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Potentials were recorded in the pituitary stalk of ewes after electrical stimulation of the inguinal nerves or dilatation of the vagina. The modifications provoked by destruction of sensory pathways at different levels in the central nervous system were studied with a view to defining the tracts which carry the impulses to the pituitary stalk. The potentials obtained with bipolar concentric electrodes were characterized by long latency and a negative wave of low amplitude and long duration. The apparent negativity of the response was due to the recording conditions. At the spinal level the tracts are bilateral but primarily contralateral. The dorsal tracts do not seem to be necessary for the transmission of impulses to the pituitary stalk and the nerve fibres are distributed diffusely in the lateral and ventral parts of the spinal cord. At the supraspinal level, the lemniscal system does not seem to be involved in this transmission. On the other hand, the passage of impulses needs the integrity of the mesencephalic reticular formation. The long latency of the responses of the pituitary stalk to electrical stimulation of the inguinal nerves was due to the transmission time of the impulses between the mesencephalic level and the pituitary stalk. This long latency does not originate in the periphery. The cause has not been determined but relay in the amygdala nuclei or in the cortex has been eliminated.

The relationship between the potentials evoked in the pituitary stalk by the stimulation of the inguinal nerves or by vaginal dilatation and the release of oxytocin is discussed.

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The pathways of the milk-ejection reflex in the ewe have been described at the spinal and mesencephalic levels (Richard, 1970; Richard, Urban & Denamur, 1970). The present paper describes the pathways followed by impulses of mammary and vaginal origin between the mesencephalic reticular formation and the neurohypophysis.

In the anaesthetized ewe the thalamus is not necessary for the transfer of impulses to the neurohypophysis as shown by studying the electrical activities evoked in the pituitary stalk by mammary or vaginal stimulation. These impulses follow a subthalamic pathway through the medial forebrain bundle. In conscious ewes small areas of coagulations in the pathways did not block the milk-ejection reflex during milking because the fibres are diffuse at all levels of the central nervous system. Larger lesions result in non-specific effects which interrupt milk secretion.

Supra-diencephalic structures are not necessary for the milk-ejection reflex.

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The milk-ejection reflex after different lesions of the sensory system was studied by mechanical milking of the ewe. Only animals with lesions which did not produce locomotor ataxia were investigated. Section of the dorsal tract of the spinal cord at different thoracic levels blocked the milk-ejection reflex. This was not due to postoperative shock, because the same type of lesion made at the sacral level was without effect. Moreover, unilateral section of this tract blocked the reflex when milking was limited to the ipsilateral mammary gland. At the cervical level, the interruption of the dorsal tract was ineffective, which can probably be explained by the existence, in sheep, of the spino-cervico-thalamic tract. The latter becomes ventral at the cervical level. Lesions of the lemniscal system in the mesencephalon (bilateral coagulation of the medial lemniscus) and in the thalamus (bilateral destruction of the ventral posterolateral nucleus) do not inhibit the milk-ejection reflex.

The role of the spinal lemniscal system is discussed in relation to the work of others and to the electrophysiological results obtained by one of us. It is suggested that two sensory systems (lemniscal and extralemniscal) have to interact to induce the release of oxytocin evoked by the stimuli of mammary origin during milking.

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C. Meyer, M. J. Freund-Mercier, Y. Guerné, and Ph. Richard


Plasma concentrations of oxytocin and vasopressin were measured in relationship to oxytocin cell firing during suckling in urethane-anaesthetized rats.

Preliminary experiments showed that plasma concentrations of oxytocin and vasopressin, which were increased immediately after anaesthesia, reverted to basal concentrations 3 h later. Moreover, it was found that exogenous oxytocin had entirely disappeared 5 min after i.v. bolus injections of known doses of oxytocin.

Suckling did not modify the basal plasma concentration of oxytocin (14·6 ± 2·9 compared with 14·±61·5 pmol/l before suckling) except during a brief period immediately after neurosecretory bursts on oxytocin cells (37·8 ± 5·2 pmol/l; P < 0·001, n = 11). The plasma concentration of oxytocin did not differ significantly from the basal concentration 1·5 min later. The plasma concentration of vasopressin never varied.

After two neurosecretory bursts of similar amplitude (total number of spikes during the burst) recorded on the same oxytocin cell, the variations in plasma concentration of oxytocin were also similar. When, for a given cell, the amplitude of neurosecretory bursts increased or decreased, the amount of oxytocin released changed in the same way.

These data demonstrate (1) that suckling induces pulsatile release of oxytocin without vasopressin, and (2) a direct relationship between the amounts of oxytocin released and the amplitude of oxytocin cell neurosecretory bursts which argue in favour of simultaneous increases or decreases in the neurosecretory burst amplitudes on all oxytocin cells.

J. Endocr. (1987) 114, 263–270

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M. E. Stoeckel, M. J. Freund-Mercier, J. M. Palacios, Ph. Richard, and A. Porte


The distribution of [3H]vasopressin- and [3H]oxytocin-binding sites was examined, using an autoradiographical technique, in the kidney of Long–Evans and Brattleboro rats. Two types of binding sites with affinities in the nanomolar range were detected: one, located on glomeruli, bound both vasopressin and oxytocin; the other, on collecting ducts, bound vasopressin selectively. In the presence of 10 μmol oxytocin/1, [3H]vasopressin labelling was abolished in glomeruli, but only reduced in collecting ducts; [3H]oxytocin labelling was completely abolished by 10 μmol vasopressin/1. These observations are discussed in relation to known effects of neurohypophysial hormones on renal physiology.

J. Endocr. (1987) 113, 179–182

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F. Moos, M. J. Freund-Mercier, Y. Guerné, J. M. Guerné, M. E. Stoeckel, and Ph. Richard


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/l 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 μmol/l solution) significantly reduced basal oxytocin release and blocked the stimulatory effect normally induced by exogenous oxytocin, as did gallopamil hydrochloride (D600, 10 μmol/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.

J. Endocr. (1984) 102, 63–72