Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Milk Ejection”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1992

Lesion and electrophysiological studies on the hypothalamic afferent pathway of the milk ejection reflex in the rat.

The afferent pathway of the milk ejection reflex in the hypothalamus was investigated with lesion and electrophysiological methods in anesthetized lactating rats. Destruction of the central region of the mid-hypothalamus (n = 12) blocked milk ejections induced by suckling, while that of the lateral region (n = 7) had no effect. In an electrophysiological study, extracellular recordings of neurons antidromically activated by electrical stimulation of the supraoptic nucleus were obtained from the ipsilateral hypothalamus caudal to the paraventricular nucleus (n = 84). Thirty-nine neurons were examined to see whether their firing activities changed during the milk ejection reflex. A group of 13 neurons were found to show changes in their activities prior to the reflex milk ejection; the neurons displayed a brief high-frequency burst of spikes before each milk ejection in the same manner as oxytocin neurons, and none of them antidromically responded to electrical stimulation of the neurohypophysis. The bursting neurons were recorded from the dorsomedial hypothalamic nucleus (n = 6), the region just lateral to that nucleus (n = 3) and the posterior hypothalamus (n = 4). The locations were included in a region whose destruction blocked the milk ejection reflex. These results indicate that the afferent pathway of the milk ejection reflex in the rat runs through the medial portion of the hypothalamus posterior to the paraventricular nucleus and that this region contains neurons which relay the input to the oxytocin neurons projecting in the neurohypophysis.

Afferent Pathways↗
PubMed1976

Inhibitory effect of prostaglandin F2 alpha on oxytocin release and on milk ejection in lactating rats.

The effect of prostaglandin F2 alpha (PGF2alpha) on milk ejection and on oxytocin release during suckling for one or two periods of 30 min was studied in lactating rats. Doses of PGF2 alpha (20 or 40 phi g) were injected i.p. 15 min before the suckling period. Control rats were injected with physiological saline. An inhibition of milk ejection proportional to the dose of drug administered was obtained. A normal milk ejection response was induced with a small dose of oxytocin injected immediately before nursing to mothers treated with PGF2 alpha, indicating that the blocking effect was not due to a lack of mammary gland response. Two groups of mothers were injected with 40 phi g PGF2 alpha 2 and 4 h respectively before suckling. In both groups milk ejection was partially but significantly inhibited. In rats pre-treated with sodium pentobarbitone (3-5 mg/100 g body wt) to prevent the release of oxytocin induced by suckling, PGF2 alpha (10 or 20 phi g) did not modify the inhibition of milk ejection indicating that PGF2 alpha does not have milk-ejecting activity. The administration of oxytocin to anaesthetized rats, immediately before a second suckling period, induced a normal milk-ejection response while in the rats treated with PGF2 alpha, oxytocin was less effective. The results indicate that PGF2 alpha inhibited milk ejection by a central block on oxytocin release and that the lipid is not able to mimic peripherally the milk-ejecting activity of oxytocin.

Animals↗
PubMed2005

The use of ultrasound to characterize milk ejection in women using an electric breast pump.

This study aimed to use ultrasound imaging to investigate the milk ejection characteristics of women during a 10-minute expression using an electric breast pump capable of applying 2 markedly different vacuum patterns. The classic pattern (47 cycles/min) and 3-phase pattern (pre-milk ejection: 120 cycles/min, post-milk ejection: 20 cycles/min for 2 minutes post-milk ejection then 55-78 cycles/min for 8 minutes) were tested, and the milk expressed was collected in 30-second intervals. Multiple milk ejections (96%) were detected (classic: 3.27+/-2.05; 3-phase: 3.72+/-1.19) and associated with increases in milk flow. Almost half of the total volume of milk expressed was removed during the first milk ejection (classic: 41.38+/-21.48%; 3-phase: 46.72+/-26.60%). There was no correlation between the number of milk ejections and both the total volume of milk and percentage of available milk for either pattern. In conclusion, milk ejection characteristics and efficiency of milk expression did not change in response to different expression patterns.

Adult↗
PubMed1984

Spinal pathway of the milk-ejection reflex in the rat.

The effects of lesions of the spinal cord on the milk-ejection reflex evoked by suckling were studied in urethane-anesthetized lactating rats. All lesions were made between C6 and C7 vertebrae and milk ejection was monitored by recording intramammary pressure. In the first experiment on the rats with bilateral lesions, a 3-h suckling test with 5 pups on each side was performed. Eleven (84.6%) of 13 rats with the section of the dorsal funiculus (Group 2), and 12 (85.7%) of 14 rats with the combined section of the dorsal and ventral funiculi (Group 4) displayed regular milk ejection. The incidence of milk ejection in both groups was not significantly different from 81.8% (9 rats) of the 11 sham-operated rats (Group 1). In contrast, none of the 12 rats with bilateral section of the lateral funiculus (Group 3) displayed milk ejection and the incidence of milk ejection was significantly lower than that in Group 1. In the second experiment on the rats with unilateral section of the lateral funiculus, bilateral suckling with 10 pups (5 pups on each side) and unilateral suckling (both ipsilateral and contralateral to the lesion) with 5 pups were consecutively performed in the 10 rats. Milk ejection was induced in 50% by contralateral suckling and in 100% by bilateral suckling, and the incidence was significantly higher than that (0%) observed during ipsilateral suckling. A significant difference in the incidence of milk ejection was also observed between contralateral and bilateral sucklings.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1990

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

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.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Effect of rise in plasma osmotic pressure on the milk-ejection reflex in the rat.

The effect of an increase in plasma osmolality on the milk-ejection reflex of rats was studied. The lactating rats, at day 8-12 of lactation, were anesthetized with urethane (1.1 g/kg, i.p.) and 8-11 pups which had been separated from their mother 16-18 h were put to the nipples to suckle. In 21 of 47 rats studied an intermittent pattern of milk ejection was recorded with a latency of 15-74 min (group-I rats). The mean interval between recurring milk ejections was 8.3 +/- 0.6 (S.E.M.) min and the mean amount of oxytocin released at each milk ejection estimated in 11 of them was 0.26 +/- 0.04 mU. The remaining 26 rats showed no milk ejection throughout the nursing period of more than 90 min (group-II rats). The intraperitoneal injection of 1.5 M NaCl (1 ml) had no effect on the interval between milk ejections but increased the amount of oxytocin released at each milk ejection by 2.4 times in group-I rats, as the plasma osmolality changed from 297.9 +/- 2.7 mOsm/kg to 310.4 +/- 3.6 mOsm/kg. On the other hand, the 1.5 M NaCl injection induced recurring reflex milk-ejections in all of the group-II rats, while the plasma osmolality increased from 307 +/- 2.8 mOsm/kg to 320 +/- 3.1 mOsm/kg. The mean interval was not significantly different from that observed in the group-I rats. The sensitivity of the mammary gland to oxytocin was not altered by the 1.5 M NaCl injection. The injection of isotonic NaCl had no effect on the milk-ejection reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Suckling-induced serum prolactin levels are modified by interference with milk ejection in lactating rats.

The aim of this study was to determine whether suckling-induced prolactin (PRL) levels were modified when milk ejection was impaired. Milk ejection impairment was achieved in two experimental models: a) depriving the dam of sleep during suckling and b) increasing the nonsuckling intervals in lactating dams. Sleep deprivation blocked milk ejection and enhanced suckling-induced PRL levels in dams that had been previously separated from their pups. When milk ejection is blocked in litter-deprived dams, mammary glands are not evacuated and they remain engorged. Suckling stimuli were not the cause of the difference in suckling-induced serum PRL levels in control and sleep-deprived dams. The engorgement of the mammary glands may play a role, as a maximum suckling-induced PRL increase was not observed in nonseparated SD dams with nonengorged mammary glands. Moreover, suckling-induced PRL levels were decreased when engorged mammary glands of SD dams were evacuated through an oxytocin injection. A parallel increase between suckling-induced PRL levels and mammary gland weight was observed in the experiments in which milk ejection was impaired through an increase in the intervals of nonsuckling, providing additional support for a relationship between mammary gland engorgement and the regulation of suckling-induced PRL levels.

Animals↗
PubMed2004

Mammary cisternal size, cisternal milk and milk ejection in Murrah buffaloes.

The internal arrangement of the mammary gland cavity system, cisternal and alveolar milk fractions and the characteristics of milk ejection were investigated in buffaloes. Twenty-four Murrah buffaloes in three different stages of lactation and of two age groups were used. Continuous ultrasound cross-sections during milk ejection induced by exogenous oxytocin were performed to record the latency period of milk ejection. Buffaloes had small cisterns and the cavity area in the teat and gland regions were not significantly different (P > 0.05). The animals had long teat canals (3.1 +/- 0.1 cm), longer in the hind than fore quarters. Cisternal milk yield was low (0.17 +/- 0.01 kg) and cisternal fraction was only 4.9 +/- 0.1% of the total milk. The cisternal area (cm2) was 69.6 +/- 4.6, 51.61 +/- 4.8 and 26.01 +/- 4.8 while the cisternal yield (kg) was 0.32 +/- 0.05, 0.18 +/- 0.05 and 0.05 +/- 0.05 in early, mid and late lactation, respectively. A close correlation (r = 0.87, P < 0.05) existed between the ultrasound cisternal area and cisternal milk yield. The latency period of induced milk ejection was similar to that reported for cows (25 +/- 1 s) and was negatively correlated with milk yield (r = -0.75, P < 0.05). Milk ejection occurred shortly after elevated oxytocin concentrations were present. Delayed milk ejection reported earlier in this species must therefore be due to the absence of cisternal milk and delayed oxytocin release. An increase in teat length and circumference at milk ejection was also evident in the ultrasound cross sections.

Aging↗
PubMed1984

Relationship of prolactin release in lactating rats to milk ejection, sleep state, and ultrasonic vocalization by the pups.

PRL release, milk ejection, and electroencephalographic states of sleep were monitored in conscious, lactating Holtzman rats. Plasma PRL levels were low in rats separated from their litters, but they increased when pups were returned to the cage, attached to the nipples of the mother, and suckled. The pups emitted ultrasonic vocalizations upon their return to the cage and before their attachment to the nipples. Exposure of mothers to the vocalizations of pups, whereas nipple attachment was prevented, failed to increase PRL release. In confirmation of previous work, milk ejection did not occur until the suckled mother exhibited electroencephalographic signs of sleep, and milk ejection could be inhibited if sleep was prevented. In contrast, sleep was not a prerequisite for PRL release and sleep deprivation of suckled mothers could not inhibit release of PRL. In summary, suckling-induced release of PRL was followed by an increased incidence of sleep and then by milk ejection. It is hypothesized that the rise in plasma PRL induces the sleep necessary for the reflex release of oxytocin required for milk ejection.

Animals↗
PubMed1988

Inhibition of suckling-induced milk ejections in the lactating rat by delta 9-tetrahydrocannabinol.

The effect of delta 9-tetrahydrocannabinol (THC) on suckling-induced oxytocin release was investigated by recording intramammary pressure changes in suckled rats treated iv with THC (0.5 mg/kg BW) or vehicle. Latency to the first posttreatment milk ejection and posttreatment milk ejection intervals and pressure wave amplitudes were compared between THC- and vehicle-treated rats. Before treatment, intervals between milk ejections averaged 6.5 +/- 1.3 (+/- SE) and 7.0 +/- 0.7 min for vehicle- and THC-treated groups, respectively. Vehicle injections did not alter the frequency of milk ejections, which continued at an overall mean interval of 7.6 +/- 0.7 min after treatment. In contrast, THC treatment was followed by a transient suspension of milk ejections, with a latency of 59.3 +/- 7.4 min before the first posttreatment milk ejection was recorded (P less than 0.001). Intervals between subsequent ejections averaged 15.3 +/- 2.0 to 16.1 +/- 1.3 min and were lengthened relative to corresponding intervals in vehicle-treated animals (P less than 0.05). The amplitudes of pressure waves were not significantly affected by treatment. Oxytocin (0.5 mU) injections 10 or 30 min after THC treatment evoked abrupt increases in intramammary pressure, indicating continued responsiveness of the mammary gland to oxytocin stimulation. These data suggest that THC interferes with the release of oxytocin in response to suckling. To our knowledge, this provides the first evidence that THC inhibits posterior pituitary function.

Animals↗
PubMed1982

Inhibition of milk ejection by a visual stimulus in lactating rats: implication of the pineal gland.

The effect of visual and auditory stimuli on milk ejection during suckling was studied in normal and pinealectomized lactating rats. The photic and auditory stimuli were applied to each mother for 10 s every 20 s during the 30 min suckling period. Both stimuli inhibited milk ejection without altering the nursing behavior. In mothers kept in complete darkness or in which the visual stimulus shone continuously during the suckling period, milk ejection was not affected. The inhibition of milk ejection is therefore produced by the light on-off sequence. In lactating rats exposed to the stimulus during 3 consecutive days, a significant inhibition of milk ejection was obtained each day. A normal milk-ejection response occurred in both non-stimulated pinealectomized and in stimulated pinealectomized lactating rats. Pinealectomy did not prevent the inhibitory effect of the sound stimulus. Treatment with methysergide prevented the inhibition of milk ejection induced by the visual stimulus but did not prevent the inhibitory effect of the auditory stimulus. It seems that the pineal gland mediates an inhibitory visual reflex acting on oxytocin release and milk ejection.

Acoustic Stimulation↗
PubMed1975

Isolation and some observations of the properties of a bovine neurohypophysial milk-ejecting factor.

A substance possessing milk-ejecting activity has been isolated from an acetone powder preparation of bovine posterior pituitary glands by Sephadex G-25 chromatography of the neurophysin-neurohypophysial hormone complex. While the material possessed an oxytocic activity of 2.8 IU/mg as measured on the isolated rat uterus, the milk-ejecting activity was more than three fold greater, 9.6 IU/mg. The peptide had an antidiuretic activity of 0.133 IU/mg and a pressor activity of 0.083 IU/mg. Neither the uterine-stimulating action nor the pressor activity was destroyed by incubating the peptide with 0.01 M sodium thioglycollate at 65 degrees C for 5 min. The oxytocic activity was antagonized neither by 1.4 X 10(-6) M atropine nor 3.3 X 10(-7) M phenoxybenzamine.

Amino Acids↗
PubMed1984

A means to assess nursing efficiency in the pig: the study of the milk ejection reflex.

We have recently devised a method for recording the intramammary pressure in conscious lactating sows. This technique allows for unambiguous detection of milk ejection, and permits correlation with hormone release and the behaviour of the sows and their piglets. Each milk ejection is characterized by an abrupt rise in intramammary pressure lasting 8-40 sec only. This is preceded 15-30 before by a rise in plasma concentrations of the hormone oxytocin. Milk ejections only occurred when the sow was nursing her litter, lying on her side and making her teats available. She usually grunted in a rhythmic manner, with a sharp increase in the frequency of grunts about 23 sec before milk ejection. Grunting ceased within 1 min thereafter. The whole litter had to be suckling to obtain a milk ejection, which occurred about 2-4 min after the onset of the initial phase of massage of the udders, and was coincident with a brief period of quiet suckling. Milk ejections occurred about every 45 min, i.e. only once per suckling period, eventhough the period could last over 15 min. They never occurred if the mother was not nursing, or if the piglets attempted to suckle too soon after a milk ejection. Out of 144 periods of suckling, over 20% of failures to eject milk were observed, in which case there was no oxytocin release in blood. Some "incomplete" sucklings happened with no apparent reasons, but their incidence was very high when the sow appeared to be disturbed.

Animals↗
PubMed1979

Milk ejection reflex linked to slow wave sleep in nursing rats.

Correlations between cerebral activity of nursing rats and the milk ejection reflex were studied in Sprague-Dawley rats with 15- to 17-day-old litters. The stretch reaction of the pups, which expresses the onset of milk ejection, was closely correlated with the slow sleep epochs of the mother. Once the litter started suckling, milk ejection only took place when the mother fell asleep and electroencephalographic features of slow wave sleep appeared. Milk ejection was never found during paradoxical sleep nor when the mother was awake. Sleep deprivation for 30 min impaired milk ejection in spite of continuous suckling of the nipples by the pups. If the mother was allowed to sleep immediately afterwards, ejection of milk occurred. A 24-h sleep-wakefulness pattern did not show differences between nursing and controls. Our results show that suckling, although necessary, is not enough to set off milk ejection. This reflex only appears when the mother falls asleep, suggesting that oxytocin release is linked to suckling and slow wave sleep.

Animals↗
PubMed1980

Sleep: a prerequisite for reflex milk ejection in the rat.

Electroencephalographic activity (EEG) was recorded from the frontal cortex of unanaesthetized and urethane-anaesthetized lactating rats and analysed in relation to the pattern of milk ejection evoked by the nursing pups. The EEG of the anaesthetized rat fluctuated without experimental intervention between three distinctive patterns defined as synchronized, desychronized, and stage III activity, whilst reflex milk ejection recurred at intervals of about 6 min (range 2- greater than 20 min) throughout the 1-4 h period the pups were left attached to the nipples. For greater than 10 s before and for up to 60 s after each milk ejection, as judged from recordings of intramammary pressure and pup behaviour, the EEG was invariably synchronized throughout. Conversely, milk ejection (n greater than 300) was never observed during long periods of desynchronized, or stage III EEG activity. The vigorous increase in the sucking of the pups at milk ejection failed to produce a desynchronization (arousal) of the EEG as observed with other forms of sensory stimulation. Indeed, the sucking of the pups appeared to produce a soporific change i, the maternal EEG for spontaneous periods of desynchronization were not observed in the 30-60 min following the initial attachment of the pups to the nipples. Similar EEG patterns were seen in the unanaesthetized rat, though arousal from the synchronized state was more easily produced, e.g., by weak auditory signals. Milk ejection, as judged from the behaviour of the pups, recurred at intervals of 2 min or more during each 20-80 min period of nursing. The rat appeared somnolent for most of the nursing period and the EEG was always synchronized for greater than 10 s before each milk ejection (n greater than 200), though her eyes usually remained open. Arousal and desynchronization of the EEG was invariably observed in association with the increased pup behaviour at milk ejection. From these observations and the knowledge that oxytocin release from the neurohypophysis occurs about 10 s before milk ejection, we conclude that a synchronized EEG pattite for the expression of the milk-ejection reflex in the rat.

Animals↗
PubMed1997

The winged helix gene, Mf3, is required for normal development of the diencephalon and midbrain, postnatal growth and the milk-ejection reflex.

The mouse Mf3 gene, also known as Fkh5 and HFH-e5.1, encodes a winged helix/forkhead transcription factor. In the early embryo, transcripts for Mf3 are restricted to the presomitic mesoderm and anterior neurectoderm and mesoderm. By 9.5 days post coitum, expression in the nervous system is predominantly in the diencephalon, midbrain and neural tube. After midgestation, the highest level of mRNA is in the mammillary bodies, the posterior-most part of the hypothalamus. Mice homozygous for a deletion of the mf3 locus on a [129 x Black Swiss] background display variable phenotypes consistent with a requirement for the gene at several stages of embryonic and postnatal development. Approximately six percent of the mf3-/- embryos show an open neural tube in the diencephalon and midbrain region, and another five percent show a severe reduction of the posterior body axis; both these classes of affected embryos die in utero. Surviving homozygotes have an apparently normal phenotype at birth. Postnatally, however, mf3-/- pups are severely growth retarded and approximately one third die before weaning. This growth defect is not a direct result of lack of circulating growth hormone or thyrotropin. Mice that survive to weaning are healthy, but they show an abnormal clasping of the hindfeet when suspended by the tail. Although much smaller than normal, the mice are fertile. However, mf3-/- females cannot eject their milk supply to feed their pups. This nursing defect can be corrected with interperitoneal injections of oxytocin. These results provide evidence that Mf3 is required for normal hypothalamus development and suggest that Mf3 may play a role in postnatal growth and lactation.

Animals↗
PubMed1986

Regulation of the milk ejection reflex in the rat.

Extracellular recordings were made from neurones in or near the supraoptic nucleus in suckled lactating rats under urethane anaesthesia to investigate the mechanism by which the firing of oxytocin cells is synchronized during reflex milk ejection. Cells synaptically driven but not antidromically activated by neural stalk stimulation, which thus probably receive an afferent input from supraoptic neurones, were classified as 'regular' or 'bursters' on the basis of their spontaneous electrical activity. The majority (twelve out of eighteen) of synaptically excited cells (o.d.+) were bursters and the majority of inhibited (o.d.-) cells (eleven out of nineteen) were regular, but only one o.d.+ burster showed any change of activity (inhibition) before milk ejection. Putative oxytocin cells in suckled lactating rats showed a firing pattern between milk-ejection bursts which could not be distinguished from that of putative oxytocin cells in male animals. The mode interspike interval between milk ejections was 47.1 +/- 3.1 ms (mean +/- S.E. of mean) compared with 47.3 +/- 3.3 ms in male rats, and fewer than 1.4% of interspike intervals were less than 20 ms in duration. By contrast, within milk-ejection bursts 40% of interspike intervals were in the range 8-20 ms. Short trains (10 or 20) of pulses applied to the neural stalk at regular (5 min) intervals, in an attempt to simulate the initial part of the milk ejection burst, failed to trigger bursts. In only 2 of 150 tests was the interval between train and milk-ejection burst less than 10 s, and after the pulse train all but one cell showed reduced activity for 1-3 s. The trains of pulses were however not without effect: they significantly (P less than 0.01) enhanced the chance of a milk-ejection burst occurring within the next 2.5 min. Our observation that pulse trains do not trigger bursts suggests that local positive feed-back mechanisms are not responsible for orchestrating the activation of oxytocin cells during the milk-ejection reflex. Moreover, because spontaneous tiring pattern is the same in lactating and non-lactating rats, we found no evidence that the anatomical changes in the synaptic organization within the supraoptic nuclei in lactation have any influence on the firing of oxytocin cells. It is likely, however, since pulse trains alter the timing of milk ejections, that oxytocin released locally in the region of the supraoptic nucleus can influence reflex milk ejection.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1996

Effects of central GABAB receptor modulation upon the milk ejection reflex in the rat.

In order to investigate the role of central GABAB receptors in the control of the milk ejection reflex, we have examined the effects of third ventricular and bilateral supraoptic nucleus (SON) injections of a GABAB receptor agonist (baclofen) and antagonist (hydroxy-saclofen) on the milk ejection reflex in the urethane-anaesthetised rat. In addition, microdialysis studies have evaluated whether the activation of GABAB receptors in the SON is able to modulate the release of GABA and glutamate, two major neurotransmitters involved in the regulation of the milk ejection reflex. Intracerebroventricular injections of baclofen (n = 9) in doses of 10, 50 and 100 pmol inhibited the milk ejection reflex in a dose-dependent manner, without affecting the electroencephalogram or attenuating the intramammary pressure response to intravenous injection of 0.5 mU exogenous oxytocin. Hydroxy-saclofen given into the third ventricle in doses of 100 pmol (n = 2) and 500 pmol (n = 4) did not modify the pattern of the milk ejection reflex. Bilateral SON microinfusions of baclofen in doses of 80 (n = 2) and 200 pmol (n = 4) did not modify the pattern of the milk ejection reflex. In microdialysis experiments (n = 8), inclusion of baclofen into the microdialysate at a concentration of 500 microM had no effect upon basal or potassium-stimulated GABA and glutamate outflow. These results show that the activation of GABAB receptors located outside, but not within, the SON are capable of inhibiting the milk ejection reflex. In contrast to our previous findings regarding the GABAA receptor, we found no evidence for a tonic role of GABAB receptors within the neural network inducing the periodic synchronous bursting of oxytocin neurons during suckling.

Animals↗