Castration of Male Rats Reduces the Capacity of Granules Isolated from the Median Eminence to Secrete Luteinizing Hormone-Releasing Hormone in Response to Copper

Barnea, Ayalla; Cho, Gloria

doi:10.1159/000124169

Cited by 13 publications

(5 citation statements)

References 18 publications

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“…This finding is in accord with several reports in the rat (Kalra & Kalra, 1986;Kalra et al 1987). It is possible that the decreased rate of GnRH release may be a consequence of reduced GnRH avail¬ able for release, since depolarization-evoked release of GnRH was smaller from the median eminences of ovariectomized animals, as proposed for the castrated male rat (Barnea & Cho, 1985). Similarly, in the female rat, the release of GnRH from hypothalami obtained from ovariectomized animals has been reported to be lower than that of intact females (Ramirez, Dluzen & Liu, 1980) with gonadal steroid replacement therapy augmenting GnRH release both in vivo and in vitro (Levine & Ramirez, 1980;Kim & Ramirez, 1982;Leadem & Kalra, 1984).…”

Section: Discussionsupporting

confidence: 92%

Endogenous opioid peptide modulation of LH secretion in the ewe lamb: possible involvement of 5-hydroxytryptamine

Stansfield

Knight²,

Howles³

et al. 1988

Journal of Endocrinology

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Evidence from several species suggest that the endogenous opioid peptides participate in the regulation of gonadotrophin and prolactin secretion. The aim of the present study involving intact and ovariectomized prepubertal ewe lambs was to compare the effects in vivo of an opioid peptide agonist [D-Ala2,N-Phe4,Met(0)ol5]-enkephalin (FK 33-824) and antagonist, naloxone, on concentrations of LH and prolactin in plasma, and levels of neurotransmitter metabolites in cerebrospinal fluid (CSF), with their effects in vitro on the release of gonadotrophin-releasing hormone (GnRH) and neurotransmitters from isolated median eminences. Infusion of FK 33-824 (0.5 mg/30 min) in vivo depressed plasma LH levels in both intact and ovariectomized lambs; this effect could be reversed by naloxone. In ovariectomized lambs, the inhibitory action of FK 33-824 on plasma LH levels was associated with a 13% rise in the concentration of the metabolite of 5-hydroxytryptamine, 5-hydroxyindolacetic acid (5-HIAA). Concurrent administration of naloxone resulted in an abrupt 33% fall in CSF levels of 5-HIAA. No significant changes in plasma concentrations of prolactin or CSF concentrations of the metabolites of dopamine were observed in response to the administration of FK 33-824 or FK 33-824 plus naloxone. That FK 33-824 inhibited LH release through a central mechanism was confirmed using superfused median eminences in vitro. Thus FK 33-824 (1 mumol/l) greatly diminished the release of GnRH induced by the introduction of a depolarizing stimulus (36 mmol K+/l) in tissue obtained from both intact and ovariectomized ewe lambs.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 92%

Endogenous opioid peptide modulation of LH secretion in the ewe lamb: possible involvement of 5-hydroxytryptamine

Stansfield

Knight²,

Howles³

et al. 1988

Journal of Endocrinology

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“…A decrease in MBH and/or ME GnRH in response to long-term ovariectomy has been noted in the mouse (Briski et al, 1983), rat (Culler et al, 1982) and sheep (Wheaton, 1979). These results were initially interpreted as an increased release of the peptide under these conditions (Tytell et al, 1980;Millar et al, 1981;Shivers et al, 1983), but others have found an inhibition of GnRH release (Dluzen & Ramirez, 1985, 1986 or a decrease in the amount of peptide available for release (Barnea & Cho, 1985) after gonadectomy. Polkowska et al (1980) noted that ovariectomy increased the numbers of GnRH-immunoreactive granules in the ME of the sheep.…”

Section: Discussionmentioning

confidence: 99%

Immunoassay of gonadotrophin-releasing hormone in brain tissue of Booroola Merino ewes

Gale¹,

Smith²,

Truman³

et al. 1988

Reproduction

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The presence of a fecundity gene (F) in Booroola Merino ewes increases the ovulation rate. To test how F gene expression affects the gonadotrophin-releasing hormone (GnRH) concentration in hypothalamic or extrahypothalamic regions of the brain, GnRH was measured by radioimmunoassay in acetic acid extracts of various brain tissues from Booroola ewes which were homozygous (FF), heterozygous (F+) or non-carriers (++) of the F gene. The GnRH concentration in brain tissues from FF, F+ and ++ animals which had been ovariectomized 5 months previously was also evaluated. No significant F gene-specific differences were noted in any of the brain areas tested, in intact or ovariectomized animals. However, in ovariectomized ewes, the concentrations of GnRH increased about 2-fold in the median eminence of the hypothalamus, remained unchanged in the medial basal hypothalamus and dropped to less than 10% of the values in intact ++ animals in the preoptic area. These studies suggest that the changed pituitary sensitivity and increased gonadotrophin release in Booroolas carrying the F gene(s) is not attributable to increased hypothalamic GnRH concentrations in these animals.

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“…Two subcellular loci contain copper-interactive sites that could be regulated by androgens: the plasma membrane and the secretory granule membrane. Since cas tration of male rats does not alter the apparent Km of the granule-interactive sites for copper, and since castration does not alter the Vmax of copper-stimulated LHRH re lease [3], it becomes apparent that the granule-interactive sites are not the sites of androgen regulation in the process of copper-stimulated release of LHRH. Therefore, we con clude that androgens increase the responsiveness of the LHRH neuron to the stimulatory action of copper by in creasing the affinity to copper of the plasma membrane in teractive sites.…”

Section: Discussionmentioning

confidence: 99%

“…Since the median eminence content of LHRH is a function of the steroid milieu of the donor rat (table I) [1,3,11,16,[30][31][32], it becomes apparent that the maximal releasable amount of LHRH, i.e., the size of the releasable pool of LHRH, is re flective of the tissue content of the peptide. Our observa tions that the size of the releasable pool is steroid-depend ent and is proportional to the median eminence content of LHRH, but that this proportionality is steroid-independent, are consistent with the proposition [3,15,17] that the an drogen-related increase in the median eminence LHRH content is due primarily to an increase in the production and packaging of LHRH and not to a decrease in LHRH release. Thus, an important mechanism by which andro gens increase the secretory capacity of the LHRH neuron is by increasing the size of the releasable pool of LHRH in the LHRH neuron.…”

Section: Discussionmentioning

confidence: 99%

“…It can be envisioned that the amounts of LHRH released from the LHRH neuron in response to a specific stimulus such as copper is determined by the size of the re leasable pool of LHRH and by the affinity and/or number of copper-interactive sites on the LHRH secretory granule itself or on the plasma membrane of the neuron. We [3] have previously investigated the effects of castration of male rats on the Michaelis-Menten kinetic constants (Km) of the pro cess of copper-stimulated release of LHRH from isolated LHRH granules and found that neither the apparent Km for copper nor the percent of total granule content released (Vmax) of LHRH release were affected. These results are supportive of our proposal that the secretory granule itself is not a primary site of steroid regulation of LHRH release in response to copper.…”

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confidence: 99%

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Effects of Castration and Maturational Age of Male Rats on the Process of Copper-Stimulated Release of Luteinizing Hormone Releasing Hormone from Median Eminence Explants: Evidence that Androgens Increase the Affinity of the Copper-Interactive Sites for Copper

Colombani-Vidal¹,

Barnea²

1985

Neuroendocrinology

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We have previously shown that chelated copper stimulates the release of luteinizing hormone releasing hormone (LHRH) from explants of the median eminence area (MEA) incubated under in vitro conditions and that this stimulation involves a ligand-specific interaction. In this study, we addressed the question: do testicular steroids regulate the secretory response of LHRH neurons to copper? MEA, obtained from immature, mature, immature castrated and sham-operated rats, were incubated in the presence of various concentrations of copper for 15 min and then in the absence of copper for an additional period of 30 min. We noted that after a lag period of 5 min of incubation, the rate of LHRH release increased in a linear fashion for a period of 15 min. In addition, the rate of LHRHrelease as well as the rate at which LHRH release was accelerated were saturable functions of the concentration of copper. When incubation was carried out in the presence of a nonsaturating concentration of copper (50 µM), the fractional amount (percent of the total MEA content) of LHRHreleased from the MEA of castrated rats was significantly (p < 0.001) lower than that from sham-operated rats; stimulated release being 0.9% and 1.4%, respectively. Similarly, copper-stimulated release from the MEA of immature rats was lower than that from the MEA of mature rats. However, when incubation was carried out in the presence of saturating concentrations of copper (100 or 200 µM), the precentage of stimulated release from the MEA of castrated rats was similar to that of sham-operated rats and it was about 2.8%. In addition, we found that LHRHcontent of the MEA of immature and castrated rats was significantly lower than that of mature and sham-operated rats, respectively. To estimate the size of the releasable pool of LHRHin the MEA of these animals, we maximally stimulated LHRH release with 60 mM K⁺. It was found that, regardless of the physiological state of the animals, about 2.6% of the MEA content was released. These results suggest that: (1) copper interacts with a limited number of sites on the LHRH neuron; (2) testicular steroids regulate the process of copper-stimulated release of LHRH by increasing the affinity of these interactive sites to copper; (3) testicular steroids increase the size of the releasable pool of LHRH in the median eminence, and (4) the size of the releasable pool is proportional to the MEA content of the peptide and this proportionality is not steroid-dependent. We propose that testicular steroids regulate two important aspects of the secretory function of the LHRH neuron: the capacity of the neuron to release LHRH and the affinity of the copper-interactive sites for copper.

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Castration of Male Rats Reduces the Capacity of Granules Isolated from the Median Eminence to Secrete Luteinizing Hormone-Releasing Hormone in Response to Copper

Cited by 13 publications

References 18 publications

Endogenous opioid peptide modulation of LH secretion in the ewe lamb: possible involvement of 5-hydroxytryptamine

Endogenous opioid peptide modulation of LH secretion in the ewe lamb: possible involvement of 5-hydroxytryptamine

Immunoassay of gonadotrophin-releasing hormone in brain tissue of Booroola Merino ewes

Effects of Castration and Maturational Age of Male Rats on the Process of Copper-Stimulated Release of Luteinizing Hormone Releasing Hormone from Median Eminence Explants: Evidence that Androgens Increase the Affinity of the Copper-Interactive Sites for Copper

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