Acute and Long-Term Changes in Central and Pituitary Mechanisms Regulating Pulsatile Luteinizing Hormone Secretion after Ovariectomy in the Rat

Leipheimer, Robert E.; Gallo, Robert V.

doi:10.1159/000123587

Cited by 50 publications

(25 citation statements)

References 15 publications

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“…2). Many investigators have noted that the sensitivity of pituitary gonadotrophs to GnRH is not increased after castration and that the most likely cause of gonadotropin release is increased gonadotropin content in pituitary gonadotrophs [1,19]. Nevertheless, the present study demonstrates that this phenomenon could be attributed in part to an increase in the number of GnRH-R on the surface of pituitary gonadotrophs or increased GnRH release from the hypothalamus.…”

Section: Gnrh-r and Concentrations Of Gonadotro Pinscontrasting

confidence: 65%

Ovariectomy-Evoked Increase in Gonadotropin Releasing Hormone Receptor Parallels Its Messenger RNA Level, but Does not Correlate with Stimulated Gonadotropin Release.

et al. 1996

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Abstract. The amount of gonadotropin releasing hormone receptor (GnRH-R) in the anterior pituitary changes during the rat estrous cycle; in addition, it is chronically increased for several weeks in response to ovariectomy.The present study was undertaken to investigate these changes in relation to the concentrations of GnRH-R mRNA, gonadotropins and luteinizing hormone-fl (LH-fl) subunit in serum and the pituitary gland, as well as hypothalamic GnRH. GnRH-R concentrations on the day of estrus were significantly lower than that at diestrus (30% lower during 2 d), its mRNA decreased even further (by 60%), but there were no significant changes in gonadotropin.Ovariectomy increased GnRH-R significantly (by 30% during 2 wk) in parallel with receptor mRNA and with pituitary LH and LH-/3, but induced an earlier increase in serum gonadotropins. Our results suggest that transcriptional activity is more intimately linked to the number of GnRH-R in the long-term increase after ovariectomy than in the short-term change during the estrous cycle, and that the increased GnRH-R is not a major factor in ovariectomy-stimulated gonadotropin release. [5, 6]. We undertook the present study to investigate changes in the number of GnRH-R and the receptor mRNA concentrations in the anterior pituitary of ovariectomized rats, in comparison with those in the estrous cycle. In addition, we measured serum and pituitary concentrations of the gonadotropins and luteinizing hormone-fl (LH-f3) subunit, as well as hypothalamic content of GnRH and analyzed their relationship to the number of GnRH-R.

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Section: Gnrh-r and Concentrations Of Gonadotro Pinscontrasting

confidence: 65%

Ovariectomy-Evoked Increase in Gonadotropin Releasing Hormone Receptor Parallels Its Messenger RNA Level, but Does not Correlate with Stimulated Gonadotropin Release.

et al. 1996

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“…Following ovariectomy there is a rapid increase in the frequency of pulses of LH [19,32]. This change is due, most likely, to the loss of ovarian steroidal feedback on the pre sumed LHRH pulse generator [18].…”

Section: Discussionmentioning

confidence: 99%

“…The acute changes in both pulse fre quency and amplitude do not appear to reflect an increase in pituitary sensitivity to LHRH [19]. Rather, these changes are attributable to an increased frequency of LHRH release as well as an increase in the amount of LHRH released per pulse [19,26].…”

mentioning

confidence: 82%

“…Following ovariectomy there are changes in the pattern of pulsatile secretion of LH [18,19,32]. While there is evidence to suggest that the number of pulses that can be detected may be dependent upon sam pling frequency [10,31], it is apparent that within I day of ovariectomy, LH pulses increase in both frequency and am plitude [19,32]. When samples were taken every 10 min.…”

mentioning

confidence: 99%

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Hyperprolactinemia Alters the Frequency and Amplitude of Pulsatile Luteinizing Hormone Secretion in the Ovariectomized Rat

Cohen-Becker

Selmanoff

Wise³

1986

Neuroendocrinology

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Studies were undertaken to (1) examine the effects of hyperprolactinemia on the frequency and amplitude of pulses of LH, and (2) determine if changes in pituitary sensitivity to LHRH were involved in the prolactin-induced suppression of LH secretion. Rats were bilaterally ovariectomized (day 0). Ovine prolactin (4 mg/kg body weight, subcutaneously) or vehicle was administered every 8 h beginning at 09.00 h on day 4 after ovariectomy and continuing until 09.00 h on day 6. On day 6, between 07.00 and 09.00 h all animals received a right atrial cannula, using ether anesthesia. In experiment I blood samples were taken at 10-min intervals beginning at 12.00 h on day 6, for a total of 180 min. To test the effect of hyperprolactinemia on pituitary responsiveness (experiment II) animals received an intravenous injection of LHRH (25 ng/100 g body weight) after the 180-min and again after the 240-min sample. Blood was drawn every 10 min for a total of 300 min. Serum was assayed for LH. Hyperprolactinemia altered the pattern of pulsatile secretion of LH. Treatment with ovine prolactin produced a decrease in both the frequency and amplitude of the LH pulses compared to values found in control animals. However, no differences in pituitary responsiveness between hyperprolactinemic and control animals were found at the dose of LHRH given. Thus, the prolactin-induced suppression of pulsatile secretion of LH was not apparently a result of alterations in the sensitivity of the pituitary to LHRH. From these studies we suggest that hyperprolactinemia directly affects a hypothalamic site which ultimately alters the LHRH pulse generator, thereby changing the secretion of LHRH.

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“…These results support the concept that the PVN-DAF1A may be the site of a pulse generator that sets the circhoral rhythm of FSH release. Furthermore, this locus of FSH regulation appears to be independent from that controlling intermittent LHRH neurosecretion and its governance of episodic LH secretion.The pulsatile nature of FSH release was recently characte rized in the conscious ovariectomized (OVX) rat [21] and has been confirmed in a subsequent study [II], Previously, other investigators [1,13,19,29,30] had eluicidated the nature of episodic LH release in the OVX rat. It would appear that the frequencies of peak episodes of these two gonadotropins in plasma are dichotomous both in the OVX rat [ 11,21] and in the OVX hamster [6].…”

mentioning

confidence: 93%

Destruction of the Dorsal Anterior Hypothalamic Region Suppresses Pulsatile Release of Follicle Stimulating Hormone but Not Luteinizing Hormone

et al. 1989

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The region of the paraventricular nucleus-dorsal anterior hypothalamic area (PVN-DAHA) previously was implicated in the control of tonic FSH secretion. However, the role that this hypothalamic area plays in governing pulsatile FSH release is unknown. To examine this question, radiofrequency (RF) lesions were produced bilaterally in the PVN-DAHA of adult female rats which had been ovariectomized for 4 weeks. Control animals received sham lesions. After a recovery period of 1 week, all rats were fitted with jugular cannulae. The next day sequential blood samples were withdrawn from conscious, undisturbed rats at 10-min intervals for 3 h. Control animals displayed secretory peaks of FSH in plasma with a frequency of 4.0 ± 0.44/3-hour period (or 1 peak/40–50 min). LH in plasma pulsed at a frequency of 5.8 ± 0.49 peaks/3 h (or 1 peak/20–30 min). Both of these control values were in agreement with previous studies. RF lesion of the PVN-DAHA reduced FSH peak frequency to 1.2 ± 0.37 peaks/3 h (p < 0.001) and also significantly suppressed the mean peak height and trough values for FSH (p < 0.001). In contrast, none of these parameters for pulsatile LH secretion was altered by the lesion. Immediately after the 3-hour sampling period, synthetic LHRH (50 ng/100 g BW) was infused intravenously into rats and blood samples withdrawn 10 and 40 min later to determine whether the responsiveness of the pituitary gland had changed as a result of the lesion. Ablation of the PVN-DAHA failed to modify the response of the pituitary gland to the LHRH challenge since LH and FSH levels were not significantly different between sham controls and animals with lesions. Lesion of an adjacent hypothalamic area did not affect pulsatile FSH release thereby suggesting specificity of the PVN-DAHA in controlling episodic FSH release. These results support the concept that the PVN-DAHA may be the site of a pulse generator that sets the circhoral rhythm of FSH release. Furthermore, this locus of FSH regulation appears to be independent from that controlling intermittent LHRH neurosecretion and its governance of episodic LH secretion.

show abstract

Acute and Long-Term Changes in Central and Pituitary Mechanisms Regulating Pulsatile Luteinizing Hormone Secretion after Ovariectomy in the Rat

Cited by 50 publications

References 15 publications

Ovariectomy-Evoked Increase in Gonadotropin Releasing Hormone Receptor Parallels Its Messenger RNA Level, but Does not Correlate with Stimulated Gonadotropin Release.

Ovariectomy-Evoked Increase in Gonadotropin Releasing Hormone Receptor Parallels Its Messenger RNA Level, but Does not Correlate with Stimulated Gonadotropin Release.

Hyperprolactinemia Alters the Frequency and Amplitude of Pulsatile Luteinizing Hormone Secretion in the Ovariectomized Rat

Destruction of the Dorsal Anterior Hypothalamic Region Suppresses Pulsatile Release of Follicle Stimulating Hormone but Not Luteinizing Hormone

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