Electrophysiological Evidence for a Key Control Function of the Medial Preoptic Area in the Regulation of Prolactin Secretion in Cycling, Pregnant and Lactating Rats

1990 ◽  
Vol 51 (2) ◽  
pp. 162-167 ◽  
Author(s):  
Jelle Wiersma ◽  
Jan Kastelijn
2008 ◽  
pp. 109-118
Author(s):  
CM Leite ◽  
GJR Machado ◽  
RCM Dornelles ◽  
CR Franci

Dopamine (DA) is known as a primary regulator of prolactin secretion (PRL) and angiotensin II (Ang II) has been recognized as one brain inhibitory factor of this secretion. In this work, estrogen-primed or unprimed ovariectomized rats were submitted to the microinjection of saline or Ang II after previous microinjection of saline or of DA antagonist (haloperidol, sulpiride or SCH) both in the medial preoptic area (MPOA). Our study of these interactions has shown that 1) estrogen-induced PRL secretion is mediated by Ang II and DA actions in the MPOA, i.e. very high plasma PRL would be prevented by inhibitory action of Ang II, while very low levels would be prevented in part by stimulatory action of DA through D(2) receptors, 2) the inhibitory action of Ang II depends on estrogen and is mediated in part by inhibitory action of DA through D(1) receptors and in other part by inhibition of stimulatory action of DA through D(2) receptors.


1990 ◽  
Vol 51 (6) ◽  
pp. 675-682 ◽  
Author(s):  
Domingos L.W. Picanço-Diniz ◽  
Marcelo M. Valença ◽  
Celso R. Franci ◽  
José Antunes-Rodrigues

1998 ◽  
pp. 583-586 ◽  
Author(s):  
RC Dornelles ◽  
CR Franci

The aim of this work was to study the participation of alpha- and beta-adrenergic receptors on the effect of microinjection of angiotensin II (A II) into the medial preoptic area (MPOA) on the secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) in estrogen-primed ovariectomized (OVX) rats. Microinjection of A II into the MPOA increased plasma LH. This effect was reduced by previous microinjection of an alpha- (phentolamine), but not a beta- (propranolol) adrenergic blocker into the MPOA. Plasma PRL decreased after microinjection of A II into the MPOA, but this effect was unchanged by phentolamine or propranolol. There was no change in plasma FSH in any condition. These results indicate that A II in the MPOA stimulates LH secretion and inhibits PRL secretion in estrogen-primed OVX rats. The effect on secretion of LH, but not of PRL, is mediated by alpha-adrenergic receptors in the MPOA.


Endocrinology ◽  
2006 ◽  
Vol 147 (10) ◽  
pp. 4688-4694 ◽  
Author(s):  
Greg M. Anderson ◽  
David R. Grattan ◽  
Willemijn van den Ancker ◽  
Robert S. Bridges

The experience of pregnancy plus lactation produces long-term enhancements in maternal behavior as well as reduced secretion of prolactin, a key hormone for the initial establishment of maternal care. Given that prolactin acts centrally to induce maternal care as well as regulate its own secretion, we tested whether prolactin receptors in brain regions known to regulate behavioral and neuroendocrine processes were up-regulated and more responsive to prolactin in reproductively experienced females. Diestrous primiparous (8 wk after weaning) and age-matched virgin rats were treated with 250 μg ovine prolactin sc or vehicle and the brains collected 2 h later for measurement of mRNA for genes involved in prolactin signaling. Reproductively experienced rats had lower serum prolactin concentrations, compared with virgin rats, suggesting enhanced prolactin feedback on the arcuate neurons regulating prolactin secretion. In the medial preoptic area and arcuate nucleus (regions involved in regulating maternal behavior and prolactin secretion, respectively), the level of long-form prolactin receptor mRNA was higher in primiparous rats, and prolactin treatment induced a further increase in receptor expression in these animals. In the same regions, suppressors of cytokine signaling-1 and -3 mRNA levels were also markedly increased after prolactin treatment in reproductively experienced but not virgin rats. These results support the idea that reproductive experience increases central prolactin responsiveness. The induction of prolactin receptors and enhanced prolactin responsiveness as a result of pregnancy and lactation may help account for the retention of maternal behavior and shifts in prolactin secretion in reproductively experienced females.


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