Homologous desensitization of gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone secretion in vitro occurs within the duration of an endogenous GnRH pulse.

Endocrinology ◽  
1995 ◽  
Vol 136 (1) ◽  
pp. 138-143 ◽  
Author(s):  
J Weiss ◽  
C R Cote ◽  
J L Jameson ◽  
W F Crowley
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


1997 ◽  
Vol 66 (4) ◽  
pp. 246-253 ◽  
Author(s):  
Lin Ping ◽  
Virendra B. Mahesh ◽  
Ganapathy K. Bhat ◽  
Darrell W. Brann

2009 ◽  
Vol 54 (No. 3) ◽  
pp. 97-110 ◽  
Author(s):  
P. Podhorec ◽  
J. Kouril

Gonadotropin-releasing hormone in Cyprinidae as in other Vertebrates functions as a brain signal which stimulates the secretion of luteinizing hormone from the pituitary gland. Two forms of gonadotropin-releasing hormone have been identified in cyprinids, chicken gonadotropin-releasing hormone II and salmon gonadotropin-releasing hormone. Hypohysiotropic functions are fulfilled mainly by salmon gonadotropin-releasing hormone. The only known factor having an inhibitory effect on LH secretion in the family Cyprinidae is dopamine. Most cyprinids reared under controlled conditions exhibit signs of reproductive dysfunction, which is manifested in the failure to undergo final oocyte maturation and ovulation. In captivity a disruption of endogenous gonadotropin-releasing hormone stimulation occurs and sequentially that of luteinizing hormone, which is indispensible for the final phases of gametogenesis. In addition to methods based on the application of exogenous gonadotropins, the usage of a method functioning on the basis of hypothalamic control of final oocyte maturation and ovulation has become popular recently. The replacement of natural gonadotropin-releasing hormones with chemically synthesized gonadotropin-releasing hormone analogues characterized by amino acid substitutions at positions sensitive to enzymatic degradation has resulted in a centuple increase in the effectiveness of luteinizing hormone secretion induction. Combining gonadotropin-releasing hormone analogues with Dopamine inhibitory factors have made it possible to develop an extremely effective agent, which is necessary for the successful artificial reproduction of cyprinids.


Endocrinology ◽  
1990 ◽  
Vol 126 (6) ◽  
pp. 3022-3027 ◽  
Author(s):  
RICHARD J. KRIEG ◽  
JUDY M. BATSON ◽  
PAUL M. MARTHA ◽  
DENNIS W. MATT ◽  
RONALD L. SALISBURY ◽  
...  

Endocrinology ◽  
2003 ◽  
Vol 144 (2) ◽  
pp. 484-490 ◽  
Author(s):  
Cynthia L. Splett ◽  
Joseph R. Scheffen ◽  
Joshua A. Desotelle ◽  
Vicky Plamann ◽  
Angela C. Bauer-Dantoin

The hypothalamic peptide GnRH is the primary neuroendocrine signal regulating pituitary LH in females. The neuropeptide galanin is cosecreted with GnRH from hypothalamic neurons, and in vitro studies have demonstrated that galanin can act at the level of the pituitary to directly stimulate LH secretion and also augment GnRH-stimulated LH secretion. Several lines of evidence have suggested that the hypophysiotropic effects of galanin are important for the generation of preovulatory LH surges. To determine whether the pituitary actions of galanin are enhanced by the preovulatory steroidal milieu, LH responses to galanin administration (with or without GnRH) were examined in: 1) ovariectomized (OVX); 2) OVX, estrogen (E)-primed; and 3) OVX, E- and progesterone-treated female rats. Results from the study indicate that galanin enhances GnRH-stimulated LH secretion only in the presence of E (in OVX, E-primed, or E- and progesterone-treated rats). Galanin alone does not directly stimulate LH secretion under any of the steroid conditions examined. In the absence of gonadal steroids (OVX rats), galanin inhibits GnRH-stimulated LH secretion. These findings suggest that the primary pituitary effect of galanin is to modulate GnRH-stimulated LH secretion, and that the potentiating effects of galanin occur only in the presence of E.


Endocrinology ◽  
2000 ◽  
Vol 141 (3) ◽  
pp. 1050-1058 ◽  
Author(s):  
Thomas G. Harris ◽  
Deborah F. Battaglia ◽  
Martha E. Brown ◽  
Morton B. Brown ◽  
Nichole E. Carlson ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document