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F Moos

Publications and source records attributed to F Moos.

17 recordsLinked to original sources
PubMed1992

Oxytocin-containing pathway to the bed nuclei of the stria terminalis of the lactating rat brain: immunocytochemical and in vitro electrophysiological evidence.

Immunocytochemical staining within the forebrain of lactating rats revealed oxytocin-immunoreactive perikarya in a continuum running from the anterior parvocellular hypothalamic paraventricular nucleus through the anterior commissural nucleus and perifornical region. Beaded axons could be seen arising from these perikarya to enter the bed nuclei of the stria terminalis. In sections cut at a 45 degree angle to the parasagittal plane, much of this pathway could be maintained intact, and in vitro tissue slices prepared in this orientation were used for electrophysiological studies of oxytocinergic innervation of the bed nuclei. By extracellular recording, neurons of the bed nuclei of the stria terminalis were tested for their response to exogenous oxytocin and to stimulation of the paraventricular hypothalamus. Both short latency (3-40 ms) orthodromic excitation (26/78 neurons) and longer latency (greater than 100 ms) excitation (12/78 neurons) were observed following paraventricular hypothalamic stimulation, possibly representing mono- and polysynaptic inputs, respectively. Removal of extracellular Ca2+ blocked these orthodromic responses (n = 6). Antidromic invasion was seen in a further 11/78 neurons with characteristics of constant latency (mean = 5.9 +/- 0.7 ms), high frequency following (40-80 Hz) and persistence in Ca(2+)-free medium. When tested for the effect of oxytocin (10(-7) M), none (0/11) of the antidromically activated neurons were excited, but nine of 34 of the orthodromically excited neurons (both short and long latency) responded with a marked increase in activity. In three of eight cases, the orthodromic synaptic excitation following hypothalamic stimulation could be reversibly attenuated by the receptor antagonist [d(CH2)5,D-Tyr(OEt)2,Val4,Cit8]-vasopressin (0.5 or 2.5 x 10(-6) M), further substantiating the involvement of oxytocin. These data provide anatomical and electrophysiological evidence for an oxytocinergic innervation of the bed nuclei of the stria terminalis. This pathway is discussed in terms of possible involvement in mediating the facilitatory effect of oxytocin on the milk-ejection reflex of lactating rats which has been suggested to act through this part of the limbic system.

Animals↗
PubMed1989

Immunocytochemical and ultrastructural studies on allografts of the pituitary neurointermediate lobe in the third cerebral ventricle of the rat.

Neurointermediate lobes from adult or 10-day-old rats were implanted by a stereotaxic procedure into the third ventricle of adult male rats, in an area close to the paraventricular nucleus. They were examined, using immunocytochemical and ultrastructural techniques, at times ranging from 1 week to 8 months. All grafts were recovered in a healthy condition although some rejection of the tissue was detected at the 1- and 2-week stages. In the neural lobe, clusters of pituicytes were scattered among the loose network of capillaries, most of which had a fenestrated endothelium. The intermediate lobe remained organized in compact avascular lobules. Axons similar to those projecting into the neurointermediate lobe in situ, but also axons of other types (e.g., somatostatinergic, enkephalinergic) penetrated the grafts. Synapses with melanotrophic cells in the intermediate lobe and neurohaemal contacts in the neural lobe were frequent from 2 1/2 months after transplantation. Immunocytochemical and ultrastructural characteristics indicated intense secretory stimulation of the melanotrophic cells in the early stages. All cells enclosed in a same glandular lobule reacted in a similar manner. In later stages, when re-innervation occurred, the cells recovered their initial characteristics. The overall effect of the re-innervation of the intermediate lobe grafted in this location is inhibitory, as in the lobe in situ.

Animals↗
PubMed1989

Release of oxytocin within the supraoptic nucleus during the milk ejection reflex in rats.

To investigate the hypothesis that oxytocin may be released within the magnocellular nuclei in vivo, push-pull cannula perfusions were performed in anaesthetized lactating rats in one supraoptic nucleus of the hypothalamus while recording the intramammary pressure and/or the electrical activity of oxytocin cells in the contralateral supraoptic nucleus. Oxytocin content was measured in samples collected over 15 min, under various conditions: 1) with no stimulation; 2) during suckling and suckling-induced reflex milk ejections; 3) during electrical stimulation of the neuro-hypophysis by trains of pulses that mimicked oxytocin cell bursts; 4) under osmotic stimulation by i.p. injection of 2 ml of 1.5 M NaCl to evoke a tonic and sustained oxytocin release from the neurohypophysis. Oxytocin release within the supraoptic nucleus increased significantly during the milk ejection reflex and, to a lesser extent, during burst-like electrical stimulation of the neurohypophysis. In suckled rats, the increase started before the first reflex milk ejection occurred. There was no apparent correlation between the amount of oxytocin in the perfusates and the number of milk ejections and oxytocin cell bursts occurring during each perfusion period. The amount of oxytocin in the perfusates further increased-during facilitation of the milk ejection reflex by intraventricular injections of oxytocin or its analogue, isotocin. When suckling failed to evoke the milk ejection reflex, there was no change in intra-supraoptic oxytocin release. There was also no change after osmotic stimulation. When the push-pull cannula was positioned outside the supraoptic nucleus, there was no increase in the amount of oxytocin during the three types of stimulation tested. These results provide evidence for an endogenous release of oxytocin within the magnocellular nuclei in lactating rats. It is suggested that the increase in such a release induced by suckling is likely to be a prerequisite for the onset and the maintenance of the characteristic intermittent bursting electrical activity of oxytocin cells leading to milk ejections.

Animals↗
PubMed1989

Paraventricular and supraoptic bursting oxytocin cells in rat are locally regulated by oxytocin and functionally related.

1. Oxytocin was pressure injected through a glass micropipette into a supraoptic (SON) or paraventricular nucleus (PVN) while recording the electrical activities of oxytocin cells in a contralateral nucleus, to see whether oxytocin acts locally in the magnocellular nuclei to control their bursting activity and whether the oxytocin cells of the four magnocellular nuclei were functionally interconnected during suckling. To test the rapidity of these relations, similar intranuclear injections were realized with acetylcholine, known to rapidly increase the background activity of oxytocin cells. The effects of intranuclear injections of oxytocin and acetylcholine were tested before and after interhemisphere sections of various dimensions. 2. Injecting oxytocin (1 ng in 100 nl) into a magnocellular nucleus (5 times into the PVN and 15 times into the SON) facilitated the occurrence and increased the amplitude of bursts of the oxytocin cells in both the contralateral PVN and SON. This facilitatory effect was similar to that induced by intraventricular injection of the same dose of oxytocin, though slightly delayed and lower. 3. Injecting acetylcholine (0.6 microgram in 100 nl) into the SON (7 times) induced a rapid and sustained increase in the background activity of oxytocin cells in both the contralateral PVN (2 times) and SON (5 times) within the same delay (less than 15 s). This excitatory effect was similar to that induced by an intraventricular injection of 5 micrograms acetylcholine. The effects on bursting activity were not considered in this study. 4. Neither the injections of oxytocin or acetylcholine outside but near the magnocellular nuclei (200-500 microns), nor the intranuclear injection of 100-200 nl of cerebrospinal fluid-like medium, modified the background activity, the frequency and amplitude of bursts of the oxytocin cells in the nucleus contralateral to the injection site. 5. After interhemisphere sections most oxytocin cells were silent, bursts occurred in an erratic manner, and their amplitude was attenuated and irregular (more than the 20% variation normally recorded in non-operated rats). Moreover, the amplitudes of successive bursts of pair-recorded supraoptic-supraoptic (SO-SO) oxytocin cells, highly related in control conditions (correlation coefficient, r = 0.68 to 0.98) were no longer correlated after interhemisphere section (r = 0.24 to -0.61), but all bursts remained synchronized.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1988

Role of central oxytocin in the control of the milk ejection reflex.

The neuropeptide oxytocin, synthetized by magnocellular neurons in the hypothalamus, is well known for its peripheral action after it is released into the bloodstream from axons in the neurohypophysis. Less familiar is the notion that it is also released centrally to control the activity of oxytocinergic neurons themselves. When injected into the third ventricle of lactating rats during suckling, oxytocin increases the basal firing rate of oxytocinergic neurons as well as their activity at the time of each reflex milk ejection. On the other hand, centrally administered oxytocin engenders the neuronal-glial and synaptic plasticity characteristic of the oxytocin system when it is physiologically activated. From numerous in vivo and in vitro observations, it appears that central oxytocin is released in the hypothalamic nuclei themselves. For example, the use of push-pull cannulae inserted into one supraoptic nucleus of suckled rats shows that oxytocin is released inside the nucleus specifically during milk ejection. Moreover, ultrastructural immunocytochemistry reveals synaptic terminals in the supraoptic nucleus where both the pre- and postsynaptic elements are oxytocinergic. Nevertheless, the mechanism of the central release of the neuropeptide has still to be determined, especially in view of electrophysiological observations indicating that the release process in the hypothalamus is different from that within the neurohypophysis.

Animals↗
PubMed1988

Characteristics of early- and late-recruited oxytocin bursting cells at the beginning of suckling in rats.

1. Paired or single recordings of paraventricular and/or supraoptic oxytocin cells at the beginning of suckling in urethane-anaesthetized rats enabled us to study cell recruitment and compare the characteristics of the early- and late-recruited cells. This was done under different experimental conditions, i.e. when the reflex was triggered in less than 1 h suckling (control), and when its triggering was facilitated either by the intraventricular (i.c.v.) injection of oxytocin, of apomorphine (a dopamine agonist) or by the intravenous (i.v.) injection of propranolol (a beta-adrenoceptor antagonist) into suckled rats with no milk ejection. 2. Under control conditions, the amplitude (total number of spikes) of the successive bursts of the early-recruited cells progressively increased, generally reaching maximum by the 6th burst. This increase was more rapid and greater after oxytocin than under control conditions or after apomorphine injection, and was delayed and reduced after propranolol. The burst frequency was higher after oxytocin and apomorphine injections than under control conditions and very low after propranolol. 3. Late-recruited cells were observed under all experimental conditions, except after oxytocin injection, since all cells displayed bursts right away. Moreover, when injected during the recruitment period of a control reflex, oxytocin greatly speeded up the recruitment of the late-recruited cells. These cells generally displayed smaller amplitude bursts than the early-recruited cells. Moreover, the increase in burst amplitude was less marked for the late- than for the early-recruited cells and often was not sustained. 4. Neither the likelihood of recruitment of an oxytocin cell nor its burst amplitude could be correlated with background activity level and there was no clear relationship between the recruitment period or the bursting characteristics on one hand and the background activity on the other. 5. In conclusion, the differences between the early- and late-recruited cells in recruitment time and in burst amplitude reflected differences in cell excitability which may depend mainly on the presence of oxytocin in the magnocellular nuclei.

Action Potentials↗
PubMed1987

[Evaluation of perfusion technics of the magnocellular nucleus of the hypothalamus in vitro and in vivo].

In suckled rats, OT necessary for the occurrence of the neurosecretory bursts on OT cells, is probably released inside the magnocellular nuclei. In order to demonstrate this in vivo release and to precise the mechanism involved, perifusions were realized in vivo on lactating rats and in vitro with isolated magnocellular nuclei. In vivo, the push-pull perifusion of a single supraoptic nucleus (SON) was realized simultaneously with the recording of the electrical activity of OT cells in the contralateral nucleus. This would allow to determine the possible relationships between the amount of OT released in the SON and the electrical activity of OT cells (bursting activation during suckling or continuous activation during an hyperosmotic stimulation). Results obtained showed 1) that OT was released in vivo inside the SON, 2) that this release was specifically increased during the milk ejection reflex and 3) that this increase was only detectable inside the SON. However, this technique did not permit to determine either the mechanism of OT release or the neuron elements (perikaryon, dendrites, axon collaterals) responsible for this release. That is for why, in vitro perifusions were undertaken with isolated magnocellular nuclei. The first stage was to determine the stimulus able to induce a reproducible increase of OT release. Among the chemical stimuli (neurotransmitters, K+) only K+ at a 56 mM concentration increased OT release by SON but this increase was small and non significant. Repetitive electrical stimulations with short pulses (0.2 to 5 msec) were ineffective even if the pulse intensity was raised up to 10 mA and the frequency up to 80 Hz.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Paired recordings from supraoptic and paraventricular oxytocin cells in suckled rats: recruitment and synchronization.

Oxytocin cells in the paraventricular (p.v.) and contralateral supraoptic (s.o.) nuclei were pair-recorded (with two micro-electrodes) in suckled rats after being anaesthetized with urethane (1.2 g/kg), to study the synchronization of their neurosecretory bursts, the importance of cell recruitment and their firing characteristics. The synchronization of paired bursts was determined by measuring the onset time-lag (time in milliseconds between the onset of two corresponding bursts) and the maximum firing time-lag (time in milliseconds between the two shortest interspike intervals for the corresponding bursts). For each cell, the characteristics studied were: the background activity and the frequency and amplitude (total number of spikes) of the neurosecretory bursts. All paired p.v.-s.o. cells recorded were activated simultaneously 12-18 s before each milk ejection. The onset of a burst could vary either way, up to 680 ms, in relation to the other (mean onset time-lag was 206 +/- 18 ms; n = 85) but the maximum activation periods fitted more closely, the mean maximum firing time-lag being 122 +/- 14 ms (n = 64). Both parameters varied randomly, in duration and 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, whether the cells were in the p.v. or the s.o. nucleus. However, in most cases, the neurosecretory burst with the highest amplitude began and reached its peak firing rate before the corresponding burst from the other cell. Cell recruitment was observed when the milk ejection reflex began, for both the p.v. and the s.o. cells. The bursts of the non-responsive cells developed progressively with the reflex, but, as soon as a cell was recruited, all its successive bursts were simultaneous with those of the first-recruited oxytocin cells. During a regular pattern of milk ejections, the mean background activity of sixty p.v. cells (3.1 +/- 0.2 spikes/s) was significantly higher than that of their s.o. counterparts (1.9 +/- 0.2 spikes/s). Nevertheless, the mean amplitude of the neurosecretory bursts of the sixty p.v. cells (49 +/- 3 spikes) did not differ significantly from that of their s.o. counterparts (55 +/- 4 spikes).(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
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↗
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↗