A possible inter-relationship between oestrogen, α-melanotrophin (αMSH) and NA in the ventromedial nucleus (VMN) has been studied in ovariectomised-adrenalectomised rats primed with a low dose of oestradiol benzoate (2 or 5 µg OB), which induces receptivity in approximately half the rats. Priming with OB increased NA turnover in the VMN (as assessed by the decline in NA concentration 1 h after 250 mg/kg α-methyl tyrosine αMT) and also enhanced the release of NA from basal medial hypothalamic fragments in vitro. This occurred whether the rats were receptive or non-receptive. Injection of 20 µg/ rat αMSH, 4 h before autopsy in OB-primed rats, reduced NA turnover in the VMN but only in the receptive animals. αMSH had no effect on NA content in the VMN, but prevented the decline normally induced by the αMT, indicating an inhibition of release. Application of 1 µg/ml αMSH to incubated hypothalamic fragments enhanced release of NA in the tissue obtained from untreated controls and the OB-non-receptive group, but had no effect on the tissue of the OB-receptive animals. Perhaps NA release had already occurred in vivo in the latter group. αMSH (100 ng/side/rat) and NA (20, 200 and 2,000 ng/side/rat) were injected into the VMN of ovariectomised-adrenalectomised rats primed with 1 µg OB. Both agents stimulated lordosis in non-receptive animals with a peak activity at 60 min. The effect of αMSH declined over the next 2 h, but the maximum effect of 200 and 2,000 ng NA was maintained until the end of the test at 4 h. Neither agent affected behaviour in receptive animals. Intra-VMN administration of the β-adrenergic antagonists, propranolol and metoprolol (both at 400 ng/side/rat) reduced the effect of αMSH and the former also antagonised the effect of NA, while the α-adrenergic antagonist, phentolamine (200 µg), was ineffective. These results show that αMSH and NA in the VMN stimulate female sexual behaviour and the effect of αMSH may be mediated by NA acting on β-receptors. αMSH may act by enhancing the release of NA, but once receptivity is initiated, αMSH appears instead to reduce NA release and thus to terminate the period of receptivity.
In a previous study we have demonstrated that cervical stimulation (CS) induces α-MSH release. The present experiments were undertaken to (1) examine the pattern of serum α-MSH during CS-induced pseudopregnancy (PSP) and (2) assess the possibility that α-MSH contributes to the induction and maintenance of PSP. Throughout PSP serum α-MSH fluctuated in a cyclic manner demonstrating two daily surges which occurred between 12.00 and 13.00 h (diurnal surge) and between 24.00 and 04.00 h (nocturnal surge). Chronic exposure of animals to α-MSH administered via minipumps (24 µg/day, starting on the morning of estrus), induced PSP as determined by deciduoma formation and persistence of a characteristic diestrous vaginal cytology. Furthermore, insertion of an α-MSH-containing minipump at diestrus 1 (Dl) resulted in progesterone and prolactin (PRL) levels on the afternoon of diestrus 2 (D2) similar to those levels found on day 2 of PSP. Uterine weight was significantly decreased in α-MSH-treated rats and pseudopregnant rats as compared with cyclic D2 controls. α-MSH was found to release PRL indirectly, through stimulation of adrenal progesterone. This effect, however, necessitates the presence of the ovaries as a source of estradiol (EB) since it is demonstrable in intact and acutely ovariectomized rats, but not in chronically ovariectomized animals. EB treatment of chronically ovariectomized rats is capable of restoring the sequence. These results indicate that, as demonstrated for PRL, cervical stimulation initiates rhythmic daily surges of α-MSH secretion which are maintained through PSP. In addition, they suggest that α-MSH may contribute to inducing and maintaining PSP by facilitating the release of adrenal progesterone and by inducing PRL release via the increase in progesterone secretion from the adrenal.
The effect of the interaction between Pro-Leu-Gly-NH2 (PLG) and catecholamines on the release of MSH by rat pituitaries glands was studied in vitro. The catecholamines dopamine (DA) and norepinephrine (NE) inhibited the release of α-MSH from pituitary glands incubated in vitro. The DA effect appeared at low concentrations while NE was effective in concentrations 20 times greater than DA. These effects were blocked by an α-adrenergic blocker agent. On the other hand, epinephrine (E) at the concentrations tested did not modify MSH release. When 50 or 500 ng/ml of DA is added to the medium containing PLG concentrations it strengthened the inhibitory effect of PLG release, whereas the action of NE and PLG was additive; at the highest tested concentration E (5,000 ng/ml) blocked the inhibition of MSH induced by PLG. It is concluded that, whereas the inhibitory release of MSH by catecholamines is mediated by an α-adrenergic receptor, the inhibitory effect of PLG is not exerted through a catecholaminergic receptor since its action is not prevented by any of the catecholamine receptor blockers studied. Thus, it seems that specific PLG receptors are present at the pituitary level.
We have previously demonstrated that neuropeptide-EI, at high doses, stimulates the production of cAMP, in caudate putamen, through the activation of adenylate cyclase coupled to specific D1 receptors. The aim of the present work was to find evidences for a probable interaction between this neuropeptide and the dopamine D1 receptor in the mammalian central nervous system. The present data show that neuropeptide-EI, at high concentrations, affected both the maximum binding and the apparent affinity of [n-methyl-3H] (R)-(+)-8 chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol hemimaleate to the dopamine D1 receptor in a concentration-dependent manner.
The effects of Leu-enkephalin, Met-enkephalin, and beta-endorphin on melanocyte-stimulating hormone (MSH) secretion were studied in vivo and in vitro. The three opioid peptides release MSH. In vitro this reslease is dose dependent for Met-enkephalin between 10 and 1000 ng/mL and for Leu-enkephalin between 10 and 100 ng/mL. beta-Endorphin releases MSH at the low concentration of 1 ng/mL and the effect is dose dependent between 1 and 100 ng/mL. Naloxone reverses this effect. In vivo the three petptides release MSH.
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