scholarly journals Effect of electrical stimulation of hypothalamuson milk-ejection in rabbits

1956 ◽  
Vol 2 (2) ◽  
pp. 44-46
Author(s):  
A. YOKOYAMA
1988 ◽  
Vol 118 (3) ◽  
pp. 471-483 ◽  
Author(s):  
L. M. Voloschin ◽  
E. Décima ◽  
J. H. Tramezzani

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


1962 ◽  
Vol 23 (4) ◽  
pp. 375-384 ◽  
Author(s):  
B. A. CROSS ◽  
I. A. SILVER

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.


1968 ◽  
Vol 40 (2) ◽  
pp. 205-214 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS ◽  
A. TURVEY

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.


1971 ◽  
Vol 50 (1) ◽  
pp. 135-152 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS

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.


1971 ◽  
Vol 50 (4) ◽  
pp. 607-618 ◽  
Author(s):  
D. W. LINCOLN

SUMMARY Labour was induced by electrical stimulation of the infundibulum and median eminence in the conscious prepartum rabbit. The stimulus was applied for 20 s through a chronically implanted platinum—rhodium electrode and consisted of 1 mA biphasic pulses at 50/s. The first visible signs of labour occurred 1·5–3·0 min after stimulation and activity usually ceased within 25 min. This was sometimes sufficient for the delivery of the entire litter. The litters ranged from 5 to 11 pups. Frequently, labour ceased before all the young were expelled, but labour was easily restarted by a further period of stimulation. There were cases in which labour was restarted on more than four occasions before parturition reached completion. Parturition was sometimes left in a suspended state for more than 24 h. The viability of the pups was not adversely influenced by the protracted nature of such parturitions. Stimulation was most effective at inducing labour when applied close to the predicted time of parturition and the treatment was almost totally ineffective when applied more than 48 h before the predicted time. Nest-building was not precipitated by the premature birth of the young and sometimes occurred a day or more after parturition. The stimulation parameters used for the induction of labour caused large milk-ejection responses when applied to the same animals during lactation. Some of these milk-ejection responses were equal to the release of more than 100 mu. oxytocin. These results suggest that the rapid expulsion of the pups during natural labour in the rabbit could be the result of a sudden and very large release of oxytocin.


1990 ◽  
Vol 127 (2) ◽  
pp. 257-263 ◽  
Author(s):  
A. Linden ◽  
M. Eriksson ◽  
S. Hansen ◽  
K. Uvnäs-Moberg

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


1958 ◽  
Vol 16 (3) ◽  
pp. 261-276 ◽  
Author(s):  
B. A. CROSS

SUMMARY 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.


1975 ◽  
Vol 66 (1) ◽  
pp. 107-113 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS

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.


1953 ◽  
Vol 9 (1) ◽  
pp. 7-18 ◽  
Author(s):  
B. A. CROSS

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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