Gonadotrophin-binding sites in the ovary of aged rats.
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Aging↗
Biomedical subjects
J Meites
Publications and source records attributed to J Meites.
Relation between prolactin and gonadotrophin secretion in post-partum lactating rats.
In post-partum lactating rats, sucking by the young was associated with high prolactin release and maintenance of lactation but severe inhibition of LH and FSH release and suspension of oestrous cycles. Shortly after the pups were removed on day 22 post partum LH and FSH release returned to normal and oestrous cycles resumed. Twice-daily injections of ergocornine methanesulphonate (ERG) into mothers beginning at 5 or 7 days post partum, resulted in sustained inhibition of prolactin release and diminished mild secretion. By frequent exchange of pups between control and ERG-treated mothers, it was possible to maintain vigorous sucking and almost normal pup growth despite low serum prolactin levels and diminished lactation. In these rats, serum levels of LH remained low during 11 or more days of treatment with ERG, but serum FSH was consistently higher than in untreated control mothers. After 11 or more days of ERG treatment, most rats showed a return to normal LH and FSH release and resumption of oestrous cycles. These results suggest (a) that the sucking stimulus rather than high prolactin levels in the circulation is mainly responsible for inhibition of LH and FSH release during the first 11 days post partum, (b) that the sucking stimulus acts to increase prolactin and inhibit LH release by separate hypothalamic mechanisms, and (c) that administration of ERG results in diminished prolactin release and lactation, and in increased release of FSH and subsequently of LH with earlier resumption of oestrous cycles.
Animals↗
Stimulation of prolactin release in rats by GABA.
Infusion of GABA into the lateral ventricle of intact female rats on the morning of proestrus and in ovariectomized rats significantly stimulated PRL release. This response apparently is not mediated through a direct action on the pituitary since injection of GABA into hypophysectomized rats with a pituitary transplant under the kindney capsule did not alter serum prolactin levels. These observations suggest that GABA may have a role in regulating prolactin secretion.
Aminobutyrates↗
Effects of aging on LH and prolactin after LHRL L-dopa, methyl-dopa, and stress in male rat.
Hypothalamic-pituitary control of prolactin and LH secretion was tested in young (4-6 months) and aged (22-30 months) male Long-Evans rats given L-dopa, methyl dopa, LHRH, or stress treatments. Pretreatment serum LH levels were consistently higher in young than in the aged groups. The increase in serum LH after LHRH injection was only about half as much in aged as compared to young control males. Although acute stress caused a prompt increase in serum LH in young male rats, this treatment was without effect in the aged group. Methyl dopa treatment stimulated serum prolactin secretion in both young and old rats. Although L-dopa treatment caused a reduction in serum prolactin in both age groups, the sensitivity, magnitude, and duration of the reduction was smaller in the aged rats.
Aging↗
Effects of hypo- and hyperthyroidism on 5-hydroxytriptophan and chlorpromazine- induced prolactin release in the rat.
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5-Hydroxytryptophan↗
The effect of stress on serum prolactin in the female rat.
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Animals↗
Estrogen and prolactin receptor concentrations in rat mammary tumors and response to endocrine ablation.
Estrogen and prolactin receptor concentrations were measured in 24 carcinogen-induced rat mammary tumors and correlated with the tumor response to host ovariectomy or hypophysectomy. It was found that essentially all of the tumors contained some specific estrogen receptor, and all but three contained prolactin receptor. The values for each receptor comprised a continuum from very low to relatively high concentrations, suggesting that previous considerations of hormone dependence on the basis of presence or absence of hormone receptors may be oversimplified. The concentration of each receptor tended to be lower in the hormone-independent than in the hormone-dependent tumors, but there were a number of hormone-independent tumors with higher receptor levels than some of the hormone-dependent tumors had. A better correlation of tumor response to endocrine ablation resulted from a combination of the 2 receptor levels than from either receptor concentration alone. These results suggest that there is a complex relationship between mammary tumor response to endocrine ablatin and levels of estrogen and prolactin receptors and that some tumors may be dependent upon 1 or both of these hormones for growth.
9,10-Dimethyl-1,2-benzanthracene↗
Prolactin and estrogen dependency of rat mammary cancers at early and late stages of development.
An attempt was made to separate estrogen from prolactin dependency of 7,12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary tumors at 2.5 and 5 months after DMBA injection. Ovariectomy and drug and/or hormone treatments were used to produce an estrogen or prolactin deficiency for 2 weeks, followed by a 2-week period in which the deficiency was corrected. Tumors were classified as estrogen or prolactin dependent based upon regression in the absence of the hormone and resumption of growth upon hormone replacement. At 2.5 months and 5 months after DMBA injection, about 29 and 33% of the tumors, respectively, were classified as prolactin dependent, and 35 and 45%, respectively, were classified as estrogen dependent. However, the percentage of estrogen-dependent tumors was reduced to 2.2 and 9.7%, respectively, when prolactin levels were maintained after ovarierctomy. These results indicate that most DMBA-induced mammary tumors in Sprague-Dawley female rats are dependent on both estrogen and prolactin but that ovariectomy or estrogen administration do not accurately reflect estrogen dependency, since prolactin secretion also is altered by these procedures.
9,10-Dimethyl-1,2-benzanthracene↗
Stimulation of carcinogen-induced mammary tumor growth in rats by adrenalectomy.
The effect of adrenalectomy on 7,12-dimethylbenz(a)anthracene-induced mammary tumor growth was studied in Sprague-Dawley female rats. Weekly measurements revealed that adrenalectomy significantly increased both mammary tumor size and number and elevated serum prolactin levels as compared to the intact controls. Daily injection of 1 mg hydrocortisone acetate into the intact 7,12-dimethylbenz(a)anthracene-tumor bearing rats did not significantly alter tumor size, number, or serum prolactin levels but, when injected into adrenalectomized rats, it prevented increased tumor growth and prolactin release. Daily injection of ovine prolactin and hydrocortisone suppressed endogenous prolactin release but significantly increased tumore size and number. Ergocornine, a prolactin-inhibiting drug, blocked adrenalectomy-induced tumor growth and partially blocked prolactin release. These results indicate that adrenalectomy in rats stimulates tumor growth by increasing prolactin release.
9,10-Dimethyl-1,2-benzanthracene↗
Effects of high hoses of estrogen on prolactin-binding activity and growth of carcinogen-induced mammary cancers in rats.
Specific binding sites for prolactin (PRL) were present in membrane preparations from 7,12-dimethylbenz(a)-anthracene-induced rat mammary tumors. The specific binding of PRL was time and temperature dependent. A significant negative correlation was noted between administered doses of estrogen and the subsequent binding of PRL to tumor cell membranes. Injections of 10 or 25 mug estradiol benzoate daily for 10 days effectively inhibited mammary tumor growth and significantly reduced specific PRL binding to mammary tumor cell membranes.
9,10-Dimethyl-1,2-benzanthracene↗
Role of biogenic amines in the control of prolactin and growth hormone (GH) secretion.
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Animals↗
Prolactin binding activity on the crop sacs of juvenile, mature, parent and prolactin-injected pigeons.
Specific prolactin (PRL) binding activity of lactoperoxidase catalyzed 125I-labeled ovine-PRL was determined in a membrane-rich particulate fraction of pigeon crop sacs. Levels of TSH, LH or FSH as high as 1000 ng each were unable to displace the 125I-o-PRL bound to 600 mug of crop sac microsomal protein, whereas competitive displacement was achieved with as little as 0.5 ng unlabeled PRL. Ovine GH exhibited some cross reactivity when incubated in amounts greater than 500 ng, but this could be accounted for by its stated PRL contamination. Specific PRL binding activities were determined in juvenile and mature pigeons with unstimulated crop sacs, and parent pigeons with 'crop milk' and mature birds injected with PRL for 4 days. Crop sacs from juvenile birds contained approximately twice as much binding activity as crop sacs from mature pigeons. Parent and PRL injected pigeons, each with proliferated crop sac epithelium, exhibited 4-5 times as much specific PRL binding as the non-proliferated crops from juvenile or mature birds. These results show that the pigeon crop sac contains specific binding sites for PRL, and that the crop sac response to PRL is associated with an increase in PRL binding activity.
Age Factors↗
Reproductive capacity of aging female rats.
Multiparous female Long-Evans rats, 20 months or older, were seen to progress from irregular estrous cycles to a constant-estrous syndrome to a series of irregular pseudopregnancies to an anestrous state. An animal in constant estrus was characterized by ovaries with well developed and sometimes cystic follicles, no corpora lutea, an estrogen-stimulated uterus, and an anterior pituitary that appeared normal. Repeatedly pseudopregnant rats had long diestrous periods of variable length, ovaries with many corpora lutea, uteri with numerous secretory glands, and anterior pituitaries that often showed hemorrhagic or small tumorous areas. Anestrous rats had small, atrophic ovaries with no obvious follicular or luteal elements, atrophic uteri, and large pituitary tumors. Twice-daily injections of L-dopa induced the resumption of regular or irregular estrous cycles in most constant-estrous but not in pseudopregnant or anestrous rats.
Aging↗
Effects of biogenic amines and TRH on release of prolactin and TSH in the rat.
The effects of a single injection of drugs on serum prolactin and TSH were determined in male and in estrogen-primed ovariectomized rats. The precursor of serotonin, 5-hydroxytryptophan(5-HTP), produced a significant rise in serum prolactin and TSH, whereas para chloroamphetamine, a depletor of serotonin, elicited a fall in serum prolactin and TSH. alpha-methylmetatyrosine (alpha-MMT) and reserpine, both depressors of brain catecholamine (CA) and serotonin levels, evoked significant increases in serum prolactin and reductions in serum TSH. Injection of alpha-MMT or reserpine together with 5-HTP further elevated serum prolactin but prevented any significant change in serum TSH. This suggests that the ability of alpha-MMT and reserpine to inhibit TSH release is mediated through a reduction in brain serotonin and not via a decrease in CA. alpha methylparatyrosine, which inhibits CA synthesis without altering serotonin, evoked a marked increase in serum prolactin but had no effect on serum TSH. L-dopa administration significantly reduced serum prolactin values but had no significant effect on serum TSH. Synthetic TRH increased both serum prolactin and TSH levels in male rats, but when it was injected after L-dopa administration, it did not elicit any rise in serum prolactin and evoked the same increase in serum TSH. This suggest that L-dopa acts directly or indirectly on the pituitary prolactin cells to inhibit TRH stimulation of prolactin release, but does not influence the action of TRH on pituitary TSH cells. Pilocarpine decreased serum prolactin, but had no significant effect on serum TSH values. The present study suggests that only serotonergic drugs produce similar effects on release of prolactin and TSH, whereas drugs that alter CA and pilocarpine depress prolactin release but have little or no effect of TSH.
5-Hydroxytryptophan↗
Effects of acute stress on serum LH and prolactin in intact, castrate and dexamethasone-treated male rats.
The effects of handling, ether vapor anesthesia and blood sampling on serum LH and prolactin were determined in intact, castrate and dexamethasone-treated male rats. Cage removal and transport to an adjacent room increased LH and prolactin levels by 10 and 15 min after the initial animal disturbance. Intact male rats subjected to repeated ether anesthesia and blood sampling showed a more rapid increase in serum LH and prolactin than the preceding rats, since serum LH and prolactin was increased by 4, 8 and 15 min after initial cage disturbance. In a group of rats subjected to serial blood sampling over a longer time interval, both prolactin and LH levels remained higher than 90 min after initial animal handling. At 90 minutes after a single blood sampling, blood prolactin concentration remained higher than in controls. Serum LH levels returned to control levels 90 min after the stress of a single blood sampling. Although serum prolactin was increased in the castrate group subjected to serial anesthesia and blood sampling, LH concentrations were reduced under the same conditions. Injection of 5 and 50 mug of dexamethasone/100 g body wt for 8 days markedly reduced adrenocortical responsiveness to the stress of serial anesthesia and blood sampling at 1, 4, 8 and 15 min after initial rat disturbance. The 50 mug dexamethasone treatment reduced the stress-stimulated increase in serum prolactin at all blood sampling intervals. The dexamethasone-treated groups also showed smaller increases in serum LH at 8 and 15 min after first animal handling than the control rats. These results indicate that serum LH and prolactin concentrations are consistently increased by acute stress in intact male rats, the duration of the stress stimulation of LH and prolactin is at least 90 min under the conditions of this study, serum LH levels of castrate male rats are decreased by acute stress and dexamethasone administration lowers stress stimulation of LH and prolactin release.
Anesthesia↗
Effects of thyroid and ovaries on prolactin binding activity in rat liver.
125I-radiolabeled ovine prolactin (oPRL) binding activity was measured in microsomal membranes of liver tissue from intact, ovariectomized, ovariectomized-thyroidectomized, and ovariectomized-thyroidectomized rats injected with thyroxine (T4) or estradiol benzoate (EB). Thyroidectomy and ovariectomy each reduced PRL binding activity in liver tissue significantly. The combination of ovariectomy and thyroidectomy decreased PRL binding activity more than thyroidectomy or ovariectomy alone. Doses of 2.5 mug or 10 mug T4/100 g BW daily returned PRL binding activity in the thyroidectomized rats to intact control values, and in the ovariectomized-thyroidectomized rats to the ovariectomized values. A dose of 2 mug EB/rat increased PRL binding activity significantly in ovariectomized-thyroidectomized rats, and a combination of 2 mug EB and 2.5 mug T4/100E that of intact controls. Scatchard analysis showed that ovariectomy and thyroidectomy decreased the number of PRL binding sites in the liver as compared to those in intact controls or in ovariectomized-thyroidectomized rats treated with EB and T4. It is concluded that the thyroid and ovaries are important regulators of PRL binding activity in the liver of the rat.
Animals↗
Age-related changes in pituitary responsiveness to LHRH in the female rat.
Serum LH changes in response to LH-releasing hormone (LHRH) injection were measured in young (4-6 month-old) proestrous, estrous, and second-day-diestrous rats and in aged(23-30-month-old) constant estrous and irregular pseudopregnant (prolonged diestrus) female Long-Evans rats. Serum LH was measured by radioimmunoassay in serial blood samples taken before and at 15, 30 and 60 min after injection of 0, 5, 50 or 500 ng of LHRH. Serum LH also was assayed in similar groups of rats acutely pretreated with either 20 mug of estradiol benzoate (EB) or 5 mg of progesterone. Aged rats showed a smaller increase in serum LH following LHRH injection than the young groups. Within the young groups, the magnitude of response was greater in proestrous and estrous rats than in the diestrous animals. Pretreatment with EB resulted in increased serum LH after LHRH injection in young estrous and diestrous rats and in aged constant estrous rats, but did not alter serum LH levels in the aged pseudopregnant rats. Although the inccrease in serum LH after LHRH injection was greater in all young groups given progesterone pretreatment, progesterone pretreatment did not affect LHRH responsiveness in either of the aged groups. These results suggest that with aging, the pituitary becomes less capable of relasing LH in response to acute LHRH stimulation, and that the pituitaries of aged rats are less responsive to gonadal steroid sensitization to LHRH stimulation.
Aging↗
Effects of hyper- and hypothyroidism on serum LH and FSH levels in intact and gonadectomized male and female rats.
The effects of hypo- and hyper-thyroidism on serum LH and FSH were determined in both intact and castrated male and female rats. Thyro-parathyroidectomy (Tx) for 30 days in rats with intact gonads resulted in a significant reduction in serum LH and FSH, and also in a decrease in serum testosterone in males. Administration of 2.5 mug thyroxine (T4)/100 g BW to Tx rats of both sexes returned serum LH and FSH levels to those of intact rats, and in males also restored normal serum testosterone levels. Tx superimposed upon castration resulted in a significantly greater increase in serum LH and FSH than produced by castration alone. Administration of 2.5 mug T4/100 g body weight to castrate-Tx rats reduced serum LH and FSH values to those of castrate rats, whereas 10 mug T4/100 g BW evoked a further decrease in serum LH but no additional reduction in serum FSH. When both 2.5 mug T4/100 g BW and 2 mug estradiol benzoate were injected into Tx-ovariectomized rats, the decrease in serum LH and FSH was much greater than produced by T4 alone. These observations indicate that hypothyroidism results in decreased release of LH and FSH in rats with intact gonads, and in increased release of LH and FSH in castrate rats of both sexes. Administration of a replacement dose of T4 can restore LH and FSH release to normal in Tx rats with intact gonads, and to castration levels in Tx-castrate rats.
Animals↗