Induction of female and male mating patterns in female rats by gonadal steroids: Effects of neonatal or adult olfactory bulbectomy.

1981 ◽  
Vol 95 (4) ◽  
pp. 497-511 ◽  
Author(s):  
Augustus R. Lumia ◽  
Robert L. Meisel ◽  
Benjamin D. Sachs
1992 ◽  
Vol 132 (1) ◽  
pp. 39-45 ◽  
Author(s):  
A. C. Dalkin ◽  
S. J. Paul ◽  
D. J. Haisenleder ◽  
G. A. Ortolano ◽  
M. Yasin ◽  
...  

ABSTRACT Gonadal steroids can act both indirectly via gonadotrophin-releasing hormone (GnRH) and directly on the pituitary to regulate gonadotrophin subunit gene expression. Recent studies to assess a possible direct action at the pituitary have shown that testosterone, when given to males in the absence of endogenous GnRH action, selectively increases FSH-β mRNA concentrations. Conversely, in females, oestradiol appears to regulate gonadotrophin subunit mRNAs primarily via GnRH. The present study was designed to determine whether these differing results reflect specific actions of the gonadal steroids themselves or different responses of the pituitary gonadotroph cells in males and females. Rats which had been castrated 7 days earlier were given silicone elastomer implants (s.c.) containing oestradiol (plasma oestradiol 68 ± 4 ng/l) in males or testosterone (plasma testosterone 3·5 ± 0·3 μg/l) in females in the absence or presence of a GnRH antagonist. Seven days later pituitaries were removed and steady-state mRNA concentrations measured by dotblot hybridization. In males, oestradiol reduced LH-β and FSH-β but not α mRNA. The antagonist reduced levels of all three subunit mRNAs in males and the addition of oestradiol had no further effect, suggesting that oestradiol regulates gonadotrophin subunit gene expression in males by suppressing GnRH secretion. In females, testosterone reduced all three subunit mRNAs though FSH-β remained threefold higher than in intact animals. The GnRH antagonist was as effective as testosterone alone and reduced α and LH-β to levels found in intact animals. FSH-β mRNA was partially reduced by antagonist alone in ovariectomized females but the addition of testosterone increased FSH-β twofold versus antagonist alone (as has been observed in males). These findings, together with earlier data, suggest that testosterone increased FSH-β twofold versus antagonist alone (as has been observed in males). These findings, together with earlier data, suggest that testosterone reduces gonadotrophin subunit mRNAs by inhibiting GnRH secretion and also acts directly on the gonadotroph to increase steady-state FSH-β mRNA concentrations in both males and females. Journal of Endocrinology (1992) 132, 39–45


1979 ◽  
Vol 10 (2-3) ◽  
pp. 130-142 ◽  
Author(s):  
J.R. Ducharme ◽  
A.M. Morera ◽  
P. Laurin ◽  
R. Collu ◽  
L. Audi ◽  
...  

1985 ◽  
Vol 41 (3) ◽  
pp. 237-245 ◽  
Author(s):  
Charles W. Scouten ◽  
William E. Heydorn ◽  
G. Joseph Creed ◽  
Charles W. Malsbury ◽  
David M. Jacobowitz

1984 ◽  
Vol 247 (3) ◽  
pp. E312-E317 ◽  
Author(s):  
L. K. Tang ◽  
A. C. Martellock ◽  
F. Y. Tang

The role of testosterone (T) in the modulation of pituitary follicle-stimulating hormone (FSH) and luteinizing hormone (LH) sensitivity to DBcAMP was examined in the pituitary monolayer cultures prepared from intact young female rats. Hormone contents in media and cell homogenates were determined by radioimmunoassays. Incubation with 8 and 4 mM DBcAMP for 4 h consistently induced a significant (P less than 0.05) increase in FSH and LH release, respectively. Pretreatment with 10 nM T for 4 days reduced the minimal dose of DBcAMP required to stimulate FSH release (2 vs. 8 mM) but had no effect on the DBcAMP-induced LH release. Data indicate that T treatment for 4 or 7 days stimulated total FSH contents (sum of hormone contents in medium and cells). Similarly, incubation with 10 mM DBcAMP for 4 h significantly increased total FSH content per dish in both the T-treated and non-T-treated cultures. Neither T nor DBcAMP had any effect on LH production under these conditions. Intracellular cAMP was significantly increased to three- to eightfold of control after T treatment for 3 or 6 h, respectively. Furthermore, cAMP-binding activities were significantly increased after T treatment for 1 or 4 days (174 or 422% of control). Our previous data indicate that estrogen increases LH production, cAMP binding, cAMP production, and LH sensitivity to DBcAMP, and these data indicate that T exerts stimulatory effects on FSH in a similar fashion. These results support the concept that the two gonadotropins are regulated independently via different gonadal steroids.


2008 ◽  
Vol 89 (3) ◽  
pp. 314-323 ◽  
Author(s):  
Sarah L. Parylak ◽  
Joseph M. Caster ◽  
Q. David Walker ◽  
Cynthia M. Kuhn

Endocrinology ◽  
1984 ◽  
Vol 115 (4) ◽  
pp. 1256-1261 ◽  
Author(s):  
RICHARD R. GALA ◽  
WILLIAM P. CLARKE ◽  
DANIEL J. HAISENLEDER ◽  
JENN-TSER PAN ◽  
DAVID R. PIEPER

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.


Stroke ◽  
2000 ◽  
Vol 31 (1) ◽  
pp. 161-168 ◽  
Author(s):  
Nabil J. Alkayed ◽  
Stephanie J. Murphy ◽  
Richard J. Traystman ◽  
Patricia D. Hurn

1984 ◽  
Vol 102 (2) ◽  
pp. 133-141 ◽  
Author(s):  
R. Bhanot ◽  
M. Wilkinson

ABSTRACT We have attempted to clarify the physiological involvement of endogenous opiates in the steroid-mediated control of gonadotrophin release. Our studies showed that there was an acute reduction in the inhibitory effects of endogenous opiates on LH and FSH release following gonadectomy in the rat. This was indicated by a significant reduction in the ability of naloxone to stimulate serum LH/FSH levels (sampled at 15 min) in 26-day-old female rats 48 h after ovariectomy. Luteinizing hormone was highly sensitive to the inhibitory effects of the synthetic met-enkephalin analogue, FK 33-824, at this time (sampled at 90 min). An unexpected observation was that long-term absence of gonadal steroids also disrupted the ability of exogenous opiates, FK 33-824 and morphine, to influence LH release. This was seen as an inability of FK 33-824 (1·0 or 3·0 mg/kg) to inhibit LH secretion. The effects of gonadectomy on opiate control of LH occurred at all developmental stages and were not due to a disruption of sexual maturation. Opiate involvement in prolactin secretion did not appear to be adversely affected by an absence of gonadal steroids. Another novel aspect of this work was that the opiatergic component in the control of gonadotrophin secretion could be reinstated in long-term gonadectomized rats by treatment with oestradiol benzoate or testosterone propionate. Similarly, priming with increasing dosages of oestradiol benzoate which resulted in progressively lower LH levels gave larger naloxone responses. This steroid–opiate interdependency suggests that the negative feedback influence of gonadal steroids on LH secretion is conveyed, in part, by hypothalamic opiate peptides. Our results therefore provide a neurochemical basis for gonadal steroid negative feedback. J. Endocr. (1984) 102, 133–141


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