PLASMA CONCENTRATIONS OF PROLACTIN AND THYROTROPHIN DURING SUCKLING: EFFECTS OF STIMULATION OF THE MEDIAN EMINENCE

1978 ◽  
Vol 76 (3) ◽  
pp. 557-558 ◽  
Author(s):  
J. B. WAKERLEY ◽  
M. B. TER HAAR
Keyword(s):  
Direct Effect ◽  
Median Eminence ◽  
Plasma Concentrations ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Animal Physiology ◽  
Inhibiting Factor ◽  
Hypothalamic Level ◽  
Stimulation Of

A.R.C. Institute of Animal Physiology, Babraham, Cambridge, CB2 4AT (Received 1 November 1977) Thyrotrophin releasing hormone (TRH) can have a stimulatory effect on the release of both prolactin and thyrotrophin (TSH; Deis & Alonso, 1973), although in the rat, supraphysiological doses of TRH are required to affect the secretion of prolactin (Burnet & Wakerley, 1976). A more important factor in the control of the release of prolactin is considered to be prolactin release inhibiting factor (PIF), which is thought to act through the catecholamine, dopamine (MacLeod, 1976). Stimuli which cause the concomitant release of TSH and prolactin are thought to have a direct effect at the hypothalamic level such that neurones releasing TRH are excited, whereas those releasing PIF are inhibited. In the present work, we have tested this hypothesis using the suckling stimulus to elicit the simultaneous release of prolactin and TSH (Blake, 1974; Burnet & Wakerley, 1976). If

EFFECTS OF NEONATAL EXPOSURE TO MONOSODIUM GLUTAMATE ON THE ELECTRICAL ACTIVITY OF NEURONES IN THE MEDIOBASAL HYPOTHALAMUS, AND ON THE PLASMA CONCENTRATIONS OF THYROID-STIMULATING HORMONE AND PROLACTIN, FOLLOWING STIMULATION OF THE ROSTRAL HYPOTHALAMUS IN ADULT FEMALE RATS

1981 ◽  
Vol 89 (3) ◽  
pp. 379-387 ◽  
Author(s):  
D. J. SAPHIER ◽  
R. G. DYER
Keyword(s):  
Adult Female ◽  
Median Eminence ◽  
Monosodium Glutamate ◽  
Plasma Concentrations ◽  
Female Rats ◽  
Mediobasal Hypothalamus ◽  
Adult Rats ◽  
Thyrotrophin Releasing Hormone ◽  
Rostral Hypothalamus ◽  
Stimulation Of

Action potentials were recorded from 174 neurones in the mediobasal hypothalamus of ovariectomized adult female rats exposed neonatally to monosodium glutamate (MSG) and from 145 neurones in control rats. All of the animals, which were anaesthetized with urethane, had been ovariectomized for at least 3 weeks and received two injections of oestradiol benzoate (20 μg/100 g body weight, i.m.) 72 h and immediately before the recording experiments. The response of each neurone to electrical stimulation of the median eminence and rostral hypothalamus (preoptic and anterior hypothalamic areas; PO/AH) was analysed. The most striking feature of the results obtained was the significant (P < 0·001) loss of inhibitory responses in those neurones remaining in the adult rats after neonatal treatment with MSG. The loss of inhibitory responses applied to both stimulation sites. In each rat the response of one neurone, which was antidromically identified as projecting to the median eminence, was recorded before and during stimulation of the PO/AH at 50 Hz for 30 s in every min for 15 min. Before and after this stimulation blood was collected from a jugular vein for estimation by radioimmunoassay of concentrations of prolactin and TSH. In the MSG-treated rats significantly (P < 0·05) fewer neurones were inhibited by the 50 Hz stimulation than in control rats. In control rats the plasma concentrations of prolactin nearly quadrupled as an immediate consequence of this treatment, whereas in MSG-treated rats plasma concentrations barely doubled. However, in the MSG-treated rats plasma concentrations of prolactin continued to rise after stimulation ceased, possibly as a consequence of enhanced secretion of thyrotrophin releasing hormone.

Effect of immunoneutralization of thyrotrophin-releasing hormone on the release of thyrotrophin and prolactin during suckling or in response to electrical stimulation of the hypothalamus in the anaesthetized rat

1985 ◽  
Vol 106 (1) ◽  
pp. 113-119 ◽  
Author(s):  
W. J. Sheward ◽  
H. M. Fraser ◽  
G. Fink
Keyword(s):  
Electrical Stimulation ◽  
Neural Control ◽  
Brain Area ◽  
Plasma Concentrations ◽  
Female Rats ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Prolactin Response ◽  
Stimulation Of

ABSTRACT The aim of the present study was to use the technique of immunoneutralization with anti-thyrotrophin-releasing hormone (anti-TRH) serum to investigate the role of TRH in mediating the TSH and prolactin responses to electrical stimulation of the hypothalamus and the prolactin response to suckling in lactating rats. Electrical stimulation of either the median eminence or paraventricular nuclei of male or female rats anaesthetized with urethane resulted in significant increases in the plasma concentrations of both TSH and prolactin. Injection of sheep anti-TRH serum blocked the rise in plasma TSH concentration in response to stimulation of either brain area, but did not block the increase in plasma prolactin concentration. In anaesthetized, lactating female rats, the suckling stimulus produced a significant increase in the plasma prolactin concentration, but did not alter the plasma TSH concentration. Injection of anti-TRH serum, but not control non-immune or anti-bovine serum albumin, significantly decreased the basal release of TSH but did not abolish the prolactin response to suckling. These results show that TRH is the principal mediator of the neural control of TSH release in the rat, but is not crucial for the release of prolactin in response to either hypothalamic stimulation or suckling. J. Endocr. (1985) 106, 113–119

PLASMA CONCENTRATIONS OF PROLACTIN AND THYROTROPHIN DURING SUCKLING IN URETHANE-ANAESTHETIZED RATS

1976 ◽  
Vol 70 (3) ◽  
pp. 429-437 ◽  
Author(s):  
F. R. BURNET ◽  
J. B. WAKERLEY
Keyword(s):  
Plasma Concentrations ◽  
Fold Increase ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Pressure Application ◽  
Oxytocin Release ◽  
Anaesthetized Rats ◽  
Substantial Change ◽  
Anaesthetized Rat

SUMMARY Plasma levels of prolactin and TSH were determined by radioimmunoassay in urethane-anaesthetized lactating rats during suckling. Oxytocin release was monitored by recording intramammary pressure. Application of ten pups, 3 h after administration of urethane (1·1 g/kg, i.p.), evoked a parallel rise in prolactin and TSH concentrations which reached a maximum during the 3rd hour of suckling and then declined. Peak hormone concentrations represented a 25-fold increase in prolactin and a ten-fold increase in TSH. Suckling also elicited a pulsatile (every 5–10 min) release of 0·5–1·0 mu. oxytocin. The gradual rise in prolactin and TSH occurred between the 1st and 20th oxytocin pulses. Intravenous injection of thyrotrophin-releasing hormone (TRH) into unsuckled, anaesthetized lactating rats resulted in a 7- to 30-fold increase in TSH concentration, whereas prolactin levels showed no substantial change. These results indicate that suckling releases TSH as well as prolactin in the urethane-anaesthetized rat. However, the absence of prolactin release after injections of TRH makes it unlikely that both endocrine responses are regulated solely by the actions of this one releasing hormone.

Anti-fertility effects of oral medroxyprogesterone acetate in rabbits

1996 ◽  
Vol 8 (8) ◽  
pp. 1185 ◽  
Author(s):  
NO Oguge ◽  
GK Barrell
Keyword(s):  
Single Dose ◽  
Luteinizing Hormone ◽  
Medroxyprogesterone Acetate ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Multiple Dosing ◽  
Releasing Hormone ◽  
Single Meal ◽  
Gonadotrophin Releasing Hormone ◽  
Hypothalamic Level

Studies on the anti-fertility effects of medroxyprogesterone acetate (MPA) were conducted in rabbits. The bioavailability of MPA and plasma concentrations of progesterone and luteinizing hormone (LH) after mating were monitored following a single meal containing MPA (1000 mg) in entire does (n = 4); the response to gonadotrophin-releasing hormone (GnRH; 250 ng) was also observed in MPA-treated, ovariectomized does (n = 6). The reproductive tracts of rabbits mated following MPA treatment were examined 28-30 h after mating. Another group of rabbits (n = 4) received a single dose of MPA on Days 1, 10 or 19 after mating or daily for five days from Day 24. After dosage with 1000 mg MPA, plasma concentrations of MPA were detectable for eight days. However, following multiple dosing (10 mg, 5 days) MPA was detectable in the plasma for two days. MPA reduced the rate of ovulation and suppressed the increase in plasma concentrations of progesterone and LH observed after mating for four days, but had no effect on the response to GnRH. When administered late in gestation, MPA caused the death of fetuses. These results demonstrate an inhibitory effect of MPA on ovulation, probably at the hypothalamic level, and impairment of gestation or parturition.

Effects of infusion of thyrotrophin releasing hormone and dopamine either alone or in combination on plasma prolactin concentrations in the anoestrous ewe

1983 ◽  
Vol 96 (2) ◽  
pp. 353-357
Author(s):  
B. F. Fitzgerald ◽  
F. J. Cunningham
Keyword(s):  
Combined Treatment ◽  
Plasma Concentrations ◽  
Regulatory Role ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone

Plasma concentrations of prolactin in anoestrous ewes were respectively lowered or raised by the separate infusion of dopamine or thyrotrophin releasing hormone (TRH). Combined treatment with dopamine and TRH lowered the concentration of prolactin in plasma but the values increased markedly after the treatment was stopped and reached a level equivalent to that found in ewes treated with TRH alone. The results are interpreted as evidence that both dopamine and TRH play a regulatory role in determining the secretion of prolactin in the ewe.

THE INFLUENCE OF OESTROGEN ADMINISTRATION IN VIVO ON IN VITRO PROLACTIN RELEASE

1979 ◽  
Vol 92 (3) ◽  
pp. 437-447 ◽  
Author(s):  
Sandford Jaques ◽  
Richard R. Gala
Keyword(s):  
Time Of Day ◽  
Ovariectomized Rat ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Stable Pool ◽  
Releasable Pool ◽  
Storage Pools

ABSTRACT The influence of oestrogen administered to the ovariectomized rat on the interaction between dopamine (DA) and thyrotrophin releasing hormone (TRH) on the release of radioimmunoassayable (RIA) and [3H] leucine incorporated into prolactin ([3H]PRL) was examined in vitro. Dopamine had a more marked suppressing effect on newly synthetized PRL (80 %), as determined [3H]PRL, than on total PRL (50 %), as determined by RIA-PRL. The administration of 5 μg of oestradiolbenzoate (OeB) for 7 days resulted in blocking the suppressing effect of DA when RIA-PRL was measured but not when [3H]PRL was measured. The administration of 5 μg of OeB enabled TRH to partially override the suppressing effect of DA and the degree of response was more marked when RIA-PRL was measured than when [3H]PRL was measured. The administration of 50 μg of OeB for 3 days enabled TRH to override the DA blockade of prolactin release to levels comparable to that of the control when RIA-PRL was measured but had little to no effect on [3H]PRL. The results are discussed in relation to the two storage pools of PRL in the pituitary and the data suggest that DA acts predominantly to suppress the newly synthetized, rapidly releasable pool. Oestrogen acts to block DA action on the older more stable PRL pool. The ability of TRH to override the DA blockade of PRL release depends upon the presence of oestrogen; here TRH acts predominantly on the older more stable pool of PRL. Oestrogen's action on disrupting the DA suppression of PRL release appears to be related to the time of day the hormone is administered subsequent to when the pituitary is exposed to DA in vitro.

OESTRADIOL STIMULATION OF PROLACTING RELEASE FROM CANINE PITUITARY IN CULTURE

1976 ◽  
Vol 82 (3) ◽  
pp. 706-709 ◽  
Author(s):  
Gwyneth E. Jones ◽  
A. R. Boyns
Keyword(s):  
Tissue Culture ◽  
Luteinizing Hormone ◽  
Prolactin Release ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Thyrotrophic Hormone ◽  
Lh Rh ◽  
Stimulation Of

ABSTRACT Anterior canine pituitaries were maintained in tissue culture for 8 days, and the immunoreactive prolactin released, was measured by a heterologous radioimmunoassay for canine prolactin. Luteinizing hormone-releasing hormone (LH-RH) and thyrotrophic hormone-releasing hormone (TRH) did not affect prolactin release, while theophylline and oestradiol-17β stimulated the release of canine prolactin.

EVIDENCE FOR THE INVOLVEMENT OF HYPOTHALAMIC DOPAMINE AND THYROTROPHIN-RELEASING HORMONE IN SUCKLING-INDUCED RELEASE OF PROLACTIN

1981 ◽  
Vol 91 (2) ◽  
pp. 213-223 ◽  
Author(s):  
W. J. DE GREEF ◽  
T. J. VISSER
Keyword(s):  
Nerve Stimulation ◽  
Plasma Levels ◽  
Plasma Prolactin ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Dopamine Infusion ◽  
Releasing Hormone ◽  
Peripheral Plasma ◽  
Transient Decrease ◽  
Hypothalamic Dopamine

The changes in adenohypophysial and hypothalamic content and in hypothalamic release of dopamine and thyrotrophin-releasing hormone (TRH) into the hypophysial portal system during the suckling-induced release of prolactin were investigated. An increase in peripheral plasma levels of prolactin was induced by mammary nerve stimulation in urethane-anaesthetized and by suckling in unanaesthetized lactating rats. In the unanaesthetized rat, suckling caused a decrease of dopamine levels in hypothalamus and adenohypophysis and a short-lasting small increase in hypothalamic TRH. Mammary nerve stimulation induced a transient decrease in dopamine levels and an increase in TRH levels in hypophysial stalk blood. To assess the significance of the observed changes in dopamine and TRH levels for prolactin release, these changes in dopamine and TRH were mimicked in lactating rats anaesthetized with urethane and pretreated with α-methyl-p-tyrosine (AMpT, a competitive inhibitor of catecholamine synthesis). Reducing hypothalamic dopamine secretion by treatment with AMpT increased peripheral plasma levels of prolactin from 15 to 477 ng/ml; an infusion with dopamine, resulting in plasma levels similar to those measured in hypophysial stalk plasma, reduced plasma levels of prolactin to 127 ng/ml. Neither a 50% reduction in dopamine infusion rate for 15 min nor administration of 100 ng TRH caused an appreciable change in plasma prolactin levels. However, when dopamine infusion was reduced by 50% for 15 min just before TRH was injected, then an increase in plasma levels of prolactin from 172 to 492 ng/ml was observed. Thus, the effectiveness of TRH in releasing prolactin in the lactating rat was enhanced when a transient decrease of dopamine levels occurred before treatment with TRH. It is concluded that the changes observed in dopamine and TRH levels in hypophysial stalk blood are involved in the suckling-induced prolactin release in an important manner.

Effects of an analogue of thyrotrophin-releasing hormone, RX77368, on infarct size and cerebral blood flow in focal cerebral ischaemia in the rat

1989 ◽  
Vol 67 (10) ◽  
pp. 1345-1350 ◽  
Author(s):  
C. T. O'Shaughnessy ◽  
N. J. Rothwell ◽  
J. Shrewsbury-Gee
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Infarct Size ◽  
Middle Cerebral Artery ◽  
Cerebral Ischaemia ◽  
Lesion Size ◽  
Focal Cerebral Ischaemia ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Stimulation Of

Effects of a stable analogue of thyrotrophin-releasing hormone, RX77368, on cerebral blood flow and infarct size have been studied in an acute model of cerebral ischaemia in the rat. Two hours after electrocoagulation of the left middle cerebral artery (MCA), the mean area of ischaemia (± SEM), determined histochemically, was 11.5 ± 2.2% of a single hemisphere and blood flow, determined using radiolabeled microspheres, was reduced by 40% in the left forebrain (p < 0.001 compared with sham-operated animals). Administration of RX77368 (50 μg/kg, intracerebroventricularly) within 10 min of arterial occlusion caused a significant (p < 0.01) reduction in mean lesion size to 3.7 ± 1.8% and stimulation of blood flow to the left ischaemic forebrain (60% above saline treated). Peripheral administration of RX77368 (1 mg/kg intraperitoneally) also significantly stimulated blood flow to the ischaemic forebrain and caused an apparent decrease in frequency of large infarcted areas of brain tissue, although mean lesion size was not significantly affected. These findings indicate that RX77368 ameliorates tissue damage in acute focal cerebral ischaemia. Such effects may be related to stimulation of cerebral blood flow.Key words: middle cerebral artery, focal cerebral ischaemia, cerebral blood flow, thyrotrophin-releasing hormone analogue.

Sign in / Sign up

Export Citation Format

Share Document