Effects of hypothalamic dopamine (DA) on salsolinol (SAL)-induced prolactin (PRL) secretion in male goats

2013 ◽  
Vol 85 (4) ◽  
pp. 461-467 ◽  
Author(s):  
Jin Jin ◽  
Sayaka Hara ◽  
Ken Sawai ◽  
Ferenc Fülöp ◽  
György Miklos Nagy ◽  
...  
Keyword(s):  
Hypothalamic Dopamine

scholarly journals Hypothalamic dopamine signalling regulates brown fat thermogenesis

2019 ◽  
Vol 1 (8) ◽  
pp. 811-829 ◽  
Author(s):  
Cintia Folgueira ◽  
Daniel Beiroa ◽  
Begoña Porteiro ◽  
Manon Duquenne ◽  
Emma Puighermanal ◽  
...  
Keyword(s):  
Brown Fat ◽  
Hypothalamic Dopamine

Inhibition by naloxone of the rise in hypothalamic dopamine and serum prolactin induced by ethanol

1985 ◽  
Vol 87 (4) ◽  
pp. 461-463 ◽  
Author(s):  
Adriana Seilicovich ◽  
Modesto Rubio ◽  
Beatriz Duvilanski ◽  
Victor Mu�oz Maines ◽  
Valeria Rettori
Keyword(s):  
Serum Prolactin ◽  
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.

Stimulation of prolactin release by dopamine withdrawal: role of membrane hyperpolarization

1994 ◽  
Vol 267 (5) ◽  
pp. E781-E788 ◽  
Author(s):  
K. A. Gregerson ◽  
N. Golesorkhi ◽  
R. Chuknyiska
Keyword(s):  
Resting Membrane Potential ◽  
Prolactin Release ◽  
Membrane Hyperpolarization ◽  
Basal Release ◽  
K Concentration ◽  
Hypothalamic Dopamine ◽  
Ca2 Channels ◽  
Stimulation Of ◽  
External K

Hypothalamic dopamine (DA) tonically inhibits prolactin (PRL) release from the anterior pituitary gland, whereas removal of DA markedly augments its release to values exceeding pre-DA rates. We investigated whether electrical events induced by DA contribute to this secretory rebound. In primary cultured lactotropes, spontaneous Ca(2+)-dependent spiking activity was enhanced after recovery from DA-induced hyperpolarization. Voltage clamp studies showed a rapidly and a slowly inactivating Ca2+ current that were both augmented by a hyperpolarizing conditioning potential. We measured PRL release from perifused cells exposed to DA to correlate the electrical with the secretory responses. DA inhibited PRL release by 67%, whereas PRL secretion increased three- to fourfold over basal release after washout of DA. Valinomycin, used to directly hyperpolarize the cell membrane, mimicked the actions of DA, inhibiting PRL release (65%) and, upon washout, augmenting PRL secretion. Blocking the DA- or valinomycin-induced hyperpolarization by elevating external K+ concentration blocked both the inhibition and rebound of PRL release. These novel results demonstrate that hyperpolarization of the lactotrope membrane by DA is critical for the development of PRL rebound after DA withdrawal. We hypothesize the mechanism involves the removal of inactivation from a population of Ca2+ channels, leading to enhanced Ca2+ influx and PRL release upon recovery of the resting membrane potential after DA removal.

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