scholarly journals OVERVIEW: Modulation by Sex Steroids and [d-TRP6, Des-Gly-NH210]Luteinizing Hormone (LH)-Releasing Hormone Ethylamide of α-Subunit and LHβ Messenger Ribonucleic Acid Levels in the Rat Anterior Pituitary Gland

1988 ◽  
Vol 2 (9) ◽  
pp. 775-784 ◽  
Author(s):  
Jacques Simard ◽  
Claude Labrie ◽  
Jean-François Hubert ◽  
Fernand Labrie
1981 ◽  
Vol 90 (3) ◽  
pp. 345-354 ◽  
Author(s):  
KATHLEEN A. ELIAS ◽  
C. A. BLAKE

Changes at the anterior pituitary and/or hypothalamic levels which result in selective FSH release during late pro-oestrus in the cyclic rat were investigated. The possible involvement of decreasing serum concentrations of oestrogen during pro-oestrus in such changes was studied. Rats were decapitated at 12.00 h on pro-oestrus, before the onset of the LH surge and first phase of FSH release, or at 24.00 h on pro-oestrus, shortly after the onset of the second or selective phase of FSH release. Other rats were given oestrogen (OE2) at 14.00 h and killed at 24.00 h pro-oestrus. Paired hemi-anterior pituitary glands were incubated with vehicle or OE2 with or without synthetic LH-releasing hormone (LH-RH) or hypothalamic acid extracts prepared from rats killed at 12.00 or 24.00 h on pro-oestrus. At 24.00 h pro-oestrus, serum FSH concentration was high while serum LH concentration was low regardless of whether rats were given OE2. Glands collected and incubated at 24.00 h released more FSH and less LH than did glands collected and incubated at 12.00 h pro-oestrus. Administration of OE2 in vivo and/or in vitro did not affect these responses. The increments in LH and FSH release attributed to LH-RH or hypothalamic extracts in the glands incubated at 24.00 h were not different from those of the glands incubated at 12.00 h. Also, the hypothalamic extracts prepared from rats killed at 24.00 h were no more effective than the extracts prepared from rats killed at 12.00 h in releasing LH or FSH from glands incubated at 12.00 or 24.00 h pro-oestrus. Administration of OE2 in vivo caused a small suppression of LH-RH-induced FSH release. We suggest that a change occurs at the level of the anterior pituitary gland during the period of the LH surge and first phase of FSH release to increase basal FSH secretion selectively and cause, at least in part, the second phase of increased serum FSH. This change is not mediated by a decrease in serum oestrogen concentration. We failed to observe any evidence that LH-RH causes preferential FSH release during late pro-oestrus or that a hypothalamic peptide with a preferential FSH releasing ability is involved in FSH release at this time.


1984 ◽  
Vol 103 (3) ◽  
pp. 371-376 ◽  
Author(s):  
M. J. D'Occhio ◽  
B. P. Setchell

ABSTRACT The capacity of the anterior pituitary gland and testes in mature bulls (705±9 (s.e.m.) kg body wt, n = 4) to respond to graded doses of LH-releasing hormone (LHRH) was assessed relative to endogenous profiles of LH and testosterone secretion. Endogenous hormone profiles were determined by bleeding bulls at 20-min intervals for 12 h. Responses to LHRH were assessed on successive days after single intravenous injections of 1, 5, 10, 50 or 100 ng LHRH/kg body wt. Blood samples were taken at −40, −20, 0, 10, 20, 30, 40, 60 and 120 min relative to LHRH injection. During a 12-h bleed bulls showed spontaneous pulses of LH and testosterone which had peak amplitudes of 2·6±0·5 μg/l and 44·5 ± 7·1 nmol/l respectively. Respective peak LH (μg/l) and testosterone (nmol/l) responses to LVRH were as follows: 1 ng LHRH (3·0±0·7: 47·3±4·1); 5 ng LHRH (8·0±1·2; 52·8 ± 6·2); 10 ng LHRH (11·1±2·3; 57·7 ± 9·1); 50 ng LHRH (19·2±2·8; 47·9±8·6); 100 ng LHRH (19·1±4·7; 43·9 ±6·4). A dose of 1 ng LHRH/kg produced LH and testosterone responses which were comparable in amplitude to spontaneous peaks in the respective hormone. There was a linear (y = 0·28x+5·72; r = 0·81) increase in the LH response to doses of LVRH between 1 and 50 ng/kg; corresponding testosterone responses showed no relationship with the dose of LHRH. The capacity of the anterior pituitary gland to release amounts of LH eight to ten times in excess of those secreted during spontaneous peaks suggests that (1) there exists a large releasable store of LH in the anterior pituitary gland and (2) hypothalamic LHRH is a limiting factor in gonadotrophin secretion. In contrast to LH release, the androgenic response of the testes to acute gonadotrophic stimulation is determined largely by prevailing steroidogenic activity. J. Endocr. (1984) 103, 371–376


1985 ◽  
Vol 107 (1) ◽  
pp. 83-87 ◽  
Author(s):  
L. Persson ◽  
M. Nilsson ◽  
E. Rosengren

ABSTRACT The biosynthesis of polyamines, an ubiquitous group of amines shown to be essential for normal cellular growth and differentiation, was studied in the rat anterior pituitary gland during the different stages of the oestrous cycle. The activity of ornithine decarboxylase (ODC), which catalyses the rate-limiting step in the biosynthesis of polyamines, was low during oestrus, metoestrus and dioestrus. However, a marked transitory rise in ODC activity was found in the pituitary gland on the evening of pro-oestrus. The rise in ODC activity was accompanied by an increase in the pituitary content of the polyamines putrescine and spermidine. Ovariectomy did not significantly change the basal ODC activity in the pituitary gland. Oestrogen treatment of ovariectomized rats resulted in a marked stimulation of pituitary polyamine biosynthesis. The largest effects were observed when oestrogen was given as two injections 72 h apart, which gave rise to levels of ODC activity comparable to those observed on the evening of pro-oestrus. The increase in polyamine synthesis in the anterior pituitary gland during pro-oestrus appeared not to be related to the preovulatory secretion of LH or prolactin, since neither LH-releasing hormone nor thyrotrophin-releasing hormone (which induces a secretion of prolactin) affected pituitary ODC activity. The observed biosynthesis of polyamines may be associated with the cellular proliferation which occurs in the anterior pituitary gland at oestrus. J. Endocr. (1985) 107, 83–87


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