Release of oxytocin and vasopressin by magnocellular nuclei in vitro: specific facilitatory effect of oxytocin on its own release

Abstract

The release of endogenous oxytocin and vasopressin by rat paraventricular and supraoptic nuclei in vitro during a 10-min period, 30 min after beginning the incubation, was measured radioimmunologically. Mean basal hormone release per 10 min and per pair of nuclei was: 128.4 +/- 12.4 (S.E.M.) pg vasopressin (n = 15) and 39.0 +/- 3.0 pg oxytocin (n = 66) for supraoptic nuclei from male rats; 273.9 +/- 42.6 pg vasopressin (n = 11) and 34.2 +/- 3.5 pg oxytocin (n = 15) for supraoptic nuclei from lactating rats; 70.0 +/- 8.6 pg vasopressin (n = 52) and 21.8 +/- 1.3 pg oxytocin (n = 68) for paraventricular nuclei from male rats; 59.1 +/- 8.6 pg vasopressin (n = 10) and 27.0 +/- 4.6 pg oxytocin (n = 16) for paraventricular nuclei from lactating rats. In male and lactating rats, both nuclei contained and released more vasopressin than oxytocin. For oxytocin alone, the paraventricular nucleus of male rats contained and released significantly less hormone than the supraoptic nucleus. This difference was not apparent in lactating rats. For vasopressin alone, the paraventricular nucleus contained and released significantly less hormone than the supraoptic nucleus in both male and lactating rats. When the hormone released was calculated as a percentage of the total tissue content the release was about 0.9% for oxytocin from both nuclei in male and lactating rats and also for vasopressin in lactating rats, but was only about 0.5% for vasopressin from both nuclei in male rats. The influence of oxytocin and analogues of oxytocin (including one antagonist) upon the release of oxytocin and vasopressin was studied. Adding oxytocin to the incubation medium (0.4-4 nmol/1 solution) induced a dose-dependent rise in oxytocin release from both nuclei of male or lactating rats. A 4 nmol/l solution of isotocin had a similar effect to a 0.4 nmol/l solution of oxytocin, but arginine-vasopressin never affected basal release of oxytocin. In no case was vasopressin release modified. An oxytocin antagonist (1 mumol/l solution) significantly reduced basal oxytocin release and blocked the stimulatory effect normally induced by exogenous oxytocin, as did gallopamil hydrochloride (D600, 10 mumol/l solution), a Ca2+ channel blocker, or incubation in a Ca2+-free medium. These findings are discussed in relation to the literature on the central effects of neurohypophysial peptides. It may be concluded that the regulatory role of endogenous oxytocin in the hypothalamus on the milk-ejection reflex could result from its local release in the extracellular spaces of magnocellular nuclei.

Oxytocin-induced elevation of ADP-ribosyl cyclase activity, cyclic ADP-riboseor Ca2+ concentrations is involved in autoregulation of oxytocin secretionin the hypothalamus and posterior pituitary in male mice

“…As we used 10-12-week-old adult male mice, this PKC-and cADPR-dependent autoregulation of OT release is not related to female reproductive processes, but to social recognition or social behavior found in this mouse strain (Jin et al, 2007a;Liu et al, 2008). The positive feedback mechanism of OT release plays a critical and physiological role in causing uterus contraction during labor and triggering milk release from the breast tissue when infants are nursed (Moos et al, 1984;Neumann et al, 1994 and1996). A recent series of studies showed that nasal infusion of OT increases trust (Kosfeld et al, 2005), mind-reading (Domes et al, 2007), and generosity (Zak et al, 2007) in humans,…”

“…Locally released OT in the brain causes excitation of OT neurons by activating OT receptors, a class A family (2.1:OXY:1:OT: in IUPHA data base; http://www.iuphar-db.org/GPCR/ReceptorListForward?class=class%20A), expressed on both neurons of the PVN and SON and nerve endings in the posterior pituitary (Adan et al, 1995;Freund-Mercier et al, 1994;Young et al, 1997). This excitation leads to facilitative OT release, known as autoregulation (Moos et al, 1984;Neumann et al, 1996). The autoregulation of OT-induced OT release occurs during uterine contraction in labor and milk ejection in lactation (Richard et al, 1991).…”

Evidence for the presence and functioning of the spinal generator for ejaculation in the neonatal male rat

“…Present data also show that the systemic injection of oxytocin to the PO7 neonatal as well as to the adult male rat induces the immediate activation of ejaculatory rhythmic motor patterns, suggesting that the spinal oxytocinergic system is involved in the functioning of the spinal generator for ejaculation. In the adult male rat, it has been demonstrated that the source of oxytocin for the spinal cord is the hypothalamus, 18 and that electrical stimulation of the posterior hypothalamic area produces the release of important amounts of this peptide; 19 however, an endogenous source of oxytocin in the neonatal spinal cord has not been described. Thus, it is necessary to perform specific experiments to further examine the developmental organization and functioning of the spinal oxytocinergic system and its relation to ejaculation across postnatal development.…”

Neuronal Uptake of Monoclonal Anti‐Vasopressin Antibodies in vivo and Relationship with the Physiological Status of Vasopressin Neurosecretory Cells

“…This increase was directly related to the distal release of hormone and more precisely, the increase in exocytosis (26). Exocytosis (27) and VP release (28,29) also occur at central level for vasopressinergic neurons. This central release…”