MESENCEPHALIC AREAS CONTROLLING PULSATILE OXYTOCIN RELEASE IN THE SUCKLED RAT

1981 ◽  
Vol 91 (2) ◽  
pp. 233-244 ◽  
Author(s):  
T. S. JUSS ◽  
J. B. WAKERLEY
Keyword(s):  
Medial Geniculate Body ◽  
Milk Ejection ◽  
Ventral Tegmentum ◽  
Irregular Pattern ◽  
Oxytocin Release ◽  
Medial Geniculate ◽  
Radiofrequency Lesions ◽  
Milk Ejection Reflex ◽  
Bilateral Lesions ◽  
And Control

Experiments were performed on anaesthetized lactating rats to investigate the effects of radiofrequency lesions of the mesencephalon on the milk-ejection reflex. In lesioned and control rats, intramammary pressure recordings were used to estimate oxytocin release (number and relative amplitude of the intermittent milk-ejection responses) during a 3-h suckling test with ten pups. Bilateral lesions (diameter 0·5–1·5 mm) of the lateral tegmentum (near the brachium of the inferior colliculus and medial geniculate body) seriously disrupted the milk-ejection reflex, reducing the number of rats ejecting milk (two out of ten v. all 12 controls, P<0·001) and the amount of oxytocin they released (1·35±0·35 (s.e.m.) v. 15·52±2·19 mu. for controls, P<0·05). Unilateral lesions of the lateral tegmentum also impaired milk ejection and, if the suckling stimulus was restricted only to the contralateral nipples, oxytocin release was virtually abolished. Bilateral lesions placed more medially in the intermediate tegmentum were far less disruptive (eight out of nine rats ejected milk), though the amount of oxytocin released in this group (8·64±1·88 mu.) was still significantly (P<0·05) lower than controls. All rats with lesions of the central grey (nine) or ventral tegmentum (eight) displayed reflex milk ejection, as did those with multiple lesions of the tectum, central grey and ventral tegmentum (seven); in these three groups the amounts of oxytocin released (13·88±2·68, 13·10±1·90 and 11·04±1·95 mu. respectively) did not differ significantly from controls. Damage to the ventral tegmentum produced an irregular pattern of milk ejection characterized by occasional abnormally short (<2 min) milk-ejection intervals, though the overall number of responses in 3 h was less than that of controls (20·83±1·82 v. 14·50±1·30 mu., P<0·05). In conclusion, these results delineate two mesencephalic areas of particular importance in the milk-ejection reflex: (a) the lateral tegmentum, which appears to be concerned with transmission of the suckling stimulus from the contralateral nipples and is indispensable for oxytocin release, and (b) the ventral tegmentum which, although not an essential component of the reflex, may contribute to the timing of the intermittent milk-ejection responses.

AN ASCENDING PATHWAY FOR RELEASE OF PROLACTIN IN THE BRAIN OF THE RABBIT

1969 ◽  
Vol 45 (1) ◽  
pp. 111-120 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS
Keyword(s):  
Electrical Stimulation ◽  
Medial Geniculate Body ◽  
Posterior Hypothalamus ◽  
Implanted Electrodes ◽  
Oxytocin Release ◽  
Central Grey Matter ◽  
Medial Geniculate ◽  
Monopolar Electrodes ◽  
Milk Ejection Reflex ◽  
The Brain

SUMMARY Rabbits in pentobarbitone anaesthesia were implanted bilaterally with a pair of monopolar electrodes in the brainstem. Approximately 10 days after the operation, pseudopregnancy was induced by i.v. injection of human chorionic gonadotrophin, and 1 week later the rabbits received electrical stimulation with square-wave pulses through the implanted electrodes for two periods of 30 min. daily for 11 days. At autopsy on the following day the mammary glands were inspected for occurrence of lactogenesis and sites of electrode tips in the brain were determined histologically. Lactogenesis, indicating release of prolactin, occurred when electrical stimulation had been applied to sites in the lateral mesencephalic tegmentum and further forward in a region medio-ventral to the medial geniculate body. Passing rostrally, the pathway moved medially and then forwards in association with the extreme rostral central grey matter, and was traced as far forward as the posterior hypothalamus where sites were found close to, but not involving, the mammillo-thalamic tracts. When compared with our previous studies on the afferent path of the milk-ejection reflex in this species, the ascending path for release of both oxytocin and prolactin appears to be the same in the mesencephalon. However, whereas the ascending path for oxytocin release bifurcates on each side into dorsal and ventral paths which reunite in the posterior hypothalamus, that for prolactin release appears to follow only the dorsal path, since stimulation of the subthalamus, through which the ventral path passes, was ineffective. It is proposed that the pathway traced in the present study represents the mesencephalic and posterior diencephalic route by which impulses initiated by the suckling stimulus attain the hypothalamus to evoke release of prolactin from the adenohypophysis.

THE AFFERENT PATH OF THE MILK-EJECTION REFLEX IN THE BRAIN OF THE GUINEA-PIG

1967 ◽  
Vol 38 (3) ◽  
pp. 337-349 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS ◽  
A. TURVEY
Keyword(s):  
Guinea Pig ◽  
Medial Geniculate Body ◽  
Pituitary Stalk ◽  
Medial Lemniscus ◽  
Milk Ejection ◽  
Major Pathway ◽  
Ventral Thalamus ◽  
Medial Geniculate ◽  
Milk Ejection Reflex ◽  
The Brain

SUMMARY The afferent path of the milk-ejection reflex has been studied in the brain of the lactating guinea-pig in light pentobarbitone anaesthesia. Square-wave pulses were applied between an indifferent electrode in the scalp and a monopolar electrode inserted stereotaxically in the brain. The brain was transected at the mid-cerebellar level to eliminate activation of the sympathetico-adrenal system, and milk-ejection pressure was monitored to detect release of neurohypophysial hormone(s). The afferent path of the reflex in the caudal midbrain was very compact and lay in the lateral tegmentum. More rostrally, milk-ejection responses were obtained from the tectum and mesencephalic central grey, but the major pathway remained in the lateral tegmentum and passed forward to lie ventromedial to the medial geniculate body, after which it divided into two components which we have termed the dorsal and ventral paths. The dorsal path traversed dorsomedially across the brainstem to reach the parafascicular thalamic nucleus, the extreme rostral central grey and the periventricular region at the meso-diencephalic boundary, and then continued forward to reach the pituitary stalk and the medial and dorsal hypothalamus. The ventral path traversed ventromedially to enter the subthalamus and then the lateral hypothalamus, in which it passed both to the rostral basal diencephalon and to the pituitary stalk. In the diencephalon, milk-ejection responses were obtained after stimulation of part of the ventral thalamus, the lateral, dorsal and anterior hypothalamic areas, the dorsomedial, ventromedial, arcuate, supraoptic and paraventricular nuclei, and the pituitary stalk. It is suggested from these findings that in the guinea-pig the suckling stimulus ascends by the spinothalamic system, and continues rostrally to relay with the medial and ventral thalamus, the dorsal longitudinal fasciculus and the medial forebrain bundle. Other ascending pathways in the medial lemniscus and mammillary peduncle may also be involved, but appear to be of only minor significance.

THE AFFERENT PATH OF THE MILK-EJECTION REFLEX IN THE BRAIN OF THE RABBIT

1969 ◽  
Vol 43 (4) ◽  
pp. 663-671 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS ◽  
A. TURVEY
Keyword(s):  
Medial Geniculate Body ◽  
Milk Ejection ◽  
Major Pathway ◽  
Arterial Blood ◽  
Neural Substrate ◽  
Indifferent Electrode ◽  
Medial Geniculate ◽  
Milk Ejection Reflex ◽  
The Brain ◽  
Stimulation Technique

SUMMARY The afferent path of the milk-ejection reflex has been studied in the brain of the anaesthetized lactating rabbit. Electrical stimulation was applied between a monopolar electrode in the brain and an indifferent electrode in the scalp. The brain was transected at the mid-cerebellar level to eliminate sympathetico-adrenal activation, and intramammary pressure and arterial blood pressure were monitored to detect release of neurohypophysial hormones. In the mid-brain, the afferent path of the reflex is compact, lying in the lateral tegmentum of each side and passing forwards to lie medio-ventral to the medial geniculate body. On entering the diencephalon, the pathway on each side bifurcates: a dorsal path passing forwards in association with the extreme rostral central grey and periventricular region, and a ventral path ascending through the subthalamus. The dorsal and ventral paths reunite in the posterior hypothalamus. Delineating the pathway further forward in the hypothalamus, using a simple stimulation technique, was not possible because at this level it intermingles with efferent fibres descending from the paraventricular nucleus to the pituitary stalk. The afferent path of the reflex is concerned with the preferential release of oxytocin from the neurohypophysis, is not a major pathway for the release of vasopressin and its neural substrate in the mid-brain is believed to be the spinothalamic system of fibres.

The subfornical organ and relaxin-induced inhibition of reflex milk ejection in lactating rats

1987 ◽  
Vol 115 (2) ◽  
pp. 347-353 ◽  
Author(s):  
A. J. S. Summerlee ◽  
K. T. O'Byrne ◽  
S. A. Jones ◽  
L. Eltringham
Keyword(s):  
Cerebrospinal Fluid ◽  
Subfornical Organ ◽  
Behavioural Response ◽  
Milk Ejection ◽  
Blood Brain ◽  
Radiofrequency Lesions ◽  
Pressure Changes ◽  
And Control

ABSTRACT Experiments were carried out on anaesthetized, lactating rats to investigate the possible role of the subfornical organ in mediating relaxin-induced inhibition of reflex milk ejection. Milk ejection was judged by the behavioural response of the sucklings and by transient rises in intramammary pressure. Radiofrequency lesions of the subfornical organ, or control lesions in adjacent areas of the cerebrum, did not affect the pattern or the magnitude of intramammary pressure changes at reflex milk ejection. Purified porcine relaxin given by either i.v. (5 μg) or intracerebroventricular (50 ng) injection suppressed reflex milk ejection in intact, sham-lesioned and control-lesioned rats, but had no effect on either the pattern or magnitude of reflex milk ejection in rats with lesions of the subfornical organ. The subfornical organ, which is situated at the interface between the blood, brain and the cerebrospinal fluid appears to mediate, at least in part, the relaxin-induced inhibition of reflex milk ejection in the rat. J. Endocr. (1987) 115, 347–353

EFFECT OF ETHANOL ON UTERINE ACTIVITY DURING SUCKLING IN POST-PARTUM WOMEN

1968 ◽  
Vol 58 (1) ◽  
pp. 133-141 ◽  
Author(s):  
Gorm Wagner ◽  
Anna-Riitta Fuchs
Keyword(s):  
Post Partum ◽  
Blood Alcohol Concentration ◽  
Alcohol Concentration ◽  
Target Organ ◽  
Release Mechanism ◽  
Blood Alcohol ◽  
Milk Ejection ◽  
Oxytocin Release ◽  
Milk Ejection Reflex ◽  
Prior Administration

ABSTRACT Previous experiments indicated that in the rabbit, prior administration of ethyl alcohol inhibits the release of oxytocin elicited by suckling. According to preliminary studies, the same applies also in the human. In the present studies, the effect of ethanol on the milk-ejection reflex in post-partum women was investigated more thoroughly. The milk-ejection reflex was induced by suckling of the infant. The uterine response, recorded by external tocography, was used as a measure of the oxytocin release. Alcohol was administered by mouth as whisky or brandy in suitable dilutions in amounts varying from 0.5 to 1.1 g/kg body weight. By comparison of the uterine response to endogenous (released) and exogenous (injected) oxytocin, it was estimated that about 100–250 mU oxytocin are released by the suckling stimulus in the early puerperium. When alcohol was administered before the application of the stimulus, the release of oxytocin was partially or completely inhibited, but the uterus continued to respond to exogenous oxytocin. As shown previously in the rabbit, the effect of alcohol must thus be on the central release mechanism of oxytocin and not on the peripheral response of the target organ to oxytocin. The degree of inhibition of the oxytocin release was dependent on the alcohol concentration in the blood. With an average blood alcohol concentration of 0.07 per cent the uterine response to suckling during one nursing period was less than half of that observed under normal conditions.

Role of the paraventricular nucleus in controlling the frequency of milk ejection and the facilitatory effect of centrally administered oxytocin in the suckled rat

1990 ◽  
Vol 125 (3) ◽  
pp. 467-NP ◽  
Author(s):  
J. B. Wakerley ◽  
T. S. Juss ◽  
R. Farrington ◽  
C. D. Ingram
Keyword(s):  
Paraventricular Nucleus ◽  
Medial Septum ◽  
Facilitatory Effect ◽  
Milk Ejection ◽  
Before And After ◽  
Radiofrequency Lesions ◽  
Group 3 ◽  
Series Of Experiments ◽  
Milk Ejection Reflex ◽  
Facilitatory Action

ABSTRACT The milk-ejection reflex was studied in anaesthetized, lactating Wistar rats in order to evaluate the contribution of the paraventricular nucleus (PVN) to the patterning of milk ejection and the facilitatory action of centrally administered oxytocin. In the first series of experiments, radiofrequency lesions were performed and centred: (1) antero-dorsal to the PVN, damaging parts of the medial septum and anterior hypothalamus; (2) in the PVN, such that much of the parvocellular division was destroyed, but parts of the magnocellular division remained intact; or (3) in the PVN, destroying both parvocellular and magnocellular divisions. Suckling tests performed before and after lesioning showed that the milk-ejection interval was significantly increased (decreased frequency) after lesioning in groups 2 and 3, but that milk-ejection amplitude was significantly decreased only in group 3. These results suggest that damage to the parvocellular division of the PVN affects milk-ejection frequency, but that damage to the magnocellular PVN only affects amplitude. Subsequent tests on rats injected into the PVN with the neurotoxin N-methyl-d,l-aspartate revealed a fall in the amplitude and frequency of milk ejection, similar to that after complete radiofrequency lesions of the PVN. In the second series of experiments, the facilitatory action of centrally administered oxytocin (1 mU, 2.2 ng) was examined in animals bearing either sham or complete PVN lesions. In both groups, intracerebroventricular injection of oxytocin was able to increase the frequency of milk ejections, although the incidence of milk ejection was lower in the pre- and post-injection period in the PVN-lesioned animals. In conclusion, the parvocellular component of the PVN may be an important site for regulating milk-ejection frequency, possibly mediated by its centrally projecting oxytocin neurones. However, the PVN does not appear to be the principle target site by which central oxytocin exerts its facilitatory effect on the frequency of milk ejection. Journal of Endocrinology (1990) 125, 467–475

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.

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.

Inhibition of oxytocin release during repeated milking in unfamiliar surroundings: the importance of opioids and adrenal cortex sensitivity

2002 ◽  
Vol 69 (1) ◽  
pp. 63-73 ◽  
Author(s):  
JULIANA MAČUHOVÁ ◽  
VLADIMIR TANČIN ◽  
WOLF-DIETER KRAETZL ◽  
HEINRICH H. D. MEYER ◽  
RUPERT M. BRUCKMAIER
Keyword(s):  
Endogenous Opioids ◽  
Opioid Antagonist ◽  
Control Group ◽  
Research Station ◽  
Milk Ejection ◽  
Milk Flow ◽  
Oxytocin Release ◽  
And Control ◽  
Naloxone Treatment ◽  
Vaginal Stimulation

The aim of this study was to test if the opioid antagonist naloxone has a beneficial effect on normalization of oxytocin (OT) release during repeated milking of cows in unfamiliar surroundings. One control milking without naloxone treatment in all cows was performed in the familiar parlour. For four successive evening milkings, cows were transported to, and milked in, the operating theatre of the research station without (control group) or with naloxone administration (1 mg/kg BW) (naloxone group) before milking. After cessation of spontaneous milk flow, but not before 3 min of milking, vaginal stimulation was applied for 2 min. After milk flow ceased again, 10 IU of OT was injected intravenously to remove the remaining milk including residual milk. Milk flow was recorded continuously and blood samples were collected via a jugular vein cannula at 1-min intervals from 1 min before the start of milking until i.v. injection of OT. The inhibition of milk ejection and its normalization during repeated milking in unfamiliar surroundings was not influenced by naloxone treatment. Concentrations of cortisol and β-endorphin during control milking and all relocations were similar in the naloxone and control groups, although their concentrations were higher after relocations than in the control. Therefore, a role of endogenous opioids in the inhibition of milk ejection in unfamiliar surroundings could not be demonstrated. In addition, the effect of exogenous ACTH1–24 (8 IU, i.v.) on the release of cortisol related to the response of cows milked in unfamiliar surroundings was studied. Cows with totally inhibited milk ejection in response to vaginal stimulation during milking after first relocation had numerically, but not significantly lower cortisol levels (8·8±3·4 ng/ml; AUC/min) in response to ACTH than did cows with at least partial milk ejection (38·7±12·9 ng/ml). Thus animals with a higher adrenal response to ACTH seemed to have less severe inhibition of milk ejection.

Effects of medial geniculate lesions on sound localization by the rat

1985 ◽  
Vol 53 (2) ◽  
pp. 361-372 ◽  
Author(s):  
J. B. Kelly ◽  
P. W. Judge
Keyword(s):  
Auditory Cortex ◽  
Sound Localization ◽  
Mammalian Species ◽  
Medial Geniculate Body ◽  
Frequency Noise ◽  
Impaired Performance ◽  
Medial Geniculate ◽  
Speaker Separation ◽  
Bilateral Lesions ◽  
Filtered Noise

Rats with bilateral lesions of the medial geniculate body were tested on a two-choice sound-localization task that required a directional response to a distant sound source. Stimuli included both broadband and filtered noise bursts presented singly or in repetitive trains. Separate tests were conducted with loudspeakers 180 and 60 degrees apart, centered around 0 degree azimuth. With complete bilateral destruction of the medial geniculate, rats could localize both trains and single bursts of noise and were capable of high levels of performance even at small angles of speaker separation. Some evidence of impaired performance was noted with high-frequency noise bursts, but generally the deficits were not severe. Animals with lesions that extended caudally into the brachium of the inferior colliculus and lateral tegmentum were severely impaired in their ability to localize sounds even at large angles of speaker separation. Three of the four animals in this group were incapable of localizing single bursts even with loudspeakers separated by 180 degrees, and the fourth was unable to perform above chance at 60 degrees. The effects of medial geniculate lesions were very similar to those reported previously for rats with lesions of the auditory cortex, but contrasted with reports of severe impairments in sound localization following damage to the auditory cortex in other mammalian species.

Sign in / Sign up

Export Citation Format

Share Document