Role of brain epinephrine neurons in the regulation of serum prolactin and luteinizing hormone release in female rats.
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Administration of phenylethanolamine N-methyltransferase (PNMT) inhibitors to estrogen (EB)-plus progesterone (PG)-treated ovariectomized (OVX) female rats produced significant reductions in hypothalamic epinephrine (Epi) levels and serum luteinizing hormone (LH) levels, but no effect on serum prolactin (Prl) levels. These results suggest that brain Epi neurons may participate in the regulation of LH release but not in controlling the surge of Prl induced by EB-plus PG-treatment in OVX rats.Cite
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Administration of phenylethanolamine N-methyltransferase (PNMT) inhibitors to estrogen (EB)-plus progesterone (PG)-treated ovariectomized (OVX) female rats produced significant reductions in hypothalamic epinephrine (Epi) levels and serum luteinizing hormone (LH) levels, but no effect on serum prolactin (Prl) levels. These results suggest that brain Epi neurons may participate in the regulation of LH release but not in controlling the surge of Prl induced by EB-plus PG-treatment in OVX rats.
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Although a relatively low dose of estradiol benzoate (E.B.) suppressed LH levels in both mature and aged ovariectomized (OVX) rats, a higher dose of E.B. induced an LH surge in mature OVX-E.B. primed rats, but failed to do so in aged OVX-E.B. primed rats. GnRH administration, however, was as effective in triggering an LH release in both mature and aged OVX-E.B. primed rats. Therefore, the cessation of reproductive cycles in the aged female rat appears to involve alterations within the “positive estrogen feedback center” of the anterior hypothalamus rather than in the pituitary or “negative estrogen feedback center”.
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Altered Negative Feedback Response to Ovariectomy and Estrogen in Prepubertal Restricted-diet Rats 1
Studies were conducted to explore the hypothesis that the delayed sexual maturation of female rats induced by reduced food intake (R) may result partially from an altered negative feedback response to estrogen. Animals were placed on 60% of normal food intake at 20 days of age. Controls (C) were fed ad libitum. Rats were used for three different experiments at 31-32 days of age. In Experiment I, rats were ovariectomized (OVX) and injected subcutaneously for 4 days with varying doses of estradiol benzoate (EB). They were killed the day after the last injection. In Experiment II, rats were ovariectomized and killed in groups at 4, 12, 24, 48, 72, and 120 h after OVX. In Experiment III, they were castrated and 1 wk later received a single injection of 0.5 microgram EB. Groups were killed at 1, 2, 4, 8, and 24 h after injection. Sera from all experiments were assayed for follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin. Results of Experiment I indicate that the efficacy of EB for suppressing LH, but not FSH, secretion is increased significantly in R rats. In Experiment II, OVX resulted in a delayed increase in serum LH, but not FSH, concentrations of R rats when compared to C animals. Results of Experiment III indicate a delayed, but more prolonged, suppression of LH secretion by EB in R rats when compared to C rats. Prolactin secretion, on the other hand, increased earlier in R rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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Observations that a pancreatic polypeptide-like substance is present in hypothalamus and may coexist with catecholamines prompted evaluation of its possible role in control of luteinizing hormone (LH) secretion. Intracerebro-ventricular administration of 0.5 or 2 µg of human pancreatic polypeptide to ovariectomized, hormonally untreated rats significantly decreased LH levels. However, when administered to ovariectomized rats pretreated with estradiol benzoate and progesternone, the neuropeptide significantly increased circulating LH in a dose-related manner. These results, which are similar to those reported for centrally administered norepinephrine, raise the possibility that pancreatic polypeptide, or a similar peptide, may participate in the physiologic regulation of LH release, either independently or perhaps as a neuromodulator or a cotransmitter with catecholamines.
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There are data indicating that stress-induced prolactin (PRL) release is blunted in the lactating rat like the release of other stress-associated hormones. In this experiment, the PRL release evoked by administration of estrogen, which is another principal stimulus for PRL release, was examined in ovariectomized lactating rats 8-15 days after delivery. Estradiol benzoate (EB, 20 µg) injections into ovariectomized nonlactating rats induced a PRL surge starting between 13:00 and 15:00 h with a peak at 17:00 h 2 days after the treatment, whereas the EB-induced PRL surge was absent in ovariectomized lactating rats separated from their pups at 09:00 h on the day or in mothers without separation from their pups. Injection of either thyrotropin-releasing hormone (TRH; 10 µg/kg) or pimozide (0.5 mg/kg) elevated serum PRL concentrations similarly in lactating and nonlactating rats when examined just before the beginning of the expected estrogen-induced PRL surge. Thus, the main cause for the reduced PRL response to estrogen in lactating rats seems not to be in the pituitary gland but in the brain. Progesterone, which is know to induce a PRL surge in ovariectomized estrogen-primed rats by acting on the mediobasal hypothalamus, also failed to evoke a PRL surge in lactating rats. Recovery from the inhibitory influence of suckling on PRL response to EB followed a time course similar to that observed in response to immobilization stress or to morphine injection; estrogen-induced PRL surge started to recover at 6 days and was almost fully recovered 8 days after weaning. These facts indicate that suckling stimuli may cause functional alterations in the neural systems responsible for PRL release, resulting in refractoriness of the PRL response to ovarian steroids.
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It has been shown that the stimulatory feedback effects of ovarian hormones on LH release in ovariectomized rats can be blocked by selective inhibition of epinephrine (EPI) synthesis. The purpose of these experiments was to characterize further the role of central and/or peripheral EPI systems in the neural regulation of LH, GH, and PRL secretion in the female rat. Ovariectomized rats were treated with either oil vehicle or a sequential, stimulatory estradiol plus progesterone regimen. Animals in each condition were pretreated with saline vehicle, centrally active EPI synthesis inhibitors (SK & F 64139 or SK & F83593), or SK & F 29661, an EPI synthesis inhibitor that does not cross the blood-brain barrier. The centrally active EPI antagonists blocked the surge of LH, but not the increase in PRL, that occurred after estrogen plus progesterone treatment. These drugs also decreased hypothalamic concentrations of EPI without affecting the other catecholamines. The peripherally active SK & F 29661 did not prevent either LH or PRL surges and did not affect hypothalamic catecholamines. None of the compounds affected LH or PRL concentrations in oil-treated, ovariectomized rats. Neither SK & F 64139 nor SK & F 29661 altered the pulsatile release of LH in ovariectomized, hormonally untreated rats, but SK & F 64139 completely blocked the episodic secretion of GH. The release of LH in response to iv LHRH was minimally affected after EPI synthesis inhibition. SK & F 64139 did not prevent the afternoon rise in PRL induced by estradiol. These experiments indicate that 1) central EPI systems may mediate the positive feedback actions of ovarian hormones on LH secretion, but not the estrogen-induced increase in PRL secretion; 2) central adrenergic systems are involved in the regulation of episodic GH secretion; and 3) central EPI systems do not appear to be involved in the neural regulation of pulsatile LH secretion.
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The effects of estrogen (E) and progesterone (P) on synthesis rates and endogenous levels of hypothalamic norepinephrine (NE) and dopamine (DA) were determined in individual ovariectomized (OVX) rats. 3H-tyrosine (3H-T) was injected intra-arterially and the rate of its incorporation into 3H-DA and 3H-NE was determined at 10, 15, 30, and 45 min. Steroid treatment for 2 days effectively decreased plasma LH levels and elevated plasma prolactin (Prl) levels while endogenous levels of NE and DA were not affected. NE synthesis was not affected by steroid treatment. A significant increase in DA synthesis was correlated with low plasma LH levels, suggesting that DA inhibits LH release. The elevated plasma Prl levels seen in steroid-treated rats were correlated with increased DA synthesis in the hypothalamus. This may indicate that elevated plasma Prl levels stimulate dopaminergic neurons in a short-loop negative feedback fashion.
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