Increased dopaminergic inhibition of prolactin in the hypoprolactinaemic IPL nude rat

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

1976 ◽  
Vol 68 (3) ◽  
pp. 355-368 ◽  
Author(s):  
A. A. VAN DER GUGTEN ◽  
P. C. SAHULEKA ◽  
G. H. VAN GALEN ◽  
H. G. KWA

SUMMARY Many investigations of the regulation of prolactin synthesis and release are based on single plasma prolactin determinations. The purpose of the present experiment was to ascertain whether groups of rats (i.e. young or adult, male or female animals, being either intact, gonadectomized or gonadectomized and treated with oestrone), differing in age and/or endocrine status, will react to a single dose of perphenazine by an acute release of pituitary prolactin in proportion to their initial plasma prolactin levels. No consistent relation existed between the classification of the twelve groups of rats into three categories of basal plasma prolactin levels (i.e. < 20, 25–50, > 125 ng/ml) and their response to perphenazine. Even though all groups showed a highly significant increase of plasma prolactin levels the magnitude of the maximum prolactin response at 30 min varied greatly within the groups of one category and thus was not related to the initial prolactin levels. The effect of 14 days of oestrone treatment in increasing plasma prolactin levels in gonadectomized animals was greatest in young and adult male rats, less in young females and not significant in adult females. The results obtained after perphenazine treatment in the latter group made it clear that the effect of oestrogen treatment on prolactin release can be completely blocked by increasing synthesis and/or release of the prolactin-release inhibiting factor (PIF). Since perphenazine induces decrease of pituitary prolactin and a concomitant increase of plasma prolactin levels through lowered PIF-action, the positive effect of oestrogens on prolactin release (as observed in gonadectomized male and young female rats) apparently is caused by a different mode of action. The implications of these findings for the regulation of prolactin release, as affected by the endocrine status of the rat, is discussed. Moreover, comparison of prolactin lost from the pituitary and gained in the circulation of the experimental animals, with amounts of prolactin that were observed to disappear from plasma during the experiment, provided suggestive evidence that the capacity to synthesize and/or eliminate prolactin, after a sudden provoked release of the hormone, differed among the groups. The rates of synthesis by the pituitary, of release from the pituitary into the circulation as well as of elimination of the hormone from the circulation (equally involved in determining actual plasma levels) are thought, therefore, to be far more important for the elucidation of prolactin regulation than single plasma prolactin determinations.


1970 ◽  
Vol 46 (2) ◽  
pp. 237-241 ◽  
Author(s):  
A. DANON ◽  
S. DIKSTEIN ◽  
F. G. SULMAN

SUMMARY Treatment of intact adult male rats with 10 mg. perphenazine (Trilafon)/kg. resulted in a decrease in the prolactin content of the pituitary within 1 hr. This decrease was probably due to suppression of the hypothalamic prolactin-inhibiting factor (PIF). Subsequent intracarotid infusion of neutralized acid extracts of rat hypothalamus restored the pituitary prolactin content. This effect was dose-dependent within a range of ½-2 hypothalami. Infusion of extracts of cerebral cortex failed to increase pituitary prolactin. The response to the hypothalamic extracts is considered to be specific for PIF and is proposed as an assay method for PIF.


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.


1977 ◽  
Vol 233 (3) ◽  
pp. E235 ◽  
Author(s):  
A De Lean ◽  
F Labrie

Daily administration of estradiol benzoate (10 microgram/100 g body wt) to intact male rats led to a twofold increase of the plasma TSH (thyroid-stimulating hormone) response to thyrotropin-releasing hormone (TRH) after 4 and 7 days of treatment whereas the basal plasma TSH level was not affected. The basal plasma PRL concentration and the PRL response to TRH were both markedly increased by estrogen treatment. The TSH pituitary content remained unchanged, whereas the PRL pituitary content increased in parallel with the effect on PRL secretion. Treatment with estrogens for 1 wk sensitized the TSH secretory response to low doses of TRH (10 ng), whereas no significant effect on the response was found at high doses of the neurohormone. The present data show that the stimulatory effect of estrogens on the TSH response to TRH is due to true sensitization of the thyrotrophs to the action of the neurohormone, whereas that on prolactin secretion can result partly from increased pituitary prolactin content.


2005 ◽  
Vol 155 (1) ◽  
pp. 87-96 ◽  
Author(s):  
A. Lafuente ◽  
A. González-Carracedo ◽  
A. Romero ◽  
T. Cabaleiro ◽  
A.I. Esquifino

1969 ◽  
Vol 45 (2) ◽  
pp. 183-NP ◽  
Author(s):  
C. S. NICOLL ◽  
J. A. PARSONS ◽  
R. P. FIORINDO ◽  
C. W. NICHOLS

SUMMARY A procedure for estimating rat prolactin and growth hormone (somatotrophin, STH), by measuring the optical density of the electrophoretically isolated and stained hormone bands in polyacrylamide gel columns, is described and evaluated. A simple and inexpensive densitometer is also described. Prolactin levels in adenohypophyses and in medium from pituitary incubates were measured by electrophoresis-densitometry (ED) and by the pigeon crop-sac assay. The two methods showed a high degree of correlation. The validity of the ED method for estimating prolactin levels in adenohypophysial tissue and in incubation medium was demonstrated by comparing the prolactin content of adult male and female and of oestrogen-treated male glands and by experiments in vitro. The female pituitary contained about three times more prolactin than the male and the glands of oestrogen-treated males had levels about the same as those of females. It was also shown that the ED method could be used to demonstrate the inhibitory effects of extract of rat hypothalamic tissue on prolactin secretion in vitro by the rat pituitary. Levels of STH in adult male glands, as measured by this method, were comparable to results obtained by others using immunoassays. Propylthiouracil-induced hypothyroidism depressed the STH and prolactin levels in male rat pituitaries, in agreement with the observations of others. The stainability of the prolactin band in rat adenohypophyses was observed to decrease with time when the glands were stored on dry ice. No such change occurred in the staining characteristics of the STH band. Other aspects of the ED method are discussed, including its precision, efficiency, sensitivity, economy and utility.


1972 ◽  
Vol 54 (2) ◽  
pp. 263-NP ◽  
Author(s):  
R. RELKIN ◽  
M. ADACHI ◽  
S. A. KAHAN

SUMMARY The effects of constant light, constant darkness and diurnal lighting, in combination with pinealectomy or sham-pinealectomy, on pituitary and plasma concentrations of radioimmunoassayable prolactin were investigated in 8-week-old male and virgin female rats. Two to three days after operation random groups of pinealectomized and sham-pinealectomized animals of the same sex were placed together in either continous light, continuous darkness or diurnal light, and killed 21 days later. Compared with sham-operated diurnally-illuminated controls, constant darkness caused a decrease in pituitary prolactin content and a rise in plasma prolactin levels. Pinealectomy or constant illumination reversed the effect of constant darkness, resulting in an increase in pituitary prolactin content and a fall in plasma prolactin levels when compared with sham-operated diurnally-illuminated controls. Electron microscopy of lactotrophic cells of the sham-pinealectomized animals exposed to constant darkness revealed few cytoplasmic granules, whereas these cells in the sham-pinealectomized animals exposed to constant light contained abundant granules; compared with the former groups, lactotrophic cells of sham-pinealectomized rats exposed to diurnal lighting revealed an intermediate degree of granulation.


2009 ◽  
Vol 185 (3) ◽  
pp. 175-179 ◽  
Author(s):  
A. Caride ◽  
B. Fernández-Pérez ◽  
T. Cabaleiro ◽  
A.I. Esquifino ◽  
A. Lafuente

1979 ◽  
Vol 57 (11) ◽  
pp. 1313-1316 ◽  
Author(s):  
S. H. Shin

Male rats in which three pituitaries were grafted beneath the kidney capsule showed approximately a fourfold increase in circulating plasma prolactin concentration. The elevated plasma prolactin concentration did not remain at a constant level but fluctuated with time. The elevated prolactin concentration declined immediately after a single bolus injection of ergocristine (30 μg/kg). The slope of the prolactin decay curve, determined by sequential blood sampling, was parallel to a theoretical slope having a 7-min half-life. This result indicates that ergocristine blocked prolactin secretion immediately and completely as the decay curve (T1/2 = 6.5 min, confidence interval 4.5–11.3) resulting from the administration of ergocristine is the same as the endogenous prolactin decay curve (T1/2 = 7 min).


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