Prostaglandin E release by rat medial basal hypothalamus in vitro. Inhibition by melatonin at submicromolar concentrations

Cardinali, Daniel P.; Ritta, Mónica N.; Fuentes, A.M.; Gimeno, M.F.; Gimeno, A.L.

doi:10.1016/0014-2999(80)90025-4

Cited by 56 publications

(24 citation statements)

References 7 publications

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“…Melatonin treatment increased progesterone production in luteal cell cultures (60), while melatonin treatment decreased prostaglandin F2␣ and E2 in endometrial and hypothalamic cultures (2,11). In addition, melatonin treatment in rats caused a 59% decrease in uterine estrogen receptors and a 35% increase in uterine progesterone receptors, as well as a reduction in uterine contractile response to oxytocin compared with controls (1).…”

Section: Discussionmentioning

confidence: 99%

Melatonin supplementation alters uteroplacental hemodynamics and fetal development in an ovine model of intrauterine growth restriction

Lemley

Meyer

Camacho

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

114

109

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Section: Discussionmentioning

confidence: 99%

Melatonin supplementation alters uteroplacental hemodynamics and fetal development in an ovine model of intrauterine growth restriction

Lemley

Meyer

Camacho

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

114

109

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“…Melatonin could act theoretically at the interaction of guanine nucleo tides with the guanine nucleotide regulatory protein (or *G' unit) [26] which is known to mediate the effect of ((-adreno ceptor agonist on adenylate cyclase. Besides, melatonin could impair NE-evoked cyclic AMP increase by the inhibi tion of prostaglandin E2 synthesis described in rat MBH explants [7]. Indeed, in several glial cell preparations pros taglandins are potent stimulators of cyclic AMP production [12,19,22].…”

Section: Discussionmentioning

confidence: 99%

“…Melato nin is known to interact with presumptive receptor sites at rat medial basal hypothalamus (MBH) [8,21], and to cause changes in a number of MBH functions in vitro including depression of synaptosomal uptake and increased release of serotonin release of neuropeptides [13,25], stimulation of cyclic GMP synthesis [32] and depression of prostaglandin E? [7,15] and cyclic AMP synthesis [32]. We further examined in the pres ent work the relationship between melatonin and P-adrenoceptor-mediated increase of cyclic AMP levels in astroglial cell cultures identified according to morphological and im munochemical characteristics.…”

mentioning

confidence: 99%

Melatonin Inhibits β-Adrenoceptor-Stimulated Cyclic AMP Accumulation in Rat Astroglial Cell Cultures

Vacas¹,

Berría²,

Cardinali³

et al. 1984

Neuroendocrinology

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We investigated whether astroglial cells are a site of action for the effect of melatonin on brain cyclic AMP content. Rat astroglial cell subcultures, identified according to morphological and immunochemical criteria, were used. Addition of melatonin to the cultures did not result in changes of cyclic AMP content. However, melatonin at 0.1–1 µM concentrations was able to impair the cyclic AMP increase elicited by 1 µM norepinephrine or isoproterenol in astroglial cultures. This melatonin effect was also shared by its biologically active analogues 5-methoxytryptophol and 6-chloromelatonin. Serotonin was only effective at a 100-fold greater concentration, while the biologically inactive melatonin metabolite 6-hydroxymelatonin was devoid of activity at any concentration used. These results suggest that methoxyindoles modulate negatively β-adrenoceptor-induced cyclic AMP accumulation in cultured rat astroglial cells.

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“…Recent observations indicate that melatonin, which in hibits brain PGE2 release in vivo [40] and in vitro [10], also depresses cAMP formation, and increases cGMP formation in hypothalamic explants [72]. Hence it is tempting to postu late a possible link between the two melatonin-induced phe nomena.…”

Section: Hypothalamusmentioning

confidence: 99%

The Role of Prostaglandins in Neuroendocrine Junctions:Studies in the Pineal Gland and the Hypothalamus

Cardinali¹,

Ritta²

1983

Neuroendocrinology

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This article discusses current experimental evidence indicating a role for prostaglandins (PGs) in pineal and median eminence neuroendocrine junctions. Both tissues release PGs, particularly of the E series, upon exposure to norepinephrine (NE) and through α-adrenoceptors. Exposure of pineal and median eminence explants to nanomolar concentrations of PGE2 augments melatonin and GnRH release, respectively. In the pineal gland, this effect appears to be linked to the stimulation of adenylate cyclase. Both in vivo and in vitro PG synthesis inhibitors impair the hormone release elicited by NE. In the pineal gland, PGE2 also constitutes a trans-synaptic negative signal for NE release. PGs receptors are present in pineal and hypothalamic membranes.

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Prostaglandin E release by rat medial basal hypothalamus in vitro. Inhibition by melatonin at submicromolar concentrations

Cited by 56 publications

References 7 publications

Melatonin supplementation alters uteroplacental hemodynamics and fetal development in an ovine model of intrauterine growth restriction

Melatonin supplementation alters uteroplacental hemodynamics and fetal development in an ovine model of intrauterine growth restriction

Melatonin Inhibits β-Adrenoceptor-Stimulated Cyclic AMP Accumulation in Rat Astroglial Cell Cultures

The Role of Prostaglandins in Neuroendocrine Junctions:Studies in the Pineal Gland and the Hypothalamus

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