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

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

1985 ◽  
Vol 104 (2) ◽  
pp. 205-209 ◽  
Author(s):  
A. M. Horn ◽  
H. M. Fraser ◽  
G. Fink

ABSTRACT The possible role of thyrotrophin-releasing hormone (TRH) in causing the pro-oestrous surge of prolactin was investigated in conscious female rats by passive immunization with a specific anti-TRH serum raised in sheep. Blood samples were withdrawn through a previously implanted intra-atrial cannula. The i.p. injection of 1 ml anti-TRH serum, but not non-immune sheep serum, at 13.00 h of pro-oestrus delayed by about 1 h the onset of the prolactin surge, but the peak of the surge was similar to that in animals injected with the non-immune serum. The plasma concentrations of TSH were significantly reduced by the anti-TRH serum, but plasma concentrations of LH were not significantly affected. These results show that TRH may play an important role in the timing and initiation, but not the maintenance of the prolactin surge in the pro-oestrous rat. J. Endocr. (1985) 104, 205–209


1978 ◽  
Vol 76 (3) ◽  
pp. 557-558 ◽  
Author(s):  
J. B. WAKERLEY ◽  
M. B. TER HAAR

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


1983 ◽  
Vol 96 (2) ◽  
pp. 353-357
Author(s):  
B. F. Fitzgerald ◽  
F. J. Cunningham

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.


1981 ◽  
Vol 89 (3) ◽  
pp. 379-387 ◽  
Author(s):  
D. J. SAPHIER ◽  
R. G. DYER

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.


1962 ◽  
Vol 39 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Roger A. Gorski ◽  
Charles A. Barraclough

ABSTRACT We have previously suggested that the failure of the androgen-sterilized, persistent-oestrous rat to ovulate, following electrical stimulation of the median eminence structures of the hypothalamus, is due to an insufficiency in adenohypophyseal LH concentration. Using the ovarian ascorbic acid technique for quantitative determination of pituitary LH content, the present studies have demonstrated that the sterile rat pituitary gland contains one-third the LH content of the normal prooestrous gland. Furthermore, not only does progesterone priming of this persistent-oestrous rat result in a 75 % increase in LH concentration, but on hypothalamic stimulation sufficient LH is released to induce ovulation. The decrease in LH concentration which accompanies ovulation in the progesterone-primed, sterile rat is approximately 45 % of the total gland content as compared with a 51 % decrease in pituitary content in the normal cyclic rat.


1977 ◽  
Vol 72 (3) ◽  
pp. 301-311 ◽  
Author(s):  
A. E. PANERAI ◽  
IRIT GIL-AD ◽  
DANIELA COCCHI ◽  
V. LOCATELLI ◽  
G. L. ROSSI ◽  
...  

SUMMARY To determine how the sensitivity of the ectopic anterior pituitary gland to the GH-releasing effect of thyrotrophin releasing hormone (TRH) might be affected by the time lapse from transplantation, TRH (0·15 and 0·6 μg) was injected i.v. into hypophysectomized (hypox)-transplanted rats under urethane anaesthesia 1,3, 8,15, 30 and 60 days after transplantation, and plasma samples were taken 5 and 10 min later. Baseline GH values gradually decreased with time from about 16·0 ng/ml (1 day) to about 3·0 ng/ml (30 and 60 days). The TRH-induced GH release was absent 1 day after transplantation, present only with the higher TRH dose 3 and 8 days after transplantation, and clearly elicitable, also with the lower TRH dose (0·15 μg), from 15 up to 60 days. Determination of plasma prolactin concentrations showed a decline from about 85·0 ng/ml (1 day) to about 32·0 ng/ml (8 days); subsequently (15–60 days) prolactin values stabilized. Plasma prolactin levels increased 15 and 60 days after transplantation only when a dose of 0·6 μg TRH was given. In intact weight-matched rats, TRH induced a GH response only at the dose of 1·2 μg while a short-lived but clear-cut prolactin response could be obtained even with the 0·3 μg dose. The present results indicate that: (1) disconnexion between the central nervous system and the anterior pituitary gland greatly enhances GH responsiveness while blunting prolactin responsiveness to TRH; (2) the sensitivity of the anterior pituitary gland to the GH-releasing effect of TRH increases with time from transplantation; (3) TRH is a more effective prolactin-than GH-releaser on the pituitary gland in situ.


1981 ◽  
Vol 90 (2) ◽  
pp. 179-191 ◽  
Author(s):  
S. HENDRICKS ◽  
C. A. BLAKE

The effects of varying amounts of copulatory stimulation on patterns of plasma concentrations of prolactin and progesterone were evaluated in 3- and 12-month-old female rats. The 12-month-old group included rats which still exhibited oestrous cycles and rats in persistent vaginal oestrus (PVO). The extent of copulatory stimulation was defined by the number of intromissions received during mating: ≤5,15 or > 50. Blood samples were drawn over the 8 days after mating through a cannula inserted into the right external jugular vein. Plasma from the samples was assayed for prolactin and progesterone. In aged but still cyclic rats, pregnancy rates were positively correlated with the number of intromissions received during mating. Only one rat in PVO became pregnant. All animals which became pregnant and rats in PVO which, after mating, exhibited a disruption of the pattern of PVO, showed the nocturnal surge of plasma prolactin characteristic of pregnant and pseudopregnant rats. While these surges persisted until day 8 after mating in pregnant animals, they were absent by this time in the rats in PVO. Prolactin surges were present in some but not all of the aged rats which did not become pregnant. Progesterone concentrations were raised in all pregnant animals except the one pregnant rat in PVO and, while not related to the number of intromissions, concentrations were higher 8 days after mating in young compared with those in aged pregnant rats. Plasma progesterone was low in rats in PVO regardless of disruption of the pattern of PVO. We have concluded that the failure of limited copulatory stimulation to induce pregnancy in older rats results, at least in part, from its failure to initiate nocturnal prolactin surges. Nevertheless, our data suggest that matings which are not experimentally limited should provide ample stimulation to establish such surges. Although reduced plasma concentrations of prolactin and progesterone at pro-oestrus and reduced plasma progesterone through part of gestation may contribute to decreasing fertility in aged rats, other unidentified factors appear to be involved in mediating the capacity of extensive copulatory stimulation to induce pregnancy in these animals.


1979 ◽  
Vol 237 (5) ◽  
pp. R278-R284 ◽  
Author(s):  
Y. Sakuma ◽  
D. W. Pfaff

Electrical stimulation in the mesencephalic central gray (CG) and adjacent subtectum through chronically implanted electrodes in free-moving estrogen-primed ovariectomized female rats elicited a rapid and large facilitation of the lordosis reflex in response to either male mounts or manula cutaneous stimuli. Unilateral stimulation was sufficient for this effect. The facilitation increased in a graded manner to increased stimulus intensity, and was optimally evoked by stimuli delivered at 50--150 Hz. Facilitation disappeared rapidly following the end ot electrical stimulation, and within 15 min, reflex performance returned to the prestimulation level. Lordosis facilitation appeared when no aversive responses occurred; stimulation with comparable parameters at the lateral edge of CG or in the mesencephalic reticular formation often resulted in postural changes or aversive responses but was not able to facilitate lordosis. Lordosis refelx facilitation was probably mediated by projections descending from neurons in and around the CG, and represents stimulation of a functional link between ascending somatosensory and descending motor systems for the control of lordosis behavior.


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