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

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.

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.


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


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.


1971 ◽  
Vol 51 (2) ◽  
pp. 347-358 ◽  
Author(s):  
I. URBAN ◽  
R. L. MOSS ◽  
B. A. CROSS

SUMMARY Recent investigations in the rabbit have indicated the presence of well-defined afferent nervous pathways for release of neurohypophysial oxytocin. To study these pathways for later use in hypothalamic unit recording, intramammary pressure responses (milk ejection) and arterial pressure were recorded in 45 lactating rabbits with post-pontine brainstem transection. Systematic exploration of the mid-brain tegmentum and ventromedial forebrain areas was carried out with a bipolar stimulating electrode. Release of oxytocin, shown by milk-ejection responses similar to those evoked by a 1–2 mu. synthetic oxytocin occurring in the absence of detectable pressor effects, was recorded in less than half the animals. The location of positive stimulation sites was very variable between animals and reproducibility of responses from the same site was poor. It is concluded that present evidence does not support a discrete afferent path in the mid-brain for the milk-ejection reflex and a possible explanation for the inconstant results of stimulation experiments is suggested.


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 203 (2) ◽  
pp. 371-373 ◽  
Author(s):  
Paul Stark ◽  
Giovanni Fazio ◽  
Eugene S. Boyd

Intracranial self-stimulation experiments in the dog using a two-wire electrode, with each wire used as a monopolar electrode and the combination as a bipolar electrode, show that monopolar stimulation may produce either a higher or a lower rate of response than that produced by bipolar stimulation. A theoretical consideration of the changes in current density around the electrode when it is changed from a monopolar to a bipolar electrode shows that such differences are to be expected. The exact location of the structure being stimulated with reference to the two electrode tips will determine whether the structure is subjected to a higher current density on monopolar or on bipolar stimulation.


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