Ovarian Steroid Regulation of Pulsatile Luteinizing Hormone Release during the Interval between the Mornings of Diestrus 2 and Proestrus in the Rat

Leipheimer, Robert E.; Bona‐Gallo, Antonella; Gallo, Robert V.

doi:10.1159/000124185

Cited by 24 publications

(30 citation statements)

References 11 publications

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“…This finding suggests that estrogen may be responsible for the observed sex-linked differences in susceptibility to cerebral ischemia in experimental stroke. Because OVX rats had decreased plasma levels of gonadal hormones at 24 hours after OVX, 24,25 the different infarct size between the short-term and long-term OVX groups might have resulted from the different durations of gonadal hormone depletion. The effects of estrogen on regional CBF reductions during ischemia remain controversial in previous studies.…”

Section: Discussionmentioning

confidence: 99%

“…23,24 Both physiological high and physiological low doses (10 and 60 pg/mL of plasma estradiol concentration, respectively) were equally effective at reducing the size of ischemic injury. 8 Therefore, the relatively lower dose of estradiol valerate used in the present study was considered to be adequate to analyze the neuroprotective role of estrogen against brain ischemia.…”

Section: Discussionmentioning

confidence: 99%

“…The estradiol level in the estrogen replacement group remained within the physiological level, but it was slightly higher than the basal circulating estradiol level in female rats during the estrous cycle and was close to the proestrous estradiol level. 23,24 …”

Section: Methodsmentioning

confidence: 99%

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Ovariectomy Exacerbates and Estrogen Replacement Attenuates Photothrombotic Focal Ischemic Brain Injury in Rats

Fukuda

Yao

Ibayashi

et al. 2000

Stroke

103

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Background and Purpose-We previously reported the infarct volumes in female spontaneously hypertensive rats (SHR) to be significantly smaller than those in male SHR. The purpose of the present study was to determine whether estrogen is responsible for the sex difference in ischemic vulnerability in SHR. Methods-In experiment 1, 1 week (short-term) or 4 weeks (long-term) after the ovariectomy (OVX), female SHR (5 months old) were randomly subjected to photothrombotic occlusion of the middle cerebral artery, and the infarct volumes were determined. In experiment 2, the rats were randomly assigned to 3 groups (ie, the sham-ovariectomized, ovariectomized, and estrogen replacement groups). In the replacement group, estradiol valerate (200 g/kg) was subcutaneously injected once a week after the OVX. Four weeks after the OVX or sham-OVX, all rats were subjected to middle cerebral artery occlusion. Changes in regional cerebral blood flow were determined by laser-Doppler flowmetry. Results-In experiment 1, the infarct volume produced 1 week after the OVX was not different from that of the sham-ovariectomized group. In contrast, the infarct volume produced 4 weeks after the OVX was significantly larger than that of the sham-ovariectomized group (82.4Ϯ11.6 versus 54.5Ϯ16.0 mm 3 , Pϭ0.0058). In experiment 2, estradiol replacement after the OVX was observed to attenuate the infarct volume compared with the ovariectomized group (55.6Ϯ18.8 versus 78.5Ϯ21.0 mm 3 , Pϭ0.0321). The degrees of regional cerebral blood flow reduction did not differ among the sham-ovariectomized, ovariectomized, and estrogen replacement groups. Conclusions-Chronic estrogen depletion was thus found to increase the infarct size, which was attenuated by estradiol replacement. These findings indicate that estrogen contributes to the sex difference in ischemic vulnerability and that endogenous estrogen also has a neuroprotective effect against ischemic brain damage. (Stroke. 2000;31:155-160.)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Ovariectomy Exacerbates and Estrogen Replacement Attenuates Photothrombotic Focal Ischemic Brain Injury in Rats

Fukuda

Yao

Ibayashi

et al. 2000

Stroke

103

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“…Recently, we reported that mean blood LH levels rapidly increased Received: April 15. 1985 Accepted after revision: October 7, 1985 within 24 h following ovariectomy (OVX) on diestrus I (Dl) and diestrus 2 (D2) due to increases in both LH pulse amplitude and frequency, suggesting an inhibitory role for ovarian steroids on these parameters of LH secretion in the intact rat [27,28], Results of studies in which physiological levels of estradiol (E2) and/or progesterone (P) were re …”

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confidence: 99%

Influence of Estradiol and Progesterone on Pulsatile LH Secretion in 8-Day Ovariectomized Rats

Leipheimer¹,

Bona‐Gallo²,

Gallo³

1986

Neuroendocrinology

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Previous studies in our laboratory [Endocrinology 114:1605–1612 (1984); Neuroendocrinology 41:252–257 (1985)] examined the influence of ovarian steroids on pulsatile luteinizing hormone (LH) release, and involved immediate replacement following ovariectomy (OVX) of estradiol (E2) and progesterone (P) for a 24-hour period within the physiological context of the estrous cycle. The present study investigated the effects of replacing E₂ and/or P 1 week after OVX, and therefore examined whether the time elapsed following OVX influences the effects of ovarian steroids on pulsatile LH release. Immediately after jugular venous cannulation, rats were implanted with either empty silastic capsules or capsules capable of restoring physiological levels of E₂ and/or P comparable to those found in intact rats between the intervals of diestrus 1 (Dl) and diestrus 2 (D2), or D2 and proestrous morning. 24 h later, these rats were bled continuously at a rate of 50 µl whole blood/6 min for 3 h for analysis of pulsatile LH secretion. Rats with empty capsules had decreased levels of E₂ and P and elevated mean blood LH levels, pulse amplitudes and frequencies. Two groups of animals with E₂ capsules had plasma E₂ levels comparable to those seen either in the D1-D2 or D2-proestrous intervals, decreased levels of P, and in both cases significant decreases in LH pulse amplitude, but no change in LH pulse frequency or basal LH secretion. Since mean blood LH levels in 8-day ovariectomized rats are determined by LH pulse amplitude, frequency and basal LH secretion [Neuroendocrinology 37:421–426 (1983)], the E₂-induced effects on LH pulse amplitude were not sufficient to decrease mean blood LH levels. Rats with P capsules had physiological D1-D2 plasma levels of P and decreased levels of E₂, but no change in any parameter of pulsatile LH release. Rats implanted with both E₂ and P capsules had physiological D1-D2 levels of both steroids which caused a significant decrease in mean blood LH levels, due to decreases in LH pulse amplitude and pulse frequency. There was no significant difference in the extent of the decrease in pulse amplitude produced by E₂ (low) or E₂ (low) + P. This indicates that the decreased LH pulse amplitude following E₂ (low) + P is due to the E₂ (low) alone. The suppressive effects on LH pulse amplitude produced by E₂ (low or high) were mediated centrally, since the in vitro responses to LHRH of anterior pituitary (AP) fragments from E₂-implanted rats were greater than those of AP fragments from rats implanted with empty capsules. When compared with our previous studies, the present results demonstrate that some of the responses of the pulsatile LH secretory system to the negative feedback effects of ovarian steroids remain the same, while others are altered when these same levels of steroids are replaced for 24 h 1 week after OVX rather than immediately after OVX. D2-pro...

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“…This may explain why elevated levels of progesterone oc curring during diestrus I and diestrus 2 do not block pulsatile LH secretion. There is ample evidence that estradiol can act during the estrous cycle to restrain GnRH and hence LH secre tion [26,27]. Using a different protocol (rats OVX on the mor ning of proestrus and receiving various steroid regimens during proestrus), Leipheimer et al [27] concluded that estradiol secre tion during proestrus was primarily responsible for restraining LH pulse frequency on estrus, while estradiol and progesterone acted together to suppress pulse amplitude.…”

Section: Discussionmentioning

confidence: 99%

Role of Proestrous Progesterone Secretion in Suppressing Basal Pulsatile LH Secretion during Estrus of the Estrous Cycle

Smith

Fox

Chatterton³

1989

Neuroendocrinology

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These studies examined the mechanisms responsible for the paucity of basal LH pulses during estrus. We confirmed our earlier observations that constant infusion of naloxone during estrus results in the immediate appearance of pulsatile LH secretion during estrus, consisting of LH peak heights and LH interpulse intervals that are similar to those observed during other days of the estrous cycle. We then tested whether the proestrous surge of progesterone was responsible for the suppression of pulsatile LH secretion during estrus. Three treatment regimens were used on proestrus to either block progesterone secretion (pentobarbital) or block its action (progesterone antiserum or the progesterone antagonist, RU 486). After treatment at 12.00 h on proestrus, blood samples were collected during estrus every 10 min for 4 h, and the plasma samples were analyzed for the pattern of LH secretion. Treatment with pentobarbital (35 mg/kg at 12:00 h) blocked the proestrous surges of LH and progesterone and resulted in pulsatile LH secretion during estrus. The LH interpulse interval (72 ± 7 min) was somewhat slower than that observed in the naloxone-infused animals (54 ± 8 min). Simultaneous treatment with pentobarbital and progesterone at 12:00 h on proestrus completely prevented the appearance of LH pulses during estrus. Treatment with either progesterone antiserum (0.5 ml, i.v.) or RU 486 (1 mg s.c.) resulted in the initiation of pulsatile LH secretion during estrus. In the RU 486-treated animals, LH peak heights and LH interpulse intervals were similar to those observed in naloxone-infused animals and during other days of the estrous cycle. These studies demonstrate that the suppression of pulsatile LH secretion during estrus is dependent on endogenous opioid tone. In addition, the proestrous surge of progesterone may be responsible for this suppression during estrus, since blocking progesterone secretion or blocking its action restores pulsatile LH secretion on estrus. We hypothesize that the proestrous surge of progesterone may cause an increase in endogenous opioid tone which then suppresses GnRH release and pulsatile LH secretion during estrus.

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Ovarian Steroid Regulation of Pulsatile Luteinizing Hormone Release during the Interval between the Mornings of Diestrus 2 and Proestrus in the Rat

Cited by 24 publications

References 11 publications

Ovariectomy Exacerbates and Estrogen Replacement Attenuates Photothrombotic Focal Ischemic Brain Injury in Rats

Ovariectomy Exacerbates and Estrogen Replacement Attenuates Photothrombotic Focal Ischemic Brain Injury in Rats

Influence of Estradiol and Progesterone on Pulsatile LH Secretion in 8-Day Ovariectomized Rats

Role of Proestrous Progesterone Secretion in Suppressing Basal Pulsatile LH Secretion during Estrus of the Estrous Cycle

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