Search PubMed⌕ Search

Biomedical subjects

F Moos

Publications and source records attributed to F Moos.

33 records · Page 2Linked to original sources
PubMed1985

[Peptidergic control of electrical activities in the magnocellular neurons of the hypothalamus].

Although many peptides have been reported in the vicinity of hypothalamic magnocellular nuclei, their role in the control of neurohypophysial hormone release was only studied for few peptides: opiates, angiotensin II, substance P, CRF, oxytocin and vasopressin. Their effects are briefly recalled and then compared to the more detailed study of their role in the firing pattern of oxytocin and vasopressin neurones. This technique, in some cases, revealed the action site and mechanism of these peptides in the hypothalamo-neurohypophysial system.

Angiotensin II↗
PubMed1984

Synchronization of oxytocin cells in the hypothalamic paraventricular and supraoptic nuclei in suckled rats: direct proof with paired extracellular recordings.

In suckled rats, neurosecretory bursts of two oxytocin cells located in two different magnocellular nuclei were almost simultaneous before each milk ejection. The time elapsing between the onset of two corresponding neurosecretory bursts varied in duration (from 0 to 368 ms) and in order from one pair of cells to another, from one pair of bursts to another for successive bursts of a given pair of cells and independently of whether one of the two cells belonged to the paraventricular or supraoptic nuclei. However, the neurosecretory burst with the highest amplitude began before the other corresponding burst in most cases. Possible inter- and intranuclear synchronization mechanisms are discussed.

Action Potentials↗
PubMed1984

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

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.

Animals↗
PubMed1983

Serotonergic control of oxytocin release during suckling in the rat: opposite effects in conscious and anesthetized rats.

Serotonergic control over the reflex oxytocin (OT) release was investigated in anesthetized rats and in conscious rats. The effects of drugs were tested in the first case, on the electrical activity of oxytocinergic cells during sucklings and in the second case, on the litter weight gain after 30 min suckling (indirect index of OT release). In rats anesthetized with urethane (1.2 g/kg), intraventricular injection of 1 microgram serotonin interrupted the regular pattern of the neurosecretory bursts and milk ejections for about 15-20 min (inhibitory effect of the 'all-or-none' type). 10 micrograms cyproheptadine or R47465 (serotonergic antagonists) slightly but significantly decreased the mean delay between two neurosecretory bursts without modifying their amplitude and in half the cases, disturbed their periodicity with occasional appearance of very close dual neurosecretory bursts. Pretreatment with rho-chlorophenylalanine (PCPA) (250 mg/kg i.p.) did not prevent or affect the regular milk ejection pattern. The inhibitory effect of 5-HT was lengthened by fluoxetine, a 5-HT reuptake inhibitor (1 microliter of 10(-4) M solution into the 3rd ventricle) and prevented by 5 micrograms R47465. In conscious rats, all the above drugs had an opposite effect. 5-HT and 5-HTP (5-HT precursor) did not affect the milk ejection reflex, whereas serotonergic antagonists and PCPA had an inhibitory effect. Injecting 5-HT into the PCPA-treated mothers restored their ability to release OT in response to suckling. Hypotheses for these opposite effects are discussed.

Anesthesia↗
PubMed1982

Excitatory effect of dopamine on oxytocin and vasopressin reflex releases in the rat.

The involvement of dopamine in the release of oxytocin and vasopressin was investigated in lactating rats during suckling or after changes in plasma osmolality. The effects of intraventricular injections of dopamine, agonists and antagonists, were tested on electrical unit activity of oxytocinergic or vasopressinergic cells in the paraventricular nucleus, on intramammary pressure (index of oxytocin release) and diuresis (index of vasopressin release). In urethane-anaesthetized lactating suckled rats, dopamine (1 microgram), apomorphine (2.5 and 5 micrograms) facilitated the established milk-ejection reflex, increasing the frequency and the amplitude of neurosecretory bursts of oxytocinergic cells. They also triggered the reflex in lactating rats without milk-ejections during suckling. The small doses injected were in no way such as to induce an acceleration in firing rate of oxytocinergic cells or an increase in mammary pressure. In alcohol-loaded rats, during water diuresis, dopamine (2 micrograms) and apomorphine (5 micrograms) activated the depressed vasopressinergic cells and inhibited diuresis. These facilitatory effects were progressive, reaching a maximum 10-15 min after injection. Haloperidol (5 micrograms) and alpha-flupentixol (10 micrograms) had an inhibitory effect on both types of neurosecretory cells in urethane-anaesthetized rats. They prevented the reflex activation of oxytocinergic cells induced by suckling and of vasopressinergic cells after a hyperosmotic stimulus (1 ml i.p 9% NaCl solution). These inhibitory effects were not of the "all-or-none' type. So, we can postulate that dopamine regulates the reflex release of oxytocin and vasopressin in the hypothalamus. On the one hand, dopamine permits and controls the periodic activation of oxytocinergic cells as long as the mothers are being suckled. On the other hand, it modulates the activity of vasopressinergic cells whenever the plasma osmolality changes.

Animals↗
PubMed1981

Ultrastructural study of electrophysiologically identified neurones in the paraventricular nucleus of the rat.

The ultrastructural characterization of electrophysiologically identified neurones of the rat paraventricular hypothalamic nucleus was performed with extracellular labelling technique. The extracellularly recorded neurons are labelled with an electrophoretic deposit of alcian blue contained in the recording micropipette. The neurone thus labelled takes on a dark and shrunken appearance which enables its detection among neighbouring cells without, however, concealing its main morphological characteristics. 1) Spontaneously firing neurones, invaded by an antidromic action potential elicited by electrical stimulation of the neurohypophysis, were identified as magnocellular cells containing dense-cored vesicles of 200-250 nm in diameter. Dense-cored vesicles were not found in the antidromically activated neurones devoid of spontaneous activity. 2) Trans-synaptically activated neurones in the PVN or in its dorso-lateral edge were small cells devoid of dense secretory vesicles. 3) PV neurones in which neurohypophysial stimulation evoked no response, contained small, dense vesicles (100 nm in diameter) comparable with those found in parvocellular peptidergic neurones.

Action Potentials↗
PubMed1980

[Dual noradrenergic control of oxytocin release during the milk ejection reflex in the rat].

During suckling in the Rat, inhibition of oxytocin release by alpha-noradrenergic antagonist and beta-noradrenergic agonist is well established, but no result pinpointed the site where the drugs acted. Simultaneous recordings of: (1) the electrical activity of the oxytocinergic (OT) neurons in the paraventricular nucleus; (2) the intramammary pressure (p.i.m.) with observations of the behaviour of the litter, have shown two levels of control. Intraventricular injections of phentolamine (an alpha antagonist) significantly depressed the spontaneous and reflex firing of OT-cells, and during this inhibition, neither p.i.m. increases nor behavioural responses of young Rats could be detected. On the contrary, after isoproterenol (a beta agonist), the reflex OT releases did not occur but the basal firing rate of OT cells and the magnitude and frequency of bursts were not affected. The action level of the two drugs is discussed.

Animals↗
PubMed1979

Effects of dopaminergic antagonist and agonist on oxytocin release induced by various stimuli.

(1) Haloperidol, a dopaminergic antagonist was injected i.p. or into the 3rd ventricle (i.c.v.) of lactating rats to determine whether or not a dopaminergic component was involved in the reflex release of oxytocin (OT) induced by (a) vaginal dilatation (Ferguson reflex), (b) vagal stimulation (vago-pituitary reflex), (c) suckling (milk-ejection reflex). Moreover, we examined the effect of a dopaminergic agonist, apomorphine, on the milk-ejection (ME) reflex. (2) I.c.v. injection of 20 microgram haloperidol inhibited the vaginal and vagal reflexes. The inhibition of the ME reflex produced by 2, 5 or 8 mg/kg i.p. or by 20 and 40 microgram i.c.v. haloperidol was dose-dependent. Apomorphine (10 mg/kg i.p.) had no effect. (3) The results suggest that a dopaminergic component must be involved in OT release whatever the peripheral stimulus.

Animals↗
PubMed1977

Prolactin inhibiting activity of dopamine-free subcellular fractions from rat mediobasal hypothalamus.

In order to check the hypothesis of an identity of dopamine (DA) and prolactin inhibiting activity (PIF), their subcellular distribution was studied in the mediobasal hypothalamus (MBH) and the striatum, which served as a control structure. PIF was tested both in vivo and on pituitary incubates. Fractions were also assayed after adsorption of their catecholamine content on alumina, as well as in presence of haloperidol or alpha-flupentixol, potent DA receptor inhibitors. In the MBH, PIF was evenly distributed in the 17,000 g supernatant (S2) and in the crude mitochondrial fraction (P2) which contains synaptosomes. PIF activity was completely removed by alumina adsorption of S2, but not of P2 in spite of an over 99.9% elimination of DA. In contrast, striatal PIF activity was detected only in P2, and disappeared completely upon alumina adsorption, thus indicating that, in this structure, it is entirely due to DA. Addition of haloperidol (10--5M) or alpha-flupentixol (10--6M) reduced PIF activity of crude MBH homogenates, but no longer affected it after alumina adsorption. Quantitative studies suggest that only half of the total MBH PIF activity is accounted for by DA. It is concluded that the MBH contains dopamine-free PIF, which, as already shown for several other neurohormones, is exclusively distributed in nerve-endings.

Animals↗
PubMed1975

[Level of oxytocin release induced by vaginal dilatation (Ferguson reflex) and vagal stimulation (vago-pituitary reflex) in lactating rats (author's transl)].

1. Vaginal dilatation for 30 seconds caused a rapid and brief increase in intramammary pressure which was equivalent to that evoked by 160 muU of oxytocin (Syntocinon) injected intravenously. 2. The rise in mammary pressure induced by the stimulation of the central end of a severed vagus nerve for 30 seconds (5 V, 0,5 ms, 50 HZ) was similar to the response obtained with an intravenous injection of 360 muU of oxytocin. 3. The vago-pituitary reflex leads to the liberation of large amounts of antidiuretic hormone which does not interfere with the effect of oxytocin on the mammary gland, since dexamethasone phosphate prevented the vasopressor effect without significantly affecting the increase in intramammary pressure.

Animals↗
PubMed1975

[Adrenergic and cholinergic control of oxytocin release evoked by vaginal, vagal and mammary stimulation in lactating rats (author's transl)].

1. The amounts of oxytocin released during Ferguson and vago-pituitary reflexes are estimated by measurements of intramammary pressure. For the milk-ejection reflex, the gain in weight of the young over a period of 30 minutes is taken as an indirect index of the release of oxytocin. 2. Antagonists of specific cholinoceptors and adrenoceptors were injected into the third ventricle in order to delineate the role of the mediators and receptors in the control of oxytocin release. 3. The results suggest that three reflexes have a specific chemical transmission since: a) The Ferguson reflex is inhibited by the drugs that only block alpha and beta adrenoceptors. b) The vago-pituitary reflex is inhibited by the drugs that block alpha and beta adrenoceptors and muscarinic cholinoceptors. c) The milk-ejection reflex is inhibited by the drugs that block alpha adrenoceptors and muscarinic and nicotinic cholinoceptors.

Acetylcholine↗