Starvation-induced changes in the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA and the hypothalamic release of proTRH-derived peptides: role of the adrenal gland

1995 ◽  
Vol 145 (1) ◽  
pp. 143-153 ◽  
Author(s):  
G A C van Haasteren ◽  
E Linkels ◽  
W Klootwijk ◽  
H van Toor ◽  
J M M Rondeel ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Thyroid Function ◽  
Food Deprivation ◽  
Median Eminence ◽  
Plasma Corticosterone ◽  
Portal Blood ◽  
Negative Effects ◽  
Releasing Hormone ◽  
Hypophysial Portal ◽  
Adrenalectomized Rats

Abstract The purpose of this study was to investigate the mechanisms involved in the reduced thyroid function in starved, young female rats. Food deprivation for 3 days reduced the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA, the amount of proTRH-derived peptides (TRH and proTRH160–169) in the paraventricular nucleus, the release of proTRH-derived peptides into hypophysial portal blood and the pituitary levels of TSHβ mRNA. Plasma TSH was either not affected or slightly reduced by starvation, but food deprivation induced marked increases in plasma corticosterone and decreases in plasma thyroid hormones. Refeeding after starvation normalized these parameters. Since the molar ratio of TRH and proTRH160–169 in hypophysial portal blood was not affected by food deprivation, it seems unlikely that proTRH processing is altered by starvation. The median eminence content of pGlu-His-Pro-Gly (TRH-Gly, a presumed immediate precursor of TRH), proTRH160–169 or TRH were not affected by food deprivation. Since median eminence TRH-Gly levels were very low compared with other proTRH-derived peptides it is unlikely that α-amidation is a rate-limiting step in hypothalamic TRH synthesis. Possible negative effects of the increased corticosterone levels during starvation on proTRH and TSH synthesis were studied in adrenalectomized rats which were treated with corticosterone in their drinking water (0·2 mg/ml). In this way, the starvation-induced increase in plasma corticosterone could be prevented. Although plasma levels of thyroid hormones remained reduced, food deprivation no longer had negative effects on hypothalamic proTRH mRNA, pituitary TSHβ mRNA and plasma TSH in starved adrenalectomized rats. Thus, high levels of corticosteroids seem to exert negative effects on the synthesis and release of proTRH and TSH. This conclusion is corroborated by the observation that TRH release into hypophysial portal blood became reduced after administration of the synthetic glucocorticosteroid dexamethasone. On the basis of these results, it is suggested that the reduced thyroid function during starvation is due to a reduced synthesis and release of TRH and TSH. Furthermore, the reduced TRH and TSH synthesis during food deprivation are probably caused by the starvation-induced enhanced adrenal secretion of corticosterone. Journal of Endocrinology (1995) 145, 143–153

Corticotrophin-releasing peptides in rat hypophysial portal blood after paraventricular lesions: a marked reduction in the concentration of corticotrophin-releasing factor-41, but no change in vasopressin

1990 ◽  
Vol 125 (2) ◽  
pp. 175-183 ◽  
Author(s):  
F. A. Antoni ◽  
G. Fink ◽  
W. J. Sheward
Keyword(s):  
Median Eminence ◽  
Feedback Inhibition ◽  
Portal Blood ◽  
Corticotrophin Releasing Factor ◽  
Paraventricular Nuclei ◽  
Oxytocin Release ◽  
Male Wistar Rats ◽  
Hypophysial Portal ◽  
Supraoptic Nuclei

ABSTRACT Previous data show that corticotrophin-releasing factor-41 (CRF-41), arginine vasopressin (AVP) and oxytocin are released into hypophysial portal blood. It has been presumed that the CRF-41 originates mainly from parvicellular neurones of the paraventricular nuclei (PVN); however, AVP and oxytocin could also be derived as a consequence of preterminal release from magnocellular projections to the neurohypophysis. The latter has been suggested to be the case for AVP as assessed by studies of the median eminence in vitro. Here we have investigated the source of CRF-41, AVP and oxytocin in hypophysial portal blood of adult male Wistar rats 8–10 days after surgical lesioning of the PVN. In PVN-lesioned animals the output of CRF-41 into hypophysial portal blood was reduced by about 90%, and that of oxytocin by about 40%: however, the output of AVP into portal blood was reduced only by about 10%. The release of AVP into portal blood increased after adrenalectomy; this increased release could be returned to normal by treatment with dexamethasone. No change of AVP release occurred after adrenalectomy in animals in which the PVN had been lesioned. These results show (i) that most of the CRF-41 released into hypophysial portal blood is derived from the PVN, (ii) that in PVN-lesioned animals AVP and oxytocin release remains at near normal or 60% of normal respectively, suggesting that a substantial amount of both neuropeptides in portal blood is derived as a consequence of preterminal release from supraoptic nuclei projections in the median eminence, and (iii) that glucocorticoid feedback inhibition of AVP release is exerted at the level of the PVN. Journal of Endocrinology (1990) 125, 175–183

Studies on the role of TRH and corticosterone in the regulation of prolactin and thyrotrophin secretion during lactation

1996 ◽  
Vol 148 (2) ◽  
pp. 325-336 ◽  
Author(s):  
G A C van Haasteren ◽  
H van Toor ◽  
W Klootwijk ◽  
B Handler ◽  
E Linkels ◽  
...  
Keyword(s):  
Litter Size ◽  
Median Eminence ◽  
Plasma Corticosterone ◽  
Adrenal Weight ◽  
Negative Effects ◽  
Mrna Content ◽  
Basal Plasma ◽  
Thyroid Axis ◽  
Acute Changes ◽  
Plasma Prl

Abstract This study describes the effects of litter size and acute suckling on the synthesis and release of hypothalamic TRH, as indirectly estimated by determination of hypothalamic prothyrotrophin-releasing hormone (proTRH) mRNA and median eminence TRH content. The effects of litter size (five or ten pups) were studied throughout lactation, while suckling-induced acute changes were analyzed on day 13 of lactation in dams with ten pups. In view of the enhanced adrenal activity during lactation and recent evidence that corticosteroids have negative effects on hypothalamic TRH, we also studied adrenalectomized (ADX) dams treated with corticosterone to maintain basal plasma corticosterone levels. In addition to an increased plasma level of prolactin (PRL), adrenal weight and plasma corticosterone increased, while plasma TSH, tri-iodothyronine (T3), thyroxine (T4) and free T4 (FT4) levels decreased during lactation. Litter size correlated positively with plasma PRL, adrenal weight and plasma corticosterone. No effect of litter size was observed on plasma T3, but rats with ten pups had lower plasma TSH, T4 and FT4 than rats with a five-pup litter. Compared with dioestrous rats, lactating rats showed an increased hypothalamic proTRH mRNA content on day 2, but not on days 8 and 15 of lactation. Median eminence TRH in lactating rats gradually increased until day 15 and decreased thereafter. Acute suckling, after a 6-h separation of mother and pups, rapidly increased plasma PRL and corticosterone in the mothers, but had no effects on plasma TSH and thyroid hormone levels. Hypothalamic proTRH mRNA increased twofold after 0·5 h of suckling, and then gradually returned to presuckling values after 6 h. Compared with sham-operated rats, corticosterone-substituted ADX rats with ten pups had increased plasma PRL and TSH, hypothalamic proTRH mRNA and pituitary TSH β mRNA on day 15 of lactation. Moreover, while acute suckling did not enhance TSH release in sham-operated rats, it provoked not only PRL but also TSH release in corticosterone-substituted ADX dams. It is concluded that suckling exerts a rapid, positive effect on hypothalamic proTRH mRNA content. However, the concurrent enhanced adrenal activity has negative effects on hypothalamic proTRH gene expression resulting in a suppressed hypophysial-thyroid axis during lactation. While TRH appears to play a role in PRL release during the first days of lactation and during acute suckling, TRH seems not important in maintaining PRL secretion during continued suckling. Journal of Endocrinology (1996) 148, 325–336

Endopeptidase EC 3.4.24.15 Presence in the Rat Median Eminence and Hypophysial Portal Blood and its Modulation of the Luteinizing Hormone Surge

1997 ◽  
Vol 9 (11) ◽  
pp. 813-822 ◽  
Author(s):  
T. J. Wu ◽  
Adrian R. Pierotti† ◽  
Moshe Jakubowski‡ ◽  
W. John Sheward ◽  
Marc J. Glucksman ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Median Eminence ◽  
Portal Blood ◽  
Luteinizing Hormone Surge ◽  
Hypophysial Portal

Interrelationship between Thyroxine and Estradiol on the Secretion of Thyrotropin-Releasing Hormone and Dopamine into Hypophysial Portal Blood in Ovariectomized-Thyroidectomized Rats

1994 ◽  
Vol 59 (3) ◽  
pp. 202-207 ◽  
Author(s):  
Paulus S. Wang ◽  
Seng-Wong Huang ◽  
Yuh-Fan Tung ◽  
Hsiao-Fung Pu ◽  
Shiow-Chwen Tsai ◽  
...  
Keyword(s):  
Thyrotropin Releasing Hormone ◽  
Portal Blood ◽  
Releasing Hormone ◽  
Hypophysial Portal

Many Peptides that Are Present in the External Zone of the Median Eminence Are Not Secreted into the Hypophysial Portal Blood of Sheep

1993 ◽  
Vol 57 (5) ◽  
pp. 765-775 ◽  
Author(s):  
Iain Clarke ◽  
David Jessop ◽  
Robert Millar ◽  
Margaret Morris ◽  
Steven Bloom ◽  
...  
Keyword(s):  
Median Eminence ◽  
Portal Blood ◽  
External Zone ◽  
Hypophysial Portal

Effect of Thyroid Status and Paraventricular Area Lesions on the Release of Thyrotropin-Releasing Hormone and Catecholamines into Hypophysial Portal Blood

Endocrinology ◽  
1988 ◽  
Vol 123 (1) ◽  
pp. 523-527 ◽  
Author(s):  
J. M. M. RONDEEL ◽  
W. J. DE GREEF ◽  
P. VAN DER SCHOOT ◽  
B. KARELS ◽  
W. KLOOTWIJK ◽  
...  
Keyword(s):  
Thyrotropin Releasing Hormone ◽  
Portal Blood ◽  
Thyroid Status ◽  
Releasing Hormone ◽  
Hypophysial Portal

Is thyrotropin-releasing hormone immunoreactivity in peripheral blood an estimate for hypothalamic thyrotropin-releasing hormone release?

1992 ◽  
Vol 126 (3) ◽  
pp. 276-281 ◽  
Author(s):  
Wim J de Greef ◽  
Jan MM Rondeel ◽  
Rogier Heide ◽  
Wim Klootwijk ◽  
Theo J Visser
Keyword(s):  
Peripheral Blood ◽  
Thyrotropin Releasing Hormone ◽  
Portal Blood ◽  
Hormone Release ◽  
Experimental Conditions ◽  
Releasing Hormone ◽  
Two Peaks ◽  
Hypophysial Portal ◽  
Stimulation Of

The significance of TRH for pituitary function is still unresolved mainly due to limitations in determining in vivo hypothalamic TRH release. We therefore examined whether TRH immunoreactivity (TRH-IR) in peripheral blood is an index for hypothalamic TRH release. Peripheral TRH-IR varied between 10 and 55 pmol/l and was similar in euthyroid and hypothyroid rats, but lower in hyperthyroid rats. Destruction of the hypothalamic paraventricular area reduced peripheral TRH-IR, while stimulation of this area increased it. Clearance of TRH during continuous TRH infusion was 1.9±0.2, 3.5±0.3 and 5.9±0.8 ml/min in hypothyroid, euthyroid and hyperthyroid rats, respectively. These and previous data on TRH in hypophysial portal blood indicate that 5–25 pmol TRH/I peripheral blood is of hypothalamic origin. Chromatography revealed that TRH-IR from hypothalamus and portal blood co-eluted with TRH, but in peripheral blood two peaks were found, one of which was authentic TRH. Thus, peripheral TRH-IR alters in experimental conditions and part of it seems to be of hypothalamic origin. However, the presence of TRH-like material in peripheral blood not identical to TRH and the fact that experimental conditions alter TRH clearance indicate that peripheral TRH-IR is not an index for hypothalamic TRH release.

Transport of Thyrotropin-Releasing Hormone from Cerebrospinal Fluid to Hypophysial Portal Blood and the Release of Thyrotropin

Endocrinology ◽  
1975 ◽  
Vol 97 (5) ◽  
pp. 1138-1143 ◽  
Author(s):  
CHARLES OLIVER ◽  
NIRA BEN-JONATHAN ◽  
S. MICAL ◽  
JOHN C. PORTER
Keyword(s):  
Cerebrospinal Fluid ◽  
Thyrotropin Releasing Hormone ◽  
Portal Blood ◽  
Releasing Hormone ◽  
Hypophysial Portal
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