β-Endorphin-induced prolactin secretion is mediated by suppression of release of newly synthesized hypothalamic dopamine

1980 ◽  
Vol 58 (4) ◽  
pp. 436-439 ◽  
Author(s):  
Glen R. Van Loon ◽  
Errol B. De Souza ◽  
Doris Ho ◽  
S. H. Shin

Intracisternal administration of synthetic human β-endorphin in rats increased plasma prolactin. This effect of β-endorphin is blocked completely by parenteral administration of the dopamine receptor agonist, apomorphine. Increasing availability of brain dopamine with the monoamine oxidase inhibitor, pargyline, blunted the effect of β-endorphin on plasma prolactin. Although the effect of apomorphine could have been mediated either in the hypothalamus or directly on pituitary, the action of pargyline could not have occurred in pituitary, thus providing support for the hypothesis that β-endorphin-induced prolactin secretion is mediated in brain and furthermore through a dopaminergic mechanism. Additional support for both aspects of this hypothesis is provided by the finding that decreasing availability of dopamine with the dopamine synthesis inhibitor, α-methyltyrosine, potentiated the effect of β-endorphin to increase plasma prolactin concentration.Furthermore, this potentiation by α-methyltyrosine of β-endorphin-induced prolactin secretion was evident at a time when mediobasal hypothalamic dopamine concentration had not yet decreased. Because the storage pool of dopamine does not appear to have been altered at this time, these data suggest that lack of newly synthesized hypothalamic dopamine potentiated the effect of β-endorphin to increase plasma prolactin. It seems probable that inhibition of release of newly synthesized (and preferentially released) tuberoinfundibular dopamine is important in mediating β-endorphin-induced prolactin secretion. Finally, intracisternal dexamethasone inhibited the synergistic effects of α-methyltyrosine and β-endorphin on prolactin secretion, perhaps by an action on hypothalamic aminergic neurons.

1989 ◽  
Vol 120 (1) ◽  
pp. 125-134 ◽  
Author(s):  
M. C. Macnamee ◽  
P. J. Sharp

ABSTRACT An assessment was made of the possible role of hypothalamic 5-hydroxytryptamine (5-HT) in the regulation of prolactin secretion in broody bantam hens. Prolactin secretion was stimulated less in incubating hens deprived of their nests for 24 h (nest-deprived) than in laying hens after administration of the 5-HT receptor agonist quipazine, or precursor 5-hydroxytryptophan. One type of 5-HT-binding site was found in the anterior and posterior hypothalami of out-of-lay, incubating and laying hens. Differences in prolactin secretion in these birds could not be accounted for by changes in the abundance of this type of 5-HT-binding site. Another type of 5-HT-binding site, with a higher density but lower affinity, was found in the anterior hypothalami of laying hens. No specific 5-HT-binding sites were found in the anterior pituitary gland. The turnover rates of 5-HT were compared in the anterior and posterior hypothalami of laying, incubating and nest-deprived hens. The turnover rates were estimated from the rate of accumulation of 5-HT after inhibiting its catabolism using the monoamine oxidase inhibitor, pargyline, or by measuring the ratio of the concentrations of 5-HT and its major metabolite, 5-hydroxyindole acetic acid. Both methods of measurement gave the same results. The turnover of 5-HT was increased in the anterior but not posterior hypothalami of incubating hens when compared with laying or nest-deprived hens. There was also a significant increase in turnover of 5-HT in the posterior hypothalami in nest-deprived hens when compared with laying or incubating birds. These results demonstrate a strong correlation between the function of 5-HT neurones in the hypothalamus and reproductive activity. They are consistent with the view that hypothalamic 5-HT is involved in the regulation of prolactin secretion. Journal of Endocrinology (1989) 120, 125–134


1985 ◽  
Vol 107 (3) ◽  
pp. 325-329 ◽  
Author(s):  
H. Cohen ◽  
I. Sabbagh ◽  
P. Guillaumot ◽  
J. Bertrand

ABSTRACT In this study, aimed at investigating whether dopaminergic regulation of prolactin could be implicated in the hypoprolactinaemia observed in the IPL nude rat, dopaminergic inhibition of prolactin was suppressed using a catecholamine synthesis inhibitor α-methyltyrosine (MT) and a dopaminergic antagonist sulpiride. Adult male rats (IPL nude and normal) were injected through implanted atrial cannulae with either MT (250 mg/kg) or physiological saline (control). Rats were decapitated 2 h after the injection. Plasma prolactin levels, compared with basal values, increased by 15·6 ± 1·9 (s.e.m.)- and 5·89 ± 0·6-fold in IPL nude and normal rats respectively. This difference was highly significant. The pituitary prolactin content was decreased in both groups. In a second experiment, adult male IPL nude or normal rats were injected with either sulpiride (1 mg/kg) or saline and decapitated 2, 4, 8, 12, 14 and 24 h later. Plasma prolactin levels, compared with basal values, were increased in rats injected with sulpiride by 9·2 ± 1·8 and 3·4 ± 0·7-fold in IPL nude and normal rats respectively. The pituitary prolactin content was reduced more in IPL nude than in normal sulpiride-injected rats. These data suggest that prolactin secretion, as well as synthesis, is under an increased dopaminergic inhibition in the male IPL nude rat. J. Endocr. (1985) 107, 325–329


1989 ◽  
Vol 121 (1) ◽  
pp. 67-74 ◽  
Author(s):  
M. C. Macnamee ◽  
P. J. Sharp

ABSTRACT An assessment was made of the possible role of hypothalamic dopamine in the regulation of changes in plasma prolactin and LH in laying and broody bantam hens. Specific dopamine-binding sites were identified, using [3H]domperidone, in the anterior pituitary gland and in the anterior and posterior hypothalamus. The mean concentrations of dopamine-binding sites in both parts of the hypothalamus were 59–66 fmol/mg protein and did not differ between laying and incubating hens. The concentration of dopamine binding sites in the anterior pituitary gland was significantly (P<0·001) greater in laying than in incubating hens (278 ± 46 compared with 420 ± 32 fmol/mg protein, n = 5). The turnover rates of dopamine were compared in the anterior and posterior hypothalami of laying, incubating and nest-deprived hens. The turnover rates were estimated from the rate of accumulation of dopamine after inhibiting its catabolism using the monoamine oxidase inhibitor, pargyline, or by measuring the ratio of the concentrations of dopamine and its major metabolite, homovanillic acid. Both methods gave the same results. The turnover of dopamine was increased in the anterior but not posterior hypothalamus of incubating hens when compared with laying or nest-deprived hens. These results show, for the first time in birds, that the anterior pituitary gland contains specific binding sites for dopamine and that the concentration of these binding sites is inversely related to the concentration of plasma prolactin. The marked increase in dopaminergic activity in the anterior hypothalamus of incubating hens may stimulate the release of unidentified prolactin-releasing factors and/or inhibit the release of LH by exerting an inhibitory influence in the area of the hypothalamus containing LHRH cell bodies. Journal of Endocrinology (1989) 121, 67–74


1989 ◽  
Vol 4 (3) ◽  
pp. 175-181
Author(s):  
J.F. Lipinski ◽  
R.C. Alexander

SummaryThe authors have reviewed 13 published studies on methionine administration, usually in combination with a monoamine oxidase inhibitor (MAOI), to chronically psychotic patients, using modern (DSM-III) diagnostic criteria. Four of these studies contained sufficient descriptive data to allow reappraisal of the effects. The results of the review suggest that a proportion of the patients experienced the induction of a manic episode/antidepressant effects rather than the reported worsening of schizophrenia while treated with a methionine-MAOI combination. It is suggested that these observations are consistent with recent findings that S-adenosyl-L-methionine (SAMe) has antidepressant and mania-inducing effects.


1987 ◽  
Vol 112 (2) ◽  
pp. 317-322 ◽  
Author(s):  
J. E. Sánchez-Criado ◽  
K. Ochiai ◽  
I. Rothchild

ABSTRACT Adult female rats were hypophysectomized and their pituitary glands autotransplanted beneath the left kidney capsule on day 2 (day 1 was the day of ovulation). In such rats the pituitary secretes prolactin fairly constantly and the corpora lutea secrete progesterone for several months. To induce the luteolytic effect of prolactin the rats were first injected s.c. with 2-bromo-α-ergocryptine (CB-154) on cycle days 12, 13 and 14 (i.e. 10, 11 and 12 days after operation) to depress prolactin secretion, and then with CB-154 vehicle (70% ethanol) daily until cycle day 21, to allow prolactin secretion to resume. One ovary was removed from each rat on day 15 and the remaining one on day 22. The mean (± s.e.m.) weight of the corpora lutea on day 15 was 1·46±0·06 mg and 0·98±0·07 mg on day 22 (n = 17). In contrast, rats in which the CB-154 treatment was maintained to day 21 had corpora lutea which weighed 1·31 ±0·09 on day 15 and 1·47 ±0·08 mg on day 22 (n = 15). To investigate whether indomethacin, a prostaglandin synthesis inhibitor, affected the luteolytic action of prolactin, the experiment was repeated, but on day 15 (after the removal of one ovary) the groups in which CB-154 treatment was stopped, as well as the group in which CB-154 treatment was maintained, were each divided into two groups. In one, indomethacin-containing silicone elastomer wafers and, in the other, blank silicone elastomer wafers, were placed within the bursa of the remaining ovary. There were no differences in corpus luteum weight on day 15 among any of these groups and the two groups of the first experiment. There was no significant difference in corpus luteum weight between day 15 and day 22 in any of the six groups except for the two groups treated with the CB-154 vehicle and not with indomethacin. Thus, treatment with indomethacin prevented the fall in corpus luteum weight associated with the discontinuation of CB-154 treatment. Serum prolactin levels fell until day 15 in all rats and remained low in those in which the CB-154 treatment was maintained to day 21, but returned to control values in those treated with vehicle after day 14. Serum progesterone levels fell and remained low in all groups. Indomethacin treatment had no effect on the levels of either serum prolactin or progesterone. We conclude that some of the pharmacological effects of indomethacin are to prevent prolactin-induced luteolysis, and we suggest that prolactin induces rapid regression of the corpus luteum by stimulating intraluteal prostaglandin production or by being necessary for the effect of luteolytic prostaglandins. J. Endocr. (1987) 112, 317–322


1995 ◽  
Vol 22 (s1) ◽  
pp. S86-S87 ◽  
Author(s):  
N. Hamaue ◽  
T. Endo ◽  
M. Hirafuji ◽  
N. Yamazaki ◽  
H. Togashi ◽  
...  

2010 ◽  
Vol 3 (4) ◽  
pp. 213-215
Author(s):  
Junji Takeshita ◽  
Deborah Goebert ◽  
John Huh ◽  
Brett Lu ◽  
Diane Thompson ◽  
...  

2000 ◽  
Vol 52 (4) ◽  
pp. 451-459 ◽  
Author(s):  
B. D. SLOLEY ◽  
L. J. URICHUK ◽  
P. MORLEY ◽  
J. DURKIN ◽  
J. J. SHAN ◽  
...  

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