Indomethacin treatment had no effect on the levels of either serum prolactin or progesterone. We conclude that some of the pharmacological effects of indomethacin are to prevent prolactin-induced luteolysis, and we suggest that prolactin induces rapid regression of the corpus luteum by stimulating intraluteal prostaglandin production or by being necessary for the effect of luteolytic prostaglandins. J. Endocr. (1987) 112, 317–322

Thyrotrophin-Releasing Hormone Analogues Increase Dopamine Release from Slices of Rat Brain

1982 ◽  
Vol 39 (6) ◽  
pp. 1763-1766 ◽  
Author(s):  
Trevor Sharp ◽  
Geoffrey W. Bennett ◽  
Charles A. Marsden
Keyword(s):  
Rat Brain ◽  
Dopamine Release ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone

scholarly journals Direct Stimulatory Effects of Oxytocin in Female Rat Gonadotrophs and Somatotrophs In Vitro: Comparison With Lactotrophs

Endocrinology ◽  
2014 ◽  
Vol 156 (2) ◽  
pp. 600-612 ◽  
Author(s):  
Arturo E. Gonzalez-Iglesias ◽  
Patrick A. Fletcher ◽  
José A. Arias-Cristancho ◽  
Ruth Cristancho-Gordo ◽  
Cleyde V. Helena ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Cell Types ◽  
Pituitary Hormones ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Pituitary Cells ◽  
Female Rat ◽  
Dependent Manner ◽  
Rat Pituitary Cells

The peptide oxytocin (OT) is secreted by hypothalamic neurons and exerts numerous actions related to reproduction. OT stimulation of prolactin secretion in female rats is important during the estrous cycle, pregnancy, and lactation. Here we report that OT also stimulates transients of intracellular Ca2+ concentration in somatotrophs and gonadotrophs as well as the release of GH and LH in a dose-dependent manner with EC50 values that closely correspond to the ligand affinity of the OT receptor (OTR). Remarkably, the hormone-releasing effect of OT in these two cell types is 2 orders of magnitude more sensitive than that in lactotrophs. The specific OTR agonist [Thr4,Gly7]-oxytocin acutely stimulated the release of LH, GH, and prolactin from female rat pituitary cells in primary culture and increased intracellular Ca2+ concentration in gonadotrophs, somatotrophs, and lactotrophs. In these three cell types, the effects on hormone release and intracellular Ca2+ of both OT and [Thr4,Gly7]oxytocin were abolished by the specific OT receptor antagonist desGly-NH2-d(CH2)5[D-Tyr2,Thr4]OVT but not by the highly selective vasopressin V1a receptor antagonist, d(CH2)5[Tyr(Me)2,Dab5]AVP. Furthermore, 10 nM arginine vasopressin stimulated LH and GH release comparably with a dose of OT that was at least 10 times lower. Finally, the presence of the OTR-like immunoreactivity could be observed in all three cell types. Taken together, these results show that OT directly stimulates gonadotrophs, somatotrophs, and lactotrophs through OT receptors and suggest that OT signaling may serve to coordinate the release of different pituitary hormones during specific physiological conditions.

ABSENCE OF PYROGLUTAMYL-N3im-METHYL-HISTIDYL-PROLINEAMIDE (METHYL-THYROTROPHIN RELEASING HORMONE) IN THE RAT HYPOTHALAMUS

1978 ◽  
Vol 77 (3) ◽  
pp. 405-408 ◽  
Author(s):  
A. E. PEKARY ◽  
J. E. MORLEY ◽  
J. M. HERSHMAN
Keyword(s):  
Cation Exchange ◽  
Exchange Chromatography ◽  
Mammalian Brain ◽  
Synthetic Analogue ◽  
Cation Exchange Chromatography ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Hypothalamus

Pyroglutamyl-N3im-methyl-histidyl-prolineamide (methyl-thyrotrophin releasing hormone, methyl-TRH) is a potent synthetic analogue of TRH. N3im-Methyl-histidine is present in mammalian brain and it has been suggested that methyl-TRH is a physiological releasing hormone normally present in the hypothalamus. A non-gradient cation-exchange chromatography system that uses SP-Sephadex C-25 and completely resolves methyl-TRH and TRH has been developed. Because methyl-TRH cross-reacts in the immunoassay for TRH, this assay was used to measure TRH and methyl-TRH in the chromatographic fractions. By this means it has been demonstrated that the amount of methyl-TRH present in the rat is less than 0·025 ng/hypothalamus.

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