The number and distribution of detectable luteinizing hormone (LH)-releasing hormone cell bodies changes in association with the preovulatory LH surge in the brains of young but not middle-aged female rats.

Endocrinology ◽  
1994 ◽  
Vol 134 (1) ◽  
pp. 467-474 ◽  
Author(s):  
B S Rubin ◽  
J C King
1981 ◽  
Vol 88 (1) ◽  
pp. 17-25 ◽  
Author(s):  
E. M. CONVEY ◽  
J. S. KESNER ◽  
V. PADMANABHAN ◽  
T. D. CARRUTHERS ◽  
T. W. BECK

In ovariectomized heifers, oestradiol decreases concentrations of LH in serum for approximately 12 h after which LH is released in a surge comparable in size and duration to the preovulatory surge. Using this model, we measured LH release induced by LH releasing hormone (LH-RH) from pituitary explants taken from ovariectomized heifers before or after an oestradiol-induced LH surge. These changes were related to changes in LH concentrations in serum and pituitary glands and hypothalamic LH-RH content. Twenty Holstein heifers were randomly assigned to one of four treatment groups to be killed 0, 6, 12, or 24 h after the injection of 500 μg oestradiol-17β. Jugular blood was collected at −2, −1 and 0 h then at intervals of 2 h until slaughter. Pituitary glands were collected and ≃2 mm3 explants were exposed to 4 ng LH-RH/ml medium for 30 min (superfusion) or 4 ng LH-RH/ml medium for 2 h in Erlenmeyer flasks. Levels of LH were measured in the medium. Hypothalami, collected at autopsy, were assayed for LH-RH content. To determine pituitary LH content, an additional 15 ovariectomized heifers were killed, five each at 0, 12 and 24 h after the injection of 500 μg oestradiol. In both groups of heifers, oestradiol reduced serum LH concentrations to ≃ 1 ng/ml, a level which persisted for 12 h, when LH was released in a surge. Pituitary sensitivity to LH-RH was increased at 6 and 12 h after the injection of oestradiol, but was markedly decreased at 24 h, i.e. after the LH surge. Despite this twofold increase in capacity of the pituitary gland to release LH in response to LH-RH, pituitary LH content did not change during 12 h after oestradiol treatment. However, LH content decreased after the LH surge and this decrease was associated with a decrease in pituitary responsiveness to LH-RH. Hypothalamic LH-RH content was not altered by these treatments. We have interpreted our results as evidence that oestradiol exerts a positive feedback effect on the pituitary gland of ovariectomized heifers such that pituitary sensitivity to LH-RH is increased twofold by the time the LH surge is initiated. In addition, oestradiol causes a transitory inhibition of LH-RH release as shown by the fact that serum LH concentrations remained low during the interval from injection of oestradiol until the beginning of the LH surge despite the fact that pituitary sensitivity to LH-RH is increased at this time. Depletion of a readily releasable pool of pituitary LH may be the mechanism by which the LH surge is terminated.


1994 ◽  
Vol 130 (5) ◽  
pp. 540-544 ◽  
Author(s):  
Aurelia N Brito ◽  
Timothy E Sayles ◽  
Richard J Krieg ◽  
Dennis W Matt

Brito AN, Sayles TE, Krieg Jr RJ, Matt DW. Relation of attenuated proestrous luteinizing hormone surges in middle-aged female rats to in vitro pituitary gonadotropin-releasing hormone responsiveness. Eur J Endocrinol 1994;130:540–4. ISSN 0804–4643 Prior to the cessation of regular cyclicity, middle-aged rats display pre-ovulatory luteinizing hormone (LH) surges of reduced magnitude. The present study was designed to identify whether middle-aged female rats with attenuated proestrous LH surges have alterations in pituitary responsiveness to gonadotropin-releasing hormone (GnRH). Young (4 months old) and middle-aged (10–12 months old) regularly cycling females were catheterized and sampled on proestrus to characterize their LH surge profiles. On the next proestrus (12.00 h), pituitaries were perifused individually and exposed to three pulses of GnRH (30 nmol/l). The patterns of the proestrous LH surges revealed that 12 of 22 middle-aged rats had attenuated surges (< 7 μg/l) while the remaining 10 middle-aged females had surges that were similar to those of young rats. Pituitaries perifused on the next proestrus showed similar basal LH release among the middle-aged and young females. However, the LH secretory rates following the second and third administration of GnRH, as well as the overall GnRH-stimulated LH secretory rates, were significantly decreased in middle-aged females with previously attenuated LH surges as compared to those from the young proestrous rats. In contrast, middle-aged rats with normal LH surges had pituitary LH responses that were no different from those of young females. These results indicate that a decrease in pituitary LH responsiveness to GnRH is only apparent in middle-aged rats that display attenuated proestrous LH surges. Dennis W Matt. Department of Obstetrics and Gynecology, Medical College of Virginia, Box 980034, Richmond, VA 23298, USA


1982 ◽  
Vol 242 (6) ◽  
pp. E392-E397
Author(s):  
L. K. Tang ◽  
A. C. Martellock ◽  
J. K. Horiuchi

The relationship between 17 beta-estradiol (E2) stimulation of luteinizing hormone (LH) response to LH-releasing hormone (LHRH) and E2 effect on LHRH binding was examined in pituitary monolayer cultures prepared from female rats. E2 pretreatment significantly (P less than 0.05) augmented the LHRH-induced LH release to 158-180% of the non-E2-treated controls. The maximal E2-priming effect could be observed after 1 day of treatment. E2 treatment for 3 days stimulated [D-Ala6]luteinizing hormone-releasing hormone (LHRHa) binding to about 1.5-fold that of the non-E2-treated controls without affecting the dissociation constant of LHRH receptor (Kd = 4 X 10(-10) M). The stimulatory effect of E2 on cell proliferation as determined by [3H]thymidine incorporation was also observed 3 days after treatment. However, E2 stimulation of LH accumulation in the cultured cells could be detected as early as 4 h after treatment. These results indicate that E2-priming effect on pituitary LH response to LHRH is initially associated with an increase in cellular LH content and later associated with increases in LHRH binding and in an index of cell proliferation that may include the LH-producing cells.


1983 ◽  
Vol 103 (3) ◽  
pp. 289-292 ◽  
Author(s):  
A. Miyake ◽  
K. Tasaka ◽  
T. Sakumoto ◽  
Y. Kawamura ◽  
Y. Nagahara ◽  
...  

Abstract. The releasing effects of clomiphene citrate (clomiphene) on luteinizing hormone (LH) and LH-releasing hormone (LRH) were examined in a sequential double chamber superfusion system by superfusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normal female rats in dioestrus. When the MBH and the pituitary were superfused in sequence with medium containing 2 × 10−10 m oestradiol (E2), two significant peaks in LH release (60–130% increase, P < 0.05) were observed 40 min and 90 min after the administration of 3 × 10−8 mol clomiphene. Administration of clomiphene in medium without E2 induced a low peak (25–50% increase, P < 0.05) of LH released from the pituitary perfused in series with the MBH. Administration of clomiphene did not cause a marked increase of LH from the pituitary superfused alone, when superfused with or without E2 containing medium. The concentration of LRH in the efflux was significantly increased (50–100%) 40 min and 90 min after clomiphene administration when MBH was superfused with medium containing E2, whereas clomiphene had no effect when superfused with medium alone. These data indicate: 1) that clomiphene induces LRH release from the MBH, that it may induce LH release, in part, by acting directly at the pituitary level; 2) that changes in LH after clomiphene administration coincide with LRH release, and 3) that a certain concentration of E2 may be necessary for the secretion of LRH by clomiphene.


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