Hypothalamic dopamine is required for salsolinol-induced prolactin secretion in goats

2017 ◽  
Vol 88 (10) ◽  
pp. 1588-1594 ◽  
Author(s):  
Tsutomu Hashizume ◽  
Ryunosuke Watanabe ◽  
Yuki Inaba ◽  
Ken Sawai ◽  
Ferenc Fülöp ◽  
...  
Keyword(s):  
Prolactin Secretion ◽  
Hypothalamic Dopamine

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
Keyword(s):  
Monoamine Oxidase Inhibitor ◽  
Synergistic Effects ◽  
Oxidase Inhibitor ◽  
Prolactin Secretion ◽  
Dopamine Synthesis ◽  
Dopamine Receptor Agonist ◽  
Plasma Prolactin ◽  
Synthesis Inhibitor ◽  
Additional Support ◽  
Hypothalamic Dopamine

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.

Involvement of Hypothalamic Dopamine in the Regulation of Prolactin Secretion

1985 ◽  
Vol 22 (3) ◽  
pp. 142-152 ◽  
Author(s):  
Marianne J. Reymond ◽  
John C. Porter
Keyword(s):  
Prolactin Secretion ◽  
Hypothalamic Dopamine

Brief decreases in dopamine result in surges of prolactin secretion in monkeys

1984 ◽  
Vol 247 (6) ◽  
pp. E778-E780
Author(s):  
L. S. Frawley ◽  
J. D. Neill
Keyword(s):  
Rhesus Monkeys ◽  
Plasma Concentrations ◽  
Elevated Serum ◽  
Prolactin Secretion ◽  
Serum Prolactin ◽  
Base Line ◽  
Peripheral Plasma ◽  
Hypothalamic Dopamine

We have reported previously that the amount of dopamine in hypophysial stalk blood was sufficient to account for tonic hypothalamic inhibition of prolactin secretion in rhesus monkeys. In the present study we determined the effect on prolactin secretion of decreases in dopamine. When hypophysial stalk-transected, estrogen-treated monkeys were infused with dopamine at a rate (0.1 microgram X kg-1 X min-1) to achieve peripheral plasma concentrations similar to those previously measured in stalk blood, their elevated serum prolactin levels fell to base line (from 47.6 +/- 4.8 to 9.7 +/- 2.7 ng/ml, mean +/- SE, n = 4). Brief interruptions of the dopamine infusions lasting for 2.5, 5.0, or 7.5 min evoked rapid increases in serum prolactin concentrations (to 27.5 +/- 8.3, 52.9 +/- 3.6, and 58.9 +/- 8.1 ng/ml, respectively, at 10 min). Maximal prolactin levels were attained within 10 to 20 min after dopamine removal and serum prolactin remained elevated for an additional 35 to 150 min. Uninterrupted dopamine infusions of stalk-transected, estrogen-treated monkeys (n = 3) led to continuously suppressed prolactin values. These results demonstrate that brief decreases in dopamine lead to major increases in prolactin secretion. Thus, if a brief decrease in hypothalamic dopamine secretion occurs after a suckling stimulus in monkeys, as it does in rats, a decrease in dopamine secretion alone may account, in part, for suckling-induced prolactin secretion in monkeys.

Changes in mediobasal hypothalamic dopamine and GABA release: A possible mechanism underlying taurine-induced prolactin secretion

Amino Acids ◽  
1998 ◽  
Vol 15 (1-2) ◽  
pp. 5-11 ◽  
Author(s):  
Pablo Arias ◽  
H. Jarry ◽  
V. Convertini ◽  
M. Ginzburg ◽  
W. Wuttke ◽  
...  
Keyword(s):  
Gaba Release ◽  
Prolactin Secretion ◽  
Hypothalamic Dopamine

scholarly journals Chronic estradiol exposure induces oxidative stress in the hypothalamus to decrease hypothalamic dopamine and cause hyperprolactinemia

2011 ◽  
Vol 300 (3) ◽  
pp. R693-R699 ◽  
Author(s):  
Sheba M. J. MohanKumar ◽  
Badrinarayanan S. Kasturi ◽  
Andrew C. Shin ◽  
Priya Balasubramanian ◽  
Ebony T. Gilbreath ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Exposure ◽  
Arcuate Nucleus ◽  
Prolactin Secretion ◽  
Dependent Manner ◽  
Neuronal Function ◽  
Low Levels ◽  
Rate Limiting ◽  
Estradiol 17Β ◽  
Hypothalamic Dopamine

Estrogens are known to cause hyperprolactinemia, most probably by acting on the tuberoinfundibular dopaminergic (TIDA) system of the hypothalamus. Dopamine (DA) produced by TIDA neurons directly inhibits prolactin secretion and, therefore, to stimulate prolactin secretion, estrogens inhibit TIDA neurons to decrease DA production. However, the mechanism by which estrogen produces this effect is not clear. In the present study, we used a paradigm involving chronic exposure to low levels of estradiol-17β (E2) to mimic prolonged exposures to environmental and endogenous estrogens. We hypothesized that chronic exposure to low levels of E2 induces oxidative stress in the arcuate nucleus (AN) of the hypothalamus that contains TIDA neurons and causes nitration of tyrosine hydroxylase (TH), the rate-limiting enzyme in the synthesis of DA. This results in a significant decrease in DA and consequently, hyperprolactinemia. To investigate this, adult, intact female cycling rats were implanted with slow-release E2 pellets (20 ng/day) for 30, 60, or 90 days and were compared with old (16–18 mo old) constant estrous (OCE) rats. Chronic E2 exposure significantly increased the expression of glial fibrillary acidic protein and the concentrations of interleukin-1β (IL-1β) and nitrate in the AN that contains perikarya of TIDA neurons and increased nitration of TH in the median eminence (ME) that contains the terminals. These levels were comparable to those seen in OCE rats. We observed a significant decrease in DA concentrations in the ME and hyperprolactinemia in an exposure-dependent manner similar to that seen in OCE rats. It was concluded that chronic exposure to low levels of E2 evokes oxidative stress in the AN to inhibit TIDA neuronal function, most probably leading to hyperprolactinemia.

SPECIAL PROBLEMS IN TOXICITY TESTING OF LONG ACTING DEPOT CONTRACEPTIVES

1974 ◽  
Vol 77 (1_Suppla) ◽  
pp. S315-S354 ◽  
Author(s):  
F. Neumann ◽  
R. von Berswordt-Wallrabe ◽  
W. Elger ◽  
K.-J. Gräf ◽  
S. H. Hasan ◽  
...  
Keyword(s):  
Biological Effects ◽  
Histological Finding ◽  
Toxicity Testing ◽  
Prolactin Secretion ◽  
List Type ◽  
Human Species ◽  
Prolactin Plasma Level ◽  
Human Use ◽  
Long Acting ◽  
Reproductive Processes

ABSTRACT Two types of so-called "depot contraceptives", long-acting steroids which are of interest for human use, were studied in animals. Norethisterone oenanthate, mainly gestagenic in the human and other species, turned out to be predominantly oestrogenic in rats. This oestrogenicity caused indirectly, via an enhanced hypophysial prolactin secretion, the well-known hypophysial and mammary tumours in rats. Another synthetic gestagen, 4,6-dichloro- 17- acetoxy- 16α-methyl-4,6-pregnadiene-3,20-dione, which might be considered in its biological actions similar to preparations containing chlormadinone acetate or medroxy-progesterone acetate, induced no signs of oestrogenicity in dogs. It is surmised that its gestagenic influence indirectly, and probaby, via an enhanced hypophysial prolactin secretion caused "mammary nodules" in this "non-rodent" species. These studies have born out mainly two facts: A synthetic steroid, norethisterone oenanthate, exerted different biological effects in different species: it was a gestagen in the rabbit, whereas in rats, its predominant influence was oestrogenic. The hypophysial prolactin secretion was enhanced in various species by different mechanisms: in rats, the oestrogenicity caused an increased prolactin plasma level, whereas in dogs, a gestagen with obviously no inherent oestrogenicity, 4,6-dichloro-17-acetoxy-16α-methyl-4,6-pregnadiene-3,20-dione, converted the histological appearance of the anterior pituitary into a condition with a greatly increased number of eosinophils. This histological finding was interpreted as an indicator for a hypersecretion of prolactin. Hence, animal work with "gestagens" has only limited predictive value with respect to their possible effects in the human species. Therefore, inflexible recommendations are not helpful in solving the safety problem of long-acting steroids which affect primarily reproductive processes.

Modulation of prolactin secretion by contraceptive progestins in cultured rat pituitary cells in vitro

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S188-S189
Author(s):  
L. KIESEL ◽  
T. RABE ◽  
D. SCHOLZ ◽  
V. KIRSCHNER ◽  
B. RUNNEBAUM
Keyword(s):  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
Rat Pituitary Cells
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