Effect of adrenocorticotrophic hormone on gonadotrophin releasing hormone-induced luteinizing hormone secretion in vitro

1997 ◽  
Vol 48 (1) ◽  
pp. 53-65 ◽  
Author(s):  
J.B. Phogat ◽  
R.F. Smith ◽  
H. Dobson
1996 ◽  
Vol 134 (1) ◽  
pp. 115-122 ◽  
Author(s):  
BM Mutayoba ◽  
PD Eckersall ◽  
IA Jeffcoate ◽  
MJA Harvey ◽  
V Cestnik ◽  
...  

Mutayoba BM, Eckersall PD, Jeffcoate IA, Harvey MJA, Cestnik V. Holmes, PH. Effects of castration on luteinizing hormone secretion and response to gonadotrophin-releasing hormone in sheep infected with Trypanosoma congolense, Eur J Endocrinol 1996:134:115–22. ISSN 0804–4643 The effects of trypanosomiasis on the endocrine function of the hypothalamo-pituitary-gonadal axis were investigated before and after castration of Scottish Blackface rams infected with Trypanosoma congolense and uninfected controls. Blood samples were collected at 15-min intervals for 6 h before and at 10,20,40, 60, 80, 100 and 120 min after injection of synthetic gonadotrophin-releasing hormone (GnRH, 20 μg iv) 2 days before infection and 26 and 54 days after infection, with castration being performed 28 days after infection. Mean luteinizing hormone (LH) pulse amplitude was higher (3.3 ± 0.2 vs 2.6 ± 0.3 ng/ml) and mean plasma testosterone concentration was lower (4.1 ± 0.6 vs 7.6 ±1.2 nmol/l) in infected vs control rams 26 days after infection (p < 0.05). Mean plasma LH concentration and pulse amplitude increased in both groups after castration but both were significantly lower in infected compared to control rams (6.6 ±1.5 and 13.0 ± 2.2 ng/ml, p < 0.01; 7.7 ±0.9 and 11.6 ± 0.9 ng/ml, p < 0.001). respectively. However, LH responses to exogenous GnRH were similar in infected and control rams at each stage of the experiment, suggesting that the smaller increase in plasma LH after castration in infected rams was not caused by reduced responsiveness of the pituitary to GnRH but by alterations in GnRH secretion by the hypothalamus or its transport to the adenohypophysis. These results also demonstrate that impairment of testosterone secretion within 4 weeks of T. congolense infection in sheep may be due to testicular rather than pituitary effects. IA Jeffcoate, Department of Veterinary Physiology. University of Glasgow Veterinary School, Bearsden, Glasgow G61 1QH. UK


FEBS Letters ◽  
1990 ◽  
Vol 267 (1) ◽  
pp. 111-113 ◽  
Author(s):  
P.Anton van der Merwe ◽  
Robert P. Millar ◽  
Ian K. Wakeneld ◽  
M.Bruce Macrae ◽  
James S. Davidson

1996 ◽  
Vol 135 (4) ◽  
pp. 455-463 ◽  
Author(s):  
Hadas Lewy ◽  
Zvi Naor ◽  
Israel E Ashkenazi

Lewy H, Naor Z, Ashkenazi IE. Rhythmicity of luteinizing hormone secretion expressed in vitro. Eur J Endocrinol 1996;135:455–63. ISSN 0804–4643 In the present study we explored the possibility that the pituitary functions as an autonomous clock and is capable of generating rhythms of luteinizing hormone (LH) release independently of hypothalamic control. Pituitaries from estrous or diestrous day 1 female mice were perifused separately with Medium-199. Effluent samples were collected at 10-min intervals and assayed for LH levels. Fourier analysis and curve-fit analysis served to elucidate the presence of prominent periods whose significance was then determined by best-fit cosinor. The latter method was used to determine additional parameters for the significant rhythm. All perifused pituitaries exhibited LH release patterns that were composed of significantly long ultradian rhythms (approximately 16 and 8 h, p < 0.001). Continuous stimulation with gonadotropin-releasing hormone (GnRH) or estradiol did not alter the periods of the observed rhythms but affected other rhythm parameters. Gonadotropin-releasing hormone increased the mesor of the rhythm and estradiol increased the amplitude. The results indicate that pituitary gonadotropes are capable of producing rhythms of LH release for a long duration in vitro, in the absence of hypothalamic control. Both GnRH and estradiol affect different rhythm parameters but do not change the periods of these rhythms. Israel E Ashkenazi, Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel


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