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1. Emotional inhibition of the milk-ejection reflex in rabbits is described.

2. Injection of 5–50 μg adrenaline intravenously into does before nursing interfered with milk ejection, as shown by the failure of the young to withdraw more than three-quarters of the normal yield of milk. Injection of 150 mU (=milliunits) 'Pitocin' immediately after the adrenaline did not restore normal milk ejection.

3. Intravenous injection of 5 μg adrenaline suppressed the milk-ejection response to 50 mU posterior pituitary extract in anaesthetized rabbits with cannulated teats, provided the injection of adrenaline preceded that of the posterior pituitary extract. The inhibitory effect had not entirely disappeared in 2 min. 50μg adrenaline prevented the occurrence of milk ejection for 3½ min.

4. Intravenous doses of 5 μg adrenaline, but not smaller amounts, inhibited the milk-ejection response to electrical stimulation of the supraoptico-hypophysial tract, if injected before stimulation or during the latent period of the response. When injected after the commencement of milk ejection 5 μg adrenaline was without effect, but 50 μg abolished the response.

5. Electrical stimulation of the posterior hypothalamus produced inhibition of the milk-ejection response to injected oxytocic extract, together with pupillary dilatation and exophthalmos. The inhibition closely resembled that resulting from injection of adrenaline.

6. It is concluded that one mechanism involved in the emotional inhibition of milk ejection is an activation of the sympathetico-adrenal system, resulting in antagonism of the action of the neurohypophysial milk-ejection hormone on the contraction process within the mammary gland.

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1. Fifteen lactating rabbits were maintained on a regime of one daily nursing in which litter weights, milk yields and duration of nursing were recorded.

2. Sodium pentobarbitone anaesthesia blocked the milk-ejection reflex and prevented the removal of more than 15% of the full milk yield by the young. Intravenous injection of 50 mU oxytocin regularly restored normal milk removal; 10 and 20 mU did not.

3. In thirty-five out of forty-two experiments in which the does were suckled while under forcible restraint the amount of milk removed was reduced by 20–100%. In twenty-nine cases injection of 50 mU oxytocin restored normal milk removal. In the remaining six experiments this replacement therapy was fully effective only after the does had been anaesthetized.

4. Kymograph records of milk-ejection responses showed that normal milk removal was associated with a reflex milk-ejection response similar to that produced by 50 mU oxytocin, and incomplete milk removal with a reduced (=5 mU oxytocin) or absent milk-ejection response. Where injection of 50 mU oxytocin failed to restore normal milk removal in the conscious animal, the resulting milk-ejection response was reduced by an amount similar to that produced by injection of 1μg adrenaline.

5. The results indicate that, while activation of the sympathetico-adrenal system does occur, the main factor in emotional disturbance of the milk-ejection reflex is a partial or complete inhibition of oxytocin release from the posterior pituitary gland.

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The parturitional behaviour of full-term rabbits injected with 100 or 200 mu. oxytocin is described. Young were born at rates varying from twelve in 7 min to three in 20 min. Newborn pups suckled the doe while she was still in labour.

Labour was induced in full-term does under sodium pentobarbitone anaesthesia by injection of 50–200 mu. oxytocin or by electrical stimulation of the supraoptico-hypophysial tract. Abdominal contractions, milk ejection and delivery of young were recorded kymographically. The delivery of every pup was assisted by reflex straining movements of the doe. Though commonly labour was completed without the secretion of additional oxytocin from the neurohypophysis (as shown by the milk-ejection record), occasionally a reflex release of oxytocin did occur in amounts sufficient to influence the course of labour. In many cases labour appeared to be as efficient as in the conscious animal.

Suppression of abdominal contractions by spinal anaesthesia did not prevent effective delivery of young after injection of oxytocin. However, the time taken to expel individual pups from the vagina tended to increase, and the last of the litter was generally retained in the vagina.

The physiological mechanisms involved in parturition in the rabbit are discussed in the light of these and earlier findings.

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The spontaneous motility of the intact uterus of spayed oestrogenized rabbits under sodium pentobarbitone anaesthesia has been recorded. Both uteri of each animal behaved similarly, and contractions often appeared to be synchronous. Small changes of load affected the amplitude of contractions, but did not alter uterine responsiveness to neurohypophysial or adrenomedullary hormones. Mid-thoracic section of the spinal cord obliterated spontaneous motility of the uterus; spinal anaesthesia did not. Spontaneous motility persisted for as long as 7 hr after decerebration and removal of the pituitary gland.

The threshold dose of oxytocin for activating the oestrogenized uterus was the same as that for the lactating mammary gland, i.e. 1–5 mu. Doses up to 50 mu. usually gave an increase in frequency and amplitude of contractions. In the same dose range vasopressin either had little effect or inhibited spontaneous uterine motility, although milk ejection was stimulated. Slow infusion of oxytocin at rates of 1·5–48 mu./min produced graded increases in the rate and depth of uterine contractions and, at the same time, in similarly treated, lactating animals, rhythmic milk-ejection responses which at the higher rates of infusion merged to give a tetanic (plateau) type of milk ejection.

Adrenaline or noradrenaline in doses of 1–5 μg produced diphasic uterine responses, initial contractions being followed by inhibition of spontaneous motility. They also inhibited the uterine, as well as the milk-ejection response to oxytocin injected 10–30 sec later. The inhibitory effect of adrenaline on both organs was about twice that of noradrenaline.

The above-mentioned responses to adrenaline and oxytocin could also be elicited by electrical stimulation of the hypothalamus. Stimuli in the dorsal, lateral, perifornical and posterior hypothalamic areas produced effects equivalent to those of 1–5 μg adrenaline on both the uterus and mammary gland. These responses were abolished by mid-thoracic section of the spinal cord or by spinal anaesthesia. In such preparations responses typical of those produced by oxytocin were seen in both organs after stimulation of the paraventricular nuclei, supraoptic nuclei and the hypothalamo-hypophysial nerve pathways of the tuber cinereum and neural stalk.

Dilatation of the vagina (or rectum) gave rise to a uterine response similar to that resulting from adrenaline or noradrenaline. The response was abolished by spinal anaesthesia, but not by mid-thoracic spinal section or decerebration. The same stimuli also produced 'bearing down' contractions of the abdominal muscles. Contractions of the uterus could also be elicited by mechanical stimuli, in the absence of functional spinal connexions.

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1. Electrical stimulation of the supraoptico-hypophysial system gave rise to milk ejection from cannulated teats in anaesthetized lactating rabbits. Stimuli applied in the vicinity of the paraventricular nucleus produced signs of sympathetic activity and no milk-ejection responses in the intact animal, but after acute adrenalectomy milk-ejection responses could be elicited from this region.

2. Stimulation of the dorsal, lateral and posterior areas of the hypothalamus, but not of the ventral tuberal regions, caused pupillary dilatation, exophthalmos and hyperpnoea, and inhibited the milk-ejection response to oxytocin injected intravenously 10–15 sec after the end of the stimulus. The inhibitory effect could be simulated by injection of 1–5 μg adrenaline. It was abolished by bilateral adrenalectomy.

3. Inhibition of the milk-ejection response to oxytocin was also produced by stimulation of the splanchnic nerve supply to the adrenal glands, and of the sympathetic nerve supply to the mammary glands. After bilateral adrenalectomy some inhibitory effect on milk-ejection was apparent when oxytocin was injected during prolonged stimulation of the sympathetic centres of the hypothalamus.

4. Adrenaline was 1½ to 4 times more active in blocking the milk-ejection response to intravenous oxytocin than noradrenaline.

5. Stimulation of the hypothalamus or mammary sympathetic nerves, and injection of adrenaline or noradrenaline did not inhibit the milk-ejection response to mechanical stimuli applied direct to the mammary glands.

6. The inhibition of the milk-ejection response to oxytocin produced by stimulation of the hypothalamus was associated with inability of the young to remove milk from the mammary glands during suckling.

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1. The milk-ejection activity of highly purified oxytocic and vasopressor-antidiuretic (ADH) polypeptides was determined on the intact mammary gland of the lactating rabbit.

2. When assayed in this way, 100 units of vasopressin-ADH had an activity represented by 17 units of oxytocin.

3. The lactating rabbit mammary gland is more sensitive to oxytocin than the rat uterus, and appears to be the best means at present available for assessing milk-ejection activity.

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1. Polarographic recording of pO2 from gold-plated needle electrodes inserted into lactating mammary glands of rabbits under light urethane anaesthesia gave resting values of 15–30 mm. Hg. Expelling the milk from distended glands raised the pO2 level.

2. Myoepithelial contraction (milk ejection) induced by i.v. injection of oxytocin lowered pO2 by an amount depending on the rise in intramammary pressure.

3. Surgical shock, spinal anaesthesia or i.v. injection of adrenaline depressed mammary pO2 and reduced the milk-ejection response to i.v. oxytocin.

4. When mammary pO2 was raised by O2 breathing, or lowered by N2 breathing, the milk-ejection response to i.v. oxytocin was not affected.

5. Electrical stimulation of the lateral and posterior hypothalamic areas reduced mammary pO2 and milk ejection in a way similar to i.v. adrenaline. Bilateral electrolytic lesions in these areas produced a sustained depression of mammary pO2.

6. It is concluded that the pO2 of mammary tissues gives a measure of capillary blood flow and that this, rather than the absolute pO2 level, determines the response of the myoepithelium to circulating oxytocin.

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A polygraphic recording method was used to study unit activity in the hypothalamus (mainly the lateral hypothalamic area) and thalamus (mainly N. anteroventralis and N. ventralis) in adult female rats under light urethane anaesthesia.

The percentage of hypothalamic neurones excited by mechanical probing of the cervix in rats, 7–11 days pseudopregnant, was only one-fourth of that previously observed in cyclic rats, and a fourfold increase was procured by removing the pseudopregnant ovaries before commencing unit recording. In the ovariectomized rat initially responsive hypothalamic neurones ceased to be excited by cervix stimuli 30 min. after the i.v. injection of 400 μg. progesterone and regained their responsiveness in 1 hr.

Only small differences were recorded in the percentage of hypothalamic neurones excited by pain or cold stimuli on the tail in cyclic, pseudopregnant and ovariectomized pseudopregnant rats. There was likewise little change in the small percentage of neurones inhibited by the test stimuli in the presence or absence of pseudopregnant ovaries.

The percentage of thalamic neurones excited by cervical stimuli in pseudopregnant rats was not depressed below that of ovariectomized animals. The findings are thought to indicate that exogenous or endogenous progesterone selectively depresses the excitation of hypothalamic neurones by stimuli from the genital tract.

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Unit activity in the hypothalamus and other diencephalic regions was recorded with stereotaxically oriented steel microelectrodes in adult female rats under light urethane anaesthesia.

Spontaneous firing rates of neurones varied from < 1/10 sec. to > 50/sec., but the majority fired at 1–10/sec. Some variations in the pattern of firing are described.

Acceleration of firing rate was most readily induced by pain stimuli (64% of neurones) and then by cold (60%), probing the cervix (47%), smell (20%), light (5%) and noise (3%) in that order. A minority of neurones were inhibited by the stimuli.

Many neurones responded to several different stimuli, most commonly by accelerating to cervical probing, cold and pain. Inhibitory convergence was also observed, e.g. blockade of the response to cervical probing by an olfactory stimulus, and inhibition by cervical probing of the response to cold or pain.

The proportion of neurones excited by smell in prooestrous rats was more than double that in oestrous or dioestrous rats. Oestrous rats had relatively more neurones which were unresponsive or inhibited by the test stimuli.

Slow intravenous injection of 400 μg. progesterone induced a selective depression of the response of lateral hypothalamic neurones to cervical probing. The effect was maximal at about 30 min. and full recovery occurred in 1 hr.

The possible significance of these observations is discussed with particular reference to the neural control of luteotrophin secretion.

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1. Stimulation of the hypogastric nerves in adult male rabbits under sodium pentobarbitone anaesthesia produced immediate contractions of the cauda epididymidis, vas deferens and seminal vesicle, with emission of semen. Kymographic records were obtained of the contractions of the seminal vesicle.

2. Intravenous injections of 1–5 μg adrenaline gave similar effects, but with latencies of 7–30 sec. Measured by its action on the seminal vesicle, adrenaline was two to five times more potent than noradrenaline.

3. Electrical stimulation of the dorsal, lateral or posterior areas of the hypothalamus evoked an immediate contraction of the seminal vesicle followed by a delayed contractile effect. Contractions of the cauda epididymidis and vas deferens also occurred.

4. The immediate response of the seminal vesicle to stimulation of the hypothalamus was abolished by section of the hypogastric nerves, and the delayed effect by adrenalectomy. After these interferences the two types of response could be simulated by stimulation of the peripheral end of the cut hypogastric nerves, and by injection of 1–5 μg adrenaline, respectively.

5. Neither electrical stimulation of the neurohypophysis, nor injection of oxytocin or vasopressin induced a contraction of the seminal vesicle.

6. The results are discussed with reference to the influence of sexual excitation at coitus on the volume and quality of ejaculated semen.