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Biomedical subjects

J Meites

Publications and source records attributed to J Meites.

At least 145 records · Page 8Linked to original sources
PubMed1977

Effects of starvation in rats on serum levels of follicle stimulating hormone, luteinizing hormone, thyrotropin, growth hormone and prolactin; response to LH-releasing hormone and thyrotropin-releasing hormone.

Adult male Sprague-Dawley rats averaging 300 g each were subjected to complete food removal for 7 days (acutely starved), 7 days complete food removal followed by 2 weeks of 1/4 ad libitum food intake (chronically strved), 7 days complete food removal and 2 weeks of 1/4 ad libitum intake followed by ad libitum feeding for 7 days (refed), or fed ad libitum throughout (controls). Serum LH, FSH, TSH, PRL, and GH levels were measured by radioimmunoassays for each group of rats. The in vivo response to the combination of synthetic LHRH and TRH also was tested in each group of rats. Circulating LH, TSH, GH, and PRL were significantly depressed in acutely and chronically starved rats, and FSH was lowered only in acutely starved rats. After 7 days of refeeding, serum levels of LH and FSH were significantly greater than in ad libitum fed controls, PRL returned to control levels, and TSH and GH increased but were still below control levels. After LHRH + TRH injection serum LH and TSH were increased significantly in all groups of rats, FSH and PRL rose in acutely but not in chronically starved rats, and GH was not elevated in any group. The increases in serum LH, FSH, TSH and prolactin in response to LHRH + TRH injection in acutely or chronically starved rats were equal to or greater than in the ad libitum fed controls. These data indicate that severe reductions in food intake result in decreased release of at least 5 anterior pituitary hormones, and this is due primarily to reduced hypothalamic stimulation rather than to inability of the pituitary to secrete hormones.

Adrenal Glands↗
PubMed1977

Evidence for depressed catecholamine and enhanced serotonin metabolism in aging male rats: posssible relation to gondotropin secretion.

The steady state concentration of dopamine (DA), norepinephrine (NE), and serotonin (5HT) was determined and turnover estimated in several brain regions of young (3-4 months) and old (21 months) male Wistar rats. An estimate of DA and NE turnover was obtained by determining their depletion rates after treatment with alpha-methylpara-tyrosine, a tyrosine hydroxylase inhibitor. Serotonin turnover was estimated by determining its rate of increase after monoamine oxidase inhibition with pargyline. In old males, medial basal hypothalamic (MBH) DA concentration and depletion rate were significantly lower than in young males. DA concentration of the remaining hypothalamus also was lower in old than in young males, but depletion rates were not different. DA concentration and depletion rate in the olfactory tubercle were the same in both age groups. The steady state concentration of NE in the MBH and remaining hypothalamus, and the hypothalamic NE depletion rate, were significantly lower in old than in young animals. In both brain and hypothalamus, steady state concentrations of 5HT were the same in young and old rats, but by 30 min after monoamine oxidase inhibition with pargyline, hypothalamic, but not brain, 5HT increased more in old than in young males. This may indicate a greater turnover of 5HT in the hypothalamus of old than of young males. In non-drug treated (control) old male rats, serum LH and FSH were lower, serum prolactin was higher and serum TSH was the same in young male rats. These data suggest that a decrease in catecholamine and an increase in serotonin metabolism occur in the hypothalamus of old male rats. These changes may be related to the decrease in release of gonadotropins and increase in release of prolactin observed in these old male rats.

Aging↗
PubMed1977

Stimulation of growth of carcinogen-induced mammary cancers in rats by thyrotropin-releasing hormone.

Twice-daily injections of three different doses of synthetic thyrotropin-releasing hormone (TRH), a hormone normally produced by the hypothalamus, produced significant increases in size and number of 7,12-dimethylbenz(a)anthracene-induced mammary cancers over 0.87% NaCl solution-injected control rats. When thyroidectomized rats, bearing 7,12-dimethylbenz(a)anthracene-induced mammary tumors were given the same twice-daily injections of TRH, mammary tumor growth was increased to the same extent as in intact rats given TRH, showing that the effects of TRH were not exerted via stimulation of thyroid function. The TRH-induced increments in mammary tumor growth were accompanied by significant increases in serum prolactin levels over 0.87% NaCl solution-injected controls. A single daily injection of 2-bromo-alpha-ergocryptine (CB-154), a prolactin-release inhibitor completely blocked TRH-induced mammary tumor growth and reduced serum prolactin values. These results indicate that a twice-daily pulse of TRH can stimulate mammary tumor growth by releasing prolactin from the anterior pituitary.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1976

Effects of estrogen and testosterone on specific prolactin binding in the kidneys and adrenal of rats.

The effects of estradiol benzoate in the female rat, testosterone propionate in the male rat, and castration in both sexes on specific prolactin binding sites in the particulate membranes of the kidneys and adrenals were studied. Castration resulted in a significant increase in PRL binding activity in the kidneys of both males and females, and in a significant increase in PRL binding activity in the adrenals of the females. The increase in PRL binding with castration and the decrease seen with testosterone treatment were similar in both immature and mature rats. Progesterone administration to castrate females failed to alter PRL binding in both tissues. The present results suggest that estrogen and testosterone participate in the PRL osmoregulatory system in rat.

Adrenal Glands↗
PubMed1976

Induction of estrous cycles in old non-cyclic rats by progesterone, ACTH, ether stress or L-dopa.

Cycling was induced in old non-cyclic, constant estrous rats by daily injections of progesterone, ACTH or L-dopa or by subjection to ether stress. Progesterone and ACTH were the most effective agents used for re-establishing estrous cycles in these rats. Most of the progesterone- and ACTH-treated rats showed regular cycles, and their ovaries had many corpora lutea; they also showed proestrous serum LH surges. Ether stress and L-dopa mostly induced irregular cycles and fewer corpora lutea in the ovaries; a smaller number of these rats showed proestrous LH surges. After treatment with each of these agents was discontinued, most of the rats returned to constant estrus or irregular cycling.

Adrenocorticotropic Hormone↗
PubMed1976

Differential effects of dopamine agonists and haloperidol on release of prolactin, thyroid stimulating hormone, growth hormone and luteinizing hormone in rats.

The dose-response effects of apomorphine and ET-495 (piribedil), 2 specific dopamine (DA) receptor stimulators, and haloperidol, a DA receptor blocker, were tested on the secretion of prolactin (PRL), thyroid stimulating hormone (TSH), growth hormone (GH) and luteinizing hormone (LH) in male rats. Both apomorphine and piribedil reduced serum PRL and TSH levels, stimulated GH release at low but not at high doses and either had no effect or tended to reduce serum LH levels. The minimal effective dose of apomorphine for reducing PRL by 30 min was 0.01 mg/kg; TSH inhibition was observed with a dose of 0.1-0.3 mg/kg. The inhibitory effects of apomorphine (1.0 mg/kg) on PRL and TSH levels were maximal by 15 min and diminished by 120 min; plasma GH was highest 120 min after injection. Thyroidectomy (10 days) markedLH elevated serum TSH, had no effect on serum PRL and inhibited the ability of apomorphine (0.1 or 0.3 mg/kg) to reduce TSH but not PRL levels. These observations may indicate that separate dopaminergic control mechanisms exist for TSH and PRL secretion. Administration of haloperidol elevated serum PRL, tended to lower TSH, dramatically reduced GH and had no effect on LH levels. Haloperidol pre-treatment blocked the effects of apomorphine on PRL, TSH, and GH secretion. The overall results of this study indicate that DA agonists inhibit PRL and TSH, stimulate GH but do not stimulate LH release in male rats.

Animals↗
PubMed1976

Selective actions of prolactin on catecholamine turnover in the hypothalamus and on serum LH and FSH.

The effects of prolactin (PRL) administration on catecholamine turnover in various brain regions of ovariectomized rats were determined by observing the decline of dopamine and norepinephrine concentrations after alpha-methyltyrosine (alphaMT) administration. PRL had no effect on the steady state concentration of dopamine in the median eminence, anterior hypothalamus and corpus striatum or on the norepinephrine concentration in the anterior hypothalamus. However, PRL selectively enhanced dopamine turnover in the median eminence and anterior hypothalamus after a latent period of 10-26 h. In addition, PRL administration significantly decreased serum concentrations of LH and FSH. These results suggest that the PRL-induced increase in activity of dopaminergic neurons in the median eminence or anterior hypothalamus may be responsible for the reduction of the post-castration rise in serum concentrations of LH and FSH.

Animals↗
PubMed1976

Effects of castration, testosterone, estradiol, and prolactin on specific prolactin-binding activity in ventral prostate of male rats.

Lactoperoxidase-catalyzed 125I-labeled ovine prolactin (PRL) was found to bind specifically to particulate membrane fractions of rat ventral prostate. Unlabeled PRL readily displaced the labeled PRL, whereas ovine GH, LH, FSH, or TSH showed no such competition. Castration reduced the binding of 125I-labeled PRL to about 1/6 of that in intact rats, and injections of testosterone propionate (TP) increased PRL binding to values as great or greater than those in intact controls. Injections of TP into intact immature and mature rats also increased PRL binding. In vitro binding of labeled PRL was inhibited in prostatic tissue removed from intact immature rats 2 h after injecting unlabeled PRL, but not in ventral prostates from rats killed 26 or 74 h after injecting unlabeled prolactin. PRL injected together with TP in castrated rats produced no greater increase in prolactin binding than TP alone, while estrogen appeared to decrease PRL binding beyond that produced by castration alone.

Animals↗
PubMed1976

Reduced luteinizing hormone release by synthetic luteinizing hormone-releasing hormone (LHRH) in postpartum lactating rats.

The ability of the pituitary to release LH in response to synthetic LHRH was tested in lactating female rats on days 7 and 17 post partum, and compared with that of normal cycling female rats on diestrous day 2 (controls). Three consecutive injections of LHRH (100 ng/100 g BW, sc), each 50 min apart, were given to each rat and sequential blood samples were collected at 25-min intervals by cardiac puncture under light ether anesthesia. In all 3 groups, the 2nd and 3rd injections of LHRH produced much greater increases in serum concentrations of LH than the 1st injection. However, this self-priming effect of LHRH on LH response was markedly attenuated in the postpartum lactating rats (PPL), compared with the normal cycling female rats on diestrous day 2. Three consecutive injections of LHRH produced significantly less LH release in PPL rats than in normal cycling female rats on diestrous day 2. Both day 7 and day 17 PPL rats released equally small amounts of LH in response to LHRH administration. The total amount of LH released by anterior pituitaries (APs) during a 5 h incubation in medium-199, from day 7 or day 17 in PPL rats, was significantly less than that released by the APs from normal cycling female rats on diestrous day 2. APs from day 7 and day 17 PPL rats also released less LH in vitro in response to LHRH (50 ng) stimulation than APs from normal cycling female rats. When APs from normal cycling female rats on diestrous day 2 were incubated with LHRH, the increments in LH release were greater at the end of the 2nd and 3rd h than after the 1st h of incubation. However, such increments in LH release were relatively small when APs from day 7 or day 17 PPL rats were similarly incubated with LHRH.

Animals↗
PubMed1976

Serum and pituitary TSH and response to TRH in developing male and female rats.

Serum and pituitary thyroid-stimulating hormone (TSH) was measured by radioimmunoassay in male and female Sprague-Dawley rats from 21 through 80 days of age. In males, serum TSH levels increased progressively from days 30 through 50, and were found to be lower on days 60, 70, and 80. In females, serum TSH levels were elevated on days 40 and 50, compared with day 30, but declined on days 60-80. A sex difference in serum TSH levels, with those of the male higher than those of the female, appeared by day 30 and was maintained through day 80. The anterior pituitary (AP) content of TSH in males increased from days 21 through 50 and remained constant through day 80; in females the AP content increased between days 25 and 60 and remained constant through day 80. In males, thyrotropin-releasing hormone (TRH) induced a significant elevation in serum TSH at all ages tested, but was less effective in increasing serum TSH on day 25 than on days 15 or 40 or in 3-4-month-old rats. The response to TRH appeared to be sustained longer in adults than in all other age groups. These observations indicate that serum TSH levels increase in both male and female rats at about the time of puberty and then decline, and that changes in the response to TRH may account in part for the increase in serum TSH levels during development.

Age Factors↗
PubMed1976

Evidence for adrenergic mediation of cholinergic inhibition of prolactin release.

Pilocarpine, a cholinergic agonist, significantly reduced the high levels of serum prolactin in estrogen-primed male rats and in female rats on the late afternoon of proestrus. In male rats treated with reserpine, chlorpromazine, haloperidol, or pimozide, serum prolactin levels were greatly elevated. Subsequent treatment with pilocarpine failed to reduce serum prolactin concentrations in these rats. When atropine, a cholinergic antagonist, was injected ip in doses of 3 to 250 mg/kg into male rats, prolactin release was not altered. However, when atropine was injected prior to pilocarpine, it prevented the reduction in serum prolactin by the latter drug. Methyl-atropine, which does not enter the CNS, did not prevent pilocarpine from inhibiting prolactin release. These results suggest that cholinergic inhibition of prolactin release is mediated via adrenergic neurons, and thus support a role for a cholinergic link in hypothalamic regulation of prolactin release.

Animals↗