SYMPATHETICO-ADRENAL INHIBITION OF THE NEUROHYPOPHYSIAL MILK-EJECTION MECHANISM

1953 ◽  
Vol 9 (1) ◽  
pp. 7-18 ◽  
Author(s):  
B. A. CROSS
Keyword(s):  
Electrical Stimulation ◽  
Inhibitory Effect ◽  
Posterior Pituitary ◽  
Pituitary Extract ◽  
Milk Ejection ◽  
Emotional Inhibition ◽  
Adrenal System ◽  
Ejection Mechanism ◽  
Milk Ejection Reflex ◽  
Stimulation Of

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.

NEUROHORMONAL MECHANISMS IN EMOTIONAL INHIBITION OF MILK EJECTION

1955 ◽  
Vol 12 (1) ◽  
pp. 29-37 ◽  
Author(s):  
B. A. CROSS
Keyword(s):  
Emotional Disturbance ◽  
Posterior Pituitary ◽  
Milk Ejection ◽  
Emotional Inhibition ◽  
Conscious Animal ◽  
Adrenal System ◽  
Oxytocin Release ◽  
Posterior Pituitary Gland ◽  
Milk Ejection Reflex ◽  
Main Factor

SUMMARY 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.

THE ROLE OF THE NEUROHYPOPHYSIS IN THE MILK-EJECTION REFLEX

1952 ◽  
Vol 8 (2) ◽  
pp. 148-161 ◽  
Author(s):  
B. A. CROSS ◽  
G. W. HARRIS
Keyword(s):  
Intravenous Injection ◽  
Mammary Glands ◽  
Posterior Pituitary ◽  
Pituitary Extract ◽  
Active Process ◽  
Milk Ejection ◽  
Marked Diminution ◽  
Milk Ejection Reflex ◽  
Stimulation Of

1. Nursing and suckling behaviour of rabbits is described, and evidence given that an active process of milk ejection ('let-down') occurs in this as in other species. 2. Intravenous injection of posterior pituitary extracts in anaesthetized rabbits resulted in ejection of milk from a cannulated teat duct. The threshold dose was about 5 mU. and maximal responses were produced by 200 mU. of extract. Whole posterior pituitary extract was more effective than the oxytocic fraction, which was in turn more effective than the vasopressor fraction. 3. Stimulation of the supraopticohypophysial (s.o.h.) tract in anaesthetized rabbits also resulted in ejection of milk from a cannulated duct. Kymographic records of this response were similar to those obtained after injection of appropriate doses of posterior pituitary extract. 4. Lesions in the s.o.h. tract in lactating rabbits caused a marked diminution in the quantity of milk obtained by their litters in standard suckling tests, and incomplete evacuation of the mammary glands. Intravenous injection of posterior pituitary extract (30–200 mU.) into the does immediately before nursing gave a marked increase in the amount of milk obtained by the young and complete evacuation of the mammary glands. Stimulation of the region of the s.o.h. tract in these animals failed to elicit milk ejection from cannulated teat ducts. 5. Rabbits with hypothalamic lesions that did not involve the s.o.h. tract showed a normal milk-ejection reflex when suckled by their young, and a milk-ejection response after electrical stimulation of the s.o.h. tract.

MAMMARY OXYGEN TENSION AND THE MILK-EJECTION MECHANISM

1962 ◽  
Vol 23 (4) ◽  
pp. 375-384 ◽  
Author(s):  
B. A. CROSS ◽  
I. A. SILVER
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Mammary Glands ◽  
Capillary Blood ◽  
Milk Ejection ◽  
Electrolytic Lesions ◽  
Ejection Mechanism ◽  
Urethane Anaesthesia ◽  
Surgical Shock ◽  
Stimulation Of

SUMMARY 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.

PREFERENTIAL RELEASE OF OXYTOCIN FROM THE NEUROHYPOPHYSIS AFTER ELECTRICAL STIMULATION OF THE AFFERENT PATH OF THE MILK-EJECTION REFLEX IN THE BRAIN OF THE GUINEA-PIG

1968 ◽  
Vol 40 (2) ◽  
pp. 205-214 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS ◽  
A. TURVEY
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Guinea Pig ◽  
Arterial Blood Pressure ◽  
Pituitary Stalk ◽  
Milk Ejection ◽  
Arterial Blood ◽  
Milk Ejection Reflex ◽  
The Brain ◽  
Stimulation Of

SUMMARY Discrete portions of the afferent path of the milk-ejection reflex have been explored in the brain of the lactating guinea-pig. Both intramammary pressure and arterial blood pressure were recorded to detect release of oxytocin and vasopressin. It was found that the milk-ejection responses which occurred after electrical stimulation of the pathway in the midbrain and hypothalamus were caused by the release of oxytocin without detectable release of vasopressin. A mixture of oxytocin and vasopressin, in the ratio of approximately 3:1, was released only after electrical stimulation of the rostral tuberal region of the hypothalamus adjacent to the pituitary stalk. It is concluded that the afferent path in the brain of the guinea-pig studied is concerned with the preferential release of oxytocin from the neurohypophysis and that it is the pathway of the milk-ejection reflex.

DETERMINATION OF THE DETAILED HYPOTHALAMIC ROUTE OF THE MILK-EJECTION REFLEX IN THE GUINEA-PIG

1971 ◽  
Vol 50 (1) ◽  
pp. 135-152 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS
Keyword(s):  
Electrical Stimulation ◽  
Lateral Hypothalamus ◽  
Third Ventricle ◽  
Milk Ejection ◽  
Lateral Direction ◽  
Reflex Pathway ◽  
Oxytocin Release ◽  
Far Lateral ◽  
Milk Ejection Reflex ◽  
Stimulation Of

SUMMARY The effect of various types of surgical damage to the forebrain on the release of oxytocin in response to electrical stimulation of the discrete ascending milk-ejection reflex pathway in the mid-brain was investigated in 99 anaesthetized lactating guinea-pigs. Oxytocin release was measured by comparison of experimental milk-ejection responses with the response to i.v. injection of known amounts of synthetic oxytocin. Removal of the entire telencephalon, including cerebral cortex, hippocampi, amygdalae and forebrain rostral to the hypothalamus, did not affect the subsequent release of oxytocin after electrical stimulation of the pathway in the mid-brain, from which it was concluded that the reflex pathway within the forebrain is entirely diencephalic. Transection of the hypothalamus immediately rostral to the paraventricular (PV) nuclei was without effect, while transection immediately caudal to the PV nuclei blocked the release of oxytocin. Destruction of the PV nuclei by a radiofrequency lesion which spared the supraoptic (SO) nuclei blocked the release of oxytocin. Undercutting both PV nuclei so as to isolate them from the ventral hypothalamus blocked the release of oxytocin. Undercutting the PV nucleus ipsilateral to the stimulated side of the mid-brain blocked the release of oxytocin, while undercutting the contralateral PV nucleus had no effect. The PV nuclei, therefore, lie on the ascending path of the milk-ejection reflex, the SO nuclei do not, and, from the mid-brain forwards, the ascending pathway remains uncrossed. The course of the reflex pathway was traced rostrally from the mesodiencephalic junction by making narrow transverse knife-cuts and determining which cuts reduced or blocked the release of oxytocin after mid-brain stimulation. At this level, the pathway on each side of the brain is represented by separate dorsal and ventral paths and in the present study it was found that the ventral path is more important than the dorsal path in terms of oxytocin release. The ventral path passes forward in the medial forebrain bundle, in the far-lateral hypothalamus, while the dorsal path enters the posterior hypothalamus dorsally in the periventricular region at the top of the third ventricle and impinges on the thalamic reuniens nucleus. Shortly afterwards the dorsal path swings abruptly in the lateral direction to join the ventral path in the lateral hypothalamus. The reunited pathway then moves forward in this position until it is level with the PV nuclei, where it swings dorsomedially to relay with the lateral tip of the ipsilateral PV nucleus, and in doing so intermingles with the descending neurosecretory fibres from this nucleus.

Suckling-induced release of cholecystokinin into plasma in the lactating rat: effects of abdominal vagotomy and lesions of central pathways concerned with milk ejection

1990 ◽  
Vol 127 (2) ◽  
pp. 257-263 ◽  
Author(s):  
A. Linden ◽  
M. Eriksson ◽  
S. Hansen ◽  
K. Uvnäs-Moberg
Keyword(s):  
Electrical Stimulation ◽  
Plasma Levels ◽  
Vagal Nerve ◽  
Milk Ejection ◽  
Vagal Nerves ◽  
Plasma Cholecystokinin ◽  
Milk Ejection Reflex ◽  
Stimulation Of

ABSTRACT Plasma levels of cholecystokinin were increased in response to suckling in lactating rats. Efferent electrical stimulation of the vagal nerve increased the concentration of cholecystokinin in plasma. Abdominal vagotomy was found to block the suckling-induced release of cholecystokinin. Furthermore, lesions to the lateral midbrain, which disrupt the oxytocin-mediated milk-ejection reflex, were shown to inhibit the increase in plasma cholecystokinin. These results show that the suckling-induced release of cholecystokinin into plasma in lactating rats is dependent upon the vagal nerves and the central neural structures concerned with milk let-down. Journal of Endocrinology (1990) 127, 257–263

FURTHER STUDIES ON THE AFFERENT PATH OF THE MILK-EJECTION REFLEX IN THE BRAIN STEM OF THE RABBIT

1975 ◽  
Vol 66 (1) ◽  
pp. 107-113 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS
Keyword(s):  
Electrical Stimulation ◽  
Inhibitory Mechanism ◽  
Milk Ejection ◽  
Initial Release ◽  
Discrete Nature ◽  
Stimulation Experiments ◽  
Milk Ejection Reflex ◽  
The Brain ◽  
Guinea Pig Brain ◽  
Stimulation Of

SUMMARY When the afferent pathway of the milk-ejection reflex, which we had previously reported, was surgically severed bilaterally in the mid-brain of the lactating rabbit, the reflex release of oxytocin in response to suckling was blocked for up to 11 days; unilateral severance did not block the reflex. The position and discrete nature of the pathway were also further substantiated by electrical stimulation experiments in acute studies in the anaesthetized rabbit. Some animals, however, did not release oxytocin in response to stimulation of the pathway. Furthermore, whereas stimulation of this reflex pathway in the guinea-pig brain at intervals of a few minutes evokes release of oxytocin after each stimulation, in the present study the release of oxytocin in the rabbit in response to repeated electrical stimulation was either progressively attenuated or did not occur at all after the initial release. There appears, therefore, to be a powerful overriding central inhibitory mechanism in the rabbit which can prevent release of oxytocin, even when the appropriate stimulus for release is applied.

Cross-talk along gastrointestinal tract during electrical stimulation: effects and mechanisms of gastric/colonic stimulation on rectal tone in dogs

2005 ◽  
Vol 288 (6) ◽  
pp. G1195-G1198 ◽  
Author(s):  
Shi Liu ◽  
Lijie Wang ◽  
J. D. Z. Chen
Keyword(s):  
Electrical Stimulation ◽  
Inhibitory Effect ◽  
Adrenergic Blockade ◽  
Rectal Compliance ◽  
Rectal Tone ◽  
Before And After ◽  
Sensory Functions ◽  
Sympathetic Pathway ◽  
Colonic Electrical Stimulation ◽  
Stimulation Of

Gastric electrical stimulation (GES) has been shown to alter motor and sensory functions of the stomach. However, its effects on other organs of the gut have rarely been investigated. The study was performed in 12 dogs implanted with two pairs of electrodes, one on the serosa of the stomach and the other on the colon. The study was composed of two experiments. Experiment 1 was designed to study the effects of GES on rectal tone and compliance in nine dogs compared with colonic electrical stimulation (CES). Rectal tone and compliance were assessed before and after GES or CES. Experiment 2 was performed to study the involvement of sympathetic pathway in 8 of the 12 dogs. The rectal tone was recorded for 30–40 min at baseline and 20 min after intravenous guanethidine. GES or CES was given for 20 min 20 min after the initiation of the infusion. It was found that both GES and CES reduced rectal tone with comparable potency. Rectal compliance was altered neither with GES, nor with CES. The inhibitory effect of GES but not CES on rectal tone was abolished by an adrenergic blockade, guanethidine. GES inhibited rectal tone with a comparable potency with CES but did not alter rectal compliance. The inhibitory effect of GES on rectal tone is mediated by the sympathetic pathway. It should be noted that electrical stimulation of one organ of the gut may have a beneficial or adverse effect on another organ of the gut.

Electronmicroscopic and electrophysiological studies of the teat branch of the XIII thoracic nerve: relationship with lactation in the rat

1988 ◽  
Vol 118 (3) ◽  
pp. 471-483 ◽  
Author(s):  
L. M. Voloschin ◽  
E. Décima ◽  
J. H. Tramezzani
Keyword(s):  
Electrical Stimulation ◽  
Conduction Velocity ◽  
Action Potentials ◽  
Silent Period ◽  
High Amplitude ◽  
Milk Ejection ◽  
Nerve Activity ◽  
Thoracic Nerve ◽  
Myelinated Fibres ◽  
Stimulation Of

ABSTRACT Electrical stimulation of the XIII thoracic nerve (the 'mammary nerve') causes milk ejection and the release of prolactin and other hormones. We have analysed the route of the suckling stimulus at the level of different subgroups of fibres of the teat branch of the XIII thoracic nerve (TBTN), which innervates the nipple and surrounding skin, and assessed the micromorphology of the TBTN in relation to lactation. There were 844 ± 63 and 868 ± 141 (s.e.m.) nerve fibres in the TBTN (85% non-myelinated) in virgin and lactating rats respectively. Non-myelinated fibres were enlarged in lactating rats; the modal value being 0·3–0·4 μm2 for virgin and 0·4–0·5 μm2 for lactating rats (P > 0·001; Kolmogorov–Smirnov test). The modal value for myelinated fibres was 3–6 μm2 in both groups. The compound action potential of the TBTN in response to electrical stimulation showed two early volleys produced by the Aα- and Aδ-subgroups of myelinated fibres (conduction velocity rate of 60 and 14 m/s respectively), and a late third volley originated in non-myelinated fibres ('C') group; conduction velocity rate 1·4 m/s). Before milk ejection the suckling pups caused 'double bursts' of fibre activity in the Aδ fibres of the TBTN. Each 'double burst' consisted of low amplitude action potentials and comprised two multiple discharges (33–37 ms each) separated by a silent period of around 35 ms. The 'double bursts' occurred at a frequency of 3–4/s, were triggered by the stimulation of the nipple and were related to fast cheek movements visible only by watching the pups closely. In contrast, the Aα fibres of the TBTN showed brief bursts of high amplitude potentials before milk ejection. These were triggered by the stimulation of cutaneous receptors during gross slow sucking motions of the pup (jaw movements). Immediately before the triggering of milk ejection the mother was always asleep and a low nerve activity was recorded in the TBTN at this time. When reflex milk ejection occurred, the mother woke and a brisk increase in nerve activity was detected; this decreased when milk ejection was accomplished. In conscious rats the double-burst type of discharges in Aδ fibres was not observed, possibly because this activity cannot be detected by the recording methods currently employed in conscious animals. During milk ejection, action potentials of high amplitude were conveyed in the Aα fibres of the TBTN. During the treading time of the stretch reaction (SR), a brisk increase in activity occurred in larger fibres; during the stretching periods of the SR a burst-type discharge was again observed in slow-conducting afferents; when the pups changed nipple an abrupt increase in activity occurred in larger fibres. In summary, the non-myelinated fibres of the TBTN are increased in diameter during lactation, and the pattern of suckling-evoked nerve activity in myelinated fibres showed that (a) the double burst of Aδ fibres, produced by individual sucks before milk ejection, could be one of the conditions required for the triggering of the reflex, and (b) the nerve activity displayed during milk-ejection action may result, at least in part, from 'non-specific' stimulation of cutaneous receptors. J. Endocr. (1988) 118, 471–483

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