GnRH-Induced Desensitization of in Vitro Luteinizing Hormone Secretion in the Turtle, Trachemys scripta

1993 ◽  
Vol 89 (2) ◽  
pp. 238-247 ◽  
Author(s):  
Pei-San Tsai ◽  
Paul Licht
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Trachemys Scripta ◽  
Luteinizing Hormone Secretion

scholarly journals Galanin Enhancement of Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone Secretion in Female Rats Is Estrogen Dependent

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
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Gonadotropin Releasing Hormone ◽  
Gonadal Steroids ◽  
Female Rats ◽  
Luteinizing Hormone Secretion ◽  
Ovx Rats ◽  
Lh Secretion ◽  
Lines Of Evidence

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.

cAMP augmentation of secretagogue-induced luteinizing hormone secretion

1986 ◽  
Vol 250 (1) ◽  
pp. E62-E68 ◽  
Author(s):  
J. L. Turgeon ◽  
D. W. Waring
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Base Line ◽  
Luteinizing Hormone Secretion ◽  
Secretory Rate ◽  
Camp Analogue ◽  
Lh Release ◽  
Lh Secretion ◽  
Camp Elevation

Whether adenosine 3',5'-cyclic monophosphate (cAMP) acts as a mediator for luteinizing hormone-releasing hormone (LHRH) in either its immediate LH release action or in its self-priming action was investigated. Pituitary pieces from either proestrous or estrous rats were superfused in vitro in the presence of dibutyryl cAMP [(Bu)2cAMP], 8-bromo-cAMP (8BrcAMP), forskolin, or control for 2-3 h. For proestrous but not estrous pituitary pieces, a slight increase in base-line LH secretion rate occurred at approximately 70 min of exposure to elevated cAMP; in the same system LHRH caused an increase in LH secretory rate within 2 min in either proestrous or estrous tissue. In contrast to its ineffectiveness as a secretagogue, cAMP elevation resulted in a severalfold augmentation of both LHRH- and elevated K+-induced LH secretion from proestrous but not estrous pituitary pieces; for these experiments, superfusion with a cAMP analogue or forskolin for varying times preceded a 10-min pulse of either 8 nM LHRH or 47 mM K+. Augmentation was evident after 30 min of cAMP elevation; longer exposures were coincident with greater potentiation. Cycloheximide prevented (Bu)2cAMP augmentation of LHRH-induced secretion. These data show that cAMP does not mediate the immediate LH release action of LHRH, but cAMP does augment LHRH- or K+-induced LH secretion with characteristics in common with the self-priming action of LHRH.

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