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

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

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

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

THE RELATION BETWEEN THE HYPOTHALAMIC NEUROSECRETION AND THE CORTICOTROPHIN RELEASE IN EXPERIMENTAL CONDITIONS

1960 ◽  
Vol XXXIV (I) ◽  
pp. 8-18 ◽  
Author(s):  
E. Kivalo ◽  
U. K. Rinne
Keyword(s):  
Paraventricular Nucleus ◽  
Median Eminence ◽  
Supraoptic Nucleus ◽  
Acute Stress ◽  
Neurosecretory Material ◽  
Experimental Conditions ◽  
Hypothalamic Cells ◽  
The One ◽  
Hypophysial Portal ◽  
Acth Release

ABSTRACT Acute stress, chronic stress plus hydration, cortisone treatment, cortisone treatment plus dehydration were used as methods of investigation and the relation between the neurosecretory activity of the hypothalamic supraoptic nucleus and paraventricular nucleus and the neurosecretory material around the hypophysial portal vessels of the median eminence on the one hand and the corticotrophin release on the other hand, has been studied in the rat. Whereas stress stimulates both the activity of the above mentioned cells of the hypothalamus and the ACTH release, stress plus hydration causes a depression of these hypothalamic cells but nevertheless causes a marked ACTH release. Cortisone inhibits the activity of the cells in the supraoptic nucleus and the paraventricular nucleus as well as the ACTH release whereas cortisone plus dehydration causes stimulation but inhibits the ACTH release. In some stress and cortisone treatment groups the variations of the neurosecretory material around the hypophysial portal vessels and of the ACTH release were found to show a correlation. It is concluded that the activity of the cells of the supraoptic nucleus and the paraventricular nucleus and the ACTH release do not seem to have any definite connection, whereas some observations indicate that the neurosecretory material in the region of the median eminence around the hypophysial portal vessels may have some significance in ACTH release.

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