The Experts below are selected from a list of 246 Experts worldwide ranked by ideXlab platform
J W Blum - One of the best experts on this subject based on the ideXlab platform.
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Oxytocin Release and milk removal in ruminants
Journal of Dairy Science, 1998Co-Authors: R M Bruckmaier, J W BlumAbstract:Abstract Before milking, less than 20% of the milk yielded by dairy cows is stored within the cistern, where it is immediately available for removal. Most of the milk is available for the milking machine only after milk ejection, which occurs in response to tactile teat stimulation and Oxytocin Release. For complete milk removal, milk ejection is necessary throughout the entire milking process. The continuation of stimulatory effect of the milking machine until the end of milking is, therefore, essential. Premilking teat stimulation causes induction of alveolar milk ejection before the start of milking. Thus, bimodal milk flow curves (i.e., interruption of milk flow after removal of the cisternal milk) are avoided. Continual ejection of milk is dependent on the presence of elevated Oxytocin concentrations during the entire milking. Any interruption of the milk ejection process can disturb milk removal. Disruption of milk removal can be caused by peripheral inhibition of Oxytocin effects on the mammary gland or by inhibition of Oxytocin Release by the central nervous system. Peripheral inhibition is induced by elevated concentrations of catecholamines through stimulation of α -adrenergic receptors in the mammary gland, likely via changes in ductal resistance. Inhibition of Oxytocin Release by the central nervous system has been observed in primiparous cows immediately after parturition, during peak estrus, and during milking in unfamiliar surroundings; concentrations of β -endorphin and cortisol are elevated in this situation. However, the role of endogenous opioid peptides in the inhibition of Oxytocin Release in cows remains unclear. In conclusion, during machine-milking, the physiological requirements of the cows need to be considered, and, most importantly, stressors must be minimized.
Tatsushi Onaka - One of the best experts on this subject based on the ideXlab platform.
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effects of rfamide related peptide rfrp 1 and rfrp 3 on Oxytocin Release and anxiety related behaviour in rats
Journal of Neuroendocrinology, 2011Co-Authors: Maroot Kaewwongse, Yuki Takayanagi, Tatsushi OnakaAbstract:RFamide-related peptides (RFRP-1 and RFRP-3) are localised in neurones of the dorsomedial hypothalamus in rats. The dorsomedial hypothalamus plays an essential role in neuroendocrine and behavioural stress responses. In the present study, we examined the role of RFRP in the control of neuroendocrine and behavioural responses in rats. Stressful stimuli increased expression of Fos protein in RFRP-immunoreactive neurones of the dorsomedial hypothalamus, suggesting that stressful stimuli activate RFRP neurones. Intracerebroventricular injection of RFRPs increased the expression of Fos protein in Oxytocin neurones in the hypothalamus and plasma concentrations of adrenocorticotrophic hormone and Oxytocin. The hypothalamic paraventricular and supraoptic nuclei expressed mRNA of GPR147, the putative RFRP receptor, and application of RFRPs to isolated supraoptic nuclei facilitated Oxytocin Release, suggesting that RFRPs activate Oxytocin neurones directly. Furthermore, the administration of RFRPs induced anxiety-related behaviour in rats in open-field tests. All these data taken together suggest that RFRPs play a role in the control of neuroendocrine and behavioural stress responses in rats.
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Effects of RFamide‐Related Peptide (RFRP)‐1 and RFRP‐3 on Oxytocin Release and Anxiety‐Related Behaviour in Rats
Journal of Neuroendocrinology, 2010Co-Authors: Maroot Kaewwongse, Yuki Takayanagi, Tatsushi OnakaAbstract:RFamide-related peptides (RFRP-1 and RFRP-3) are localised in neurones of the dorsomedial hypothalamus in rats. The dorsomedial hypothalamus plays an essential role in neuroendocrine and behavioural stress responses. In the present study, we examined the role of RFRP in the control of neuroendocrine and behavioural responses in rats. Stressful stimuli increased expression of Fos protein in RFRP-immunoreactive neurones of the dorsomedial hypothalamus, suggesting that stressful stimuli activate RFRP neurones. Intracerebroventricular injection of RFRPs increased the expression of Fos protein in Oxytocin neurones in the hypothalamus and plasma concentrations of adrenocorticotrophic hormone and Oxytocin. The hypothalamic paraventricular and supraoptic nuclei expressed mRNA of GPR147, the putative RFRP receptor, and application of RFRPs to isolated supraoptic nuclei facilitated Oxytocin Release, suggesting that RFRPs activate Oxytocin neurones directly. Furthermore, the administration of RFRPs induced anxiety-related behaviour in rats in open-field tests. All these data taken together suggest that RFRPs play a role in the control of neuroendocrine and behavioural stress responses in rats.
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Oxytocin Release from the Neurohypophysis after the Taste Stimuli Previously Paired with Intravenous Cholecystokinin in Anaesthetized Rats
Journal of Neuroendocrinology, 2008Co-Authors: Tatsushi Onaka, Kinji YagiAbstract:Intravenously administered cholecystokinin octapeptide (CCK) induces Oxytocin Release from the neurohypophysis in anaesthetised rats. Memory of conditioned taste aversion can be acquired under anaesthesia. The present experiments aimed at investigating whether taste stimuli previously paired with iv CCK evoke Oxytocin Release from the neurohypophysis in urethane-anaesthetised male rats. Sucrose solution (0.75–2.0 M) paired with iv CCK or the vehicle was applied to the tongue. After 3 h, sucrose solution was applied again. The second sucrose slightly increased plasma Oxytocin concentration in rats that had received the first sucrose solution paired with the vehicle. Plasma Oxytocin concentration after the second sucrose application, however, was significantly higher in CCK-injected than in vehicle-injected rats. In rats that received CCK 1 h before the first sucrose application, a second sucrose application did not produce the Oxytocin response. The magnitude of the Oxytocin response to the second sucrose solution was increased in a manner related to CCK doses. In separate experiments, NaCl solution (0.75 M) paired with CCK or the vehicle was applied to the tongue. The second NaCl solution applied 3 h after the first one facilitated Oxytocin Release both in the rats that had received CCK or the vehicle. The increase in plasma Oxytocin, however, was significantly larger in CCK than in vehicle-injected rats. In rats that had received the first sucrose solution paired with CCK, a second sucrose solution evoked a significantly larger increase in plasma Oxytocin concentrations than a testing NaCl solution did. In rats that had received NaCl solution paired with CCK, a testing sucrose solution did not significantly change plasma Oxytocin concentrations. These data suggest that the taste stimulus previously paired with iv CCK induces Oxytocin Release from the neurohypophysis in urethane-anaesthetised rats.
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neural pathways controlling central and peripheral Oxytocin Release during stress
Journal of Neuroendocrinology, 2004Co-Authors: Tatsushi OnakaAbstract:Oxytocin is Released from the pituitary gland in response to a variety of stressful stimuli, including noxious stimuli, conditioned fear and exposure to novel environments. These responses are believed to be mediated, at least in part, by noradrenergic projections from the medulla oblongata, and some of these noradrenergic neurones also contain prolactin-releasing peptide (PrRP). Central administration of either PrRP or noradrenaline stimulates Oxytocin secretion into the circulation. Stressful stimuli activate PrRP-containing noradrenergic neurones in the medulla oblongata, and it is thus possible that PrRP/noradrenergic projections to the hypothalamus mediate Oxytocin responses to stressful stimuli. Here, the roles of brainstem PrRP/noradrenergic projections to the hypothalamus in Oxytocin responses to different kinds of stressful stimuli are reviewed, with a particular emphasis on conditioned fear. Roles of dendritic Oxytocin Release during stress and metabolic factors affecting stress pathways are also discussed.
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Neuromedin U facilitates Oxytocin Release from the pituitary via β adrenoceptors
Neuroreport, 2003Co-Authors: Kumiko Rokkaku, Tatsushi Onaka, Kazufumi Honda, Nobukazu Okada, Junichi Ideno, Akio Kawakami, Toshihiko Yada, Shun IshibashiAbstract:Neuromedin U activates noradrenergic neurones in the medulla oblongata and Oxytocin neurones in the hypothalamus. Here we examined roles of noradrenergic transmission in Oxytocin Release from the pituitary after intracerebroventricular administration of neuromedin U in rats. Neuromedin U administration facilitated noradrenaline Release in the supraoptic nucleus. Administration of a β1 adrenoceptor antagonist, metoprolol, or a β2 antagonist, ICI 118551 but not an α1 antagonist, benoxathian, reduced increases in plasma Oxytocin concentrations observed after administration of neuromedin U, but plasma ACTH concentrations were not significantly changed. All theses data suggest that neuromedin U stimulates Oxytocin Release from the pituitary, at least in part, via activation of β adrenoceptors.
Gareth Leng - One of the best experts on this subject based on the ideXlab platform.
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the involvement of voltage operated calcium channels in somato dendritic Oxytocin Release
PLOS ONE, 2011Co-Authors: Vicky A Tobin, Alison J Douglas, Gareth Leng, Mike LudwigAbstract:Magnocellular neurons of the supraoptic nucleus (SON) secrete Oxytocin and vasopressin from axon terminals in the neurohypophysis, but they also Release large amounts of peptide from their somata and dendrites, and this can be regulated both by activity-dependent Ca2+ influx and by mobilization of intracellular Ca2+. This somato-dendritic Release can also be primed by agents that mobilise intracellular Ca2+, meaning that the extent to which it is activity-dependent, is physiologically labile. We investigated the role of different Ca2+ channels in somato-dendritic Release; blocking N-type channels reduced depolarisation-induced Oxytocin Release from SONs in vitro from adult and post-natal day 8 (PND-8) rats, blocking L-type only had effect in PND-8 rats, while blocking other channel types had no significant effect. When Oxytocin Release was primed by prior exposure to thapsigargin, both N- and L-type channel blockers reduced Release, while P/Q and R-type blockers were ineffective. Using confocal microscopy, we found immunoreactivity for Cav1.2 and 1.3 channel subunits (which both form L-type channels), 2.1 (P/Q type), 2.2 (N-type) and 2.3 (R-type) in the somata and dendrites of both Oxytocin and vasopressin neurons, and the intensity of the immunofluorescence signal for different subunits differed between PND-8, adult and lactating rats. Using patch-clamp electrophysiology, the N-type Ca2+ current density increased after thapsigargin treatment, but did not alter the voltage sensitivity of the channel. These results suggest that the expression, location or availability of N-type Ca2+ channels is altered when required for high rates of somato-dendritic peptide Release.
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α melanocyte stimulating hormone stimulates Oxytocin Release from the dendrites of hypothalamic neurons while inhibiting Oxytocin Release from their terminals in the neurohypophysis
The Journal of Neuroscience, 2003Co-Authors: Nancy Sabatier, Govindan Dayanithi, Alison J Douglas, Celine Caquineau, Philip M Bull, Xiao Ming M Guan, Michael Jiang, Lex Van Der Ploeg, Gareth LengAbstract:The peptides α-melanocyte stimulating hormone (α-MSH) and Oxytocin, when administered centrally, produce similar behavioral effects. α-MSH induces Fos expression in supraoptic Oxytocin neurons, and α-MSH melanocortin-4 receptors (MC4Rs) are highly expressed in the supraoptic nucleus, suggesting that α-MSH and Oxytocin actions are not independent. Here we investigated the effects of α-MSH on the activity of supraoptic neurons. We confirmed that α-MSH induces Fos expression in the supraoptic nucleus when injected centrally and demonstrated that α-MSH also stimulates Fos expression in the nucleus when applied locally by retrodialysis. Thus α-MSH-induced Fos expression is not associated with electrophysiological excitation of supraoptic neurons because central injection of α-MSH or selective MC4 receptor agonists inhibited the electrical activity of Oxytocin neurons in the supraoptic nucleus recorded in vivo . Consistent with these observations, Oxytocin secretion into the bloodstream decreased after central injection of α-MSH. However, MC4R ligands induced substantial Release of Oxytocin from dendrites in isolated supraoptic nuclei. Because dendritic Oxytocin Release can be triggered by changes in [Ca 2+ ] i , we measured [Ca 2+ ] i responses in isolated supraoptic neurons and found that MC4R ligands induce a transient [Ca 2+ ] i increase in Oxytocin neurons. This response was still observed in low extracellular Ca 2+ concentration and probably reflects mobilization of [Ca 2+ ] i from intracellular stores rather than entry via voltage-gated channels. Taken together, these results show for the first time that a peptide, here α-MSH, can induce differential regulation of dendritic Release and systemic secretion of Oxytocin, accompanied by dissociation of Fos expression and electrical activity.
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Oxytocin Released from Magnocellular Dendrites
Annals of the New York Academy of Sciences, 2003Co-Authors: Nancy Sabatier, Alison J Douglas, Celine Caquineau, Gareth LengAbstract:: α-Melanocyte-stimulating hormone (α-MSH) is implicated in a variety of behavioral processes that are remarkably similar to those behaviors in which centrally acting Oxytocin has been implicated. Central Oxytocin derives in part from centrally projecting parvocellular neurons of the paraventricular nucleus, but large amounts of Oxytocin are also Released from dendrites of magnocellular Oxytocin neurons in the supraoptic and paraventricular nuclei of the hypothalamus. Oxytocin Release from dendrites is semi-independent of electrical activity and can be modulated by peptidergic signals independently of Release from nerve terminals. Oxytocin is Released from dendrites by stimuli that mobilize intracellular calcium stores, and such stimuli also prime dendritic stores of Oxytocin, making them available for subsequent activity-dependent secretion. Evidence exists for efferent projections to the supraoptic nucleus from the arcuate nucleus where α-MSH neurons are located, and the supraoptic and paraventricular nuclei show high levels of expression of mRNA for the melanocortin receptor MC4R. These projections may be involved specifically in the regulation of dendritic Oxytocin Release.
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neurosteroid regulation of Oxytocin and vasopressin Release from the rat supraoptic nucleus
The Journal of Physiology, 2003Co-Authors: Helene Widmer, Gareth Leng, Mike Ludwig, Frederic Bancel, Govindan DayanithiAbstract:In adult rats somato-dendritic Release of Oxytocin and vasopressin from magnocellular neurones in the supraoptic nucleus of the hypothalamus has important autoregulatory actions on the neuronal electrical activity, and in neonatal rats it plays a role in the development of dendritic arborisation. In the adult, Oxytocin effects are modulated by allopregnanolone via an interaction with inhibitory GABAA receptors. This study examined the effects of allopregnanolone, progesterone and 17β-oestradiol on Oxytocin and vasopressin Release from intact isolated supraoptic nuclei and from the neurophypophyses in rats of differing ages. In supraoptic nuclei from rats of 3–4 weeks old or less, all three neurosteroids induced Oxytocin Release from the isolated supraoptic nucleus, but only allopregnanolone induced significant Release of vasopressin. Surprisingly, in these very young rats, allopregnanolone-induced Oxytocin Release was inhibited by GABAA receptor antagonists as well as by an Oxytocin receptor antagonist. By contrast, in supraoptic nuclei from adult rats allopregnanolone-induced Oxytocin Release was much smaller, and was enhanced in the presence of bicuculline. The GABAA receptor agonist muscimol also induced Oxytocin Release from supraoptic nuclei in young rats, but had no effect in adult rats. Oxytocin cells isolated from young rats showed an increase in [Ca2+]i in response to both allopregnanolone and muscimol. Allopregnanolone had no effect on [Ca2+]i or on the Release of Oxytocin or vasopressin from neurohypophysial axon terminals in either young or old rats. We conclude that, in very young rats, (i) neurosteroids induce Oxytocin Release from the supraoptic nucleus by a mechanism that partly depends on the presence of GABA, which in young rats is depolarising to Oxytocin cells, and which also partly depends upon endogenous Oxytocin, and (ii) the effect of allopregnanolone upon Oxytocin Release changes with age, as the functional activity of GABAA receptors changes from excitation to inhibition of Oxytocin cells.
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involvement of the noradrenergic afferents from the nucleus tractus solitarii to the supraoptic nucleus in Oxytocin Release after peripheral cholecystokinin octapeptide in the rat
Neuroscience, 1995Co-Authors: T Onaka, Simon M Luckman, I Antonijevic, J R Palmer, Gareth LengAbstract:Abstract Activation of abdominal vagal afferents by peripheral injection of cholecystokinin octapeptide induces Oxytocin Release into the circulation. To test the hypothesis that cholecystokinin increases Oxytocin Release via activation of noradrenergic afferents from the brainstem, we injected rats with 5-amino-2,4-dihydroxy-α-methylphenylethylamine, a selective neurotoxin to noradrenergic fibres, into a lateral cerebral ventricle. The neurotoxin treatment reduced the noradrenaline content in the hypothalamus by 75% and reduced the Oxytocin secretion in response to cholecystokinin by over 90%. In separate experiments, the neurotoxin was injected unilaterally in the vicinity of the supraoptic nucleus to test whether direct noradrenergic afferents to the supraoptic nucleus are involved in the response to cholecystokinin. The injection reduced the immunoreactivity for dopamine β-hydroxylase in the supraoptic nucleus and significantly decreased the number of the supraoptic neurons expressing Fos-like protein after cholecystokinin but not after hypertonic saline. In further experiments, rhodamine-conjugated latex microspheres were injected into the supraoptic nucleus to retrogradely label afferent neurons, and the brains were processed with double-immunohistochemistry for tyrosine hydroxylase and Fos-like protein. In the C2/A2 but not the C1/A1 region of the brainstem, cholecystokinin increased the expression of Fos-like protein in the population of retrogradely-labelled catecholaminergic cells. In the C2/A2 region, the majority of retrogradely labelled cells expressing Fos-like protein after cholecystokinin were catecholaminergic. We conclude that noradrenergic afferents from the A2 but not from the A1 region of the brainstem to the hypothalamus mediate, at least in part, Oxytocin Release following cholecystokinin.
Inga D Neumann - One of the best experts on this subject based on the ideXlab platform.
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central vasopressin and Oxytocin Release regulation of complex social behaviours
Progress in Brain Research, 2008Co-Authors: Alexa H Veenema, Inga D NeumannAbstract:Abstract The neuropeptides arginine vasopressin (AVP) and Oxytocin (OXT) are acknowledged as important modulators of diverse social behaviours. Here we discuss recent studies using intracerebral microdialysis to investigate the dynamics of AVP and OXT Release patterns within distinct brain regions during the display of social behaviours in rats. Manipulation of local receptor-mediated actions of AVP and OXT via retrodialysis of either agonists or antagonists revealed the behavioural significance of changes in local neuropeptide Release. Alterations in local AVP and OXT within, e.g. the medio-lateral septum, the central amygdala or the hypothalamic paraventricular nucleus (PVN) were associated with intermale and maternal aggression, respectively. Moreover, increased OXT Release within the PVN was associated with male sexual behaviour and successful mating. Using retrodialysis, we found that AVP Released within the lateral septum during the resident–intruder test was associated with anxiety-related behaviour and with non-aggressive social behaviour rather than intermale aggressive behaviour. In contrast, OXT Release within the PVN and the central amygdala correlated positively with the level of maternal aggression. Interestingly, OXT Released within the PVN during sexual activity in male rats was found to be associated with a robust decrease in anxiety-related behaviour up to 4 h after mating. These data illustrate distinct modes of behavioural actions of AVP and OXT, reaching from acute regulation of the respective social behaviour to the long-term modulation of related behaviours including anxiety and social cognition. In conclusion, measuring the in vivo Release patterns of AVP and OXT within distinct brain regions during the display of diverse social behaviours and manipulation of local AVP and OXT activity has yielded new insights into the specific roles of these neuropeptides in the regulation of complex social behaviours.
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vasopressin and Oxytocin Release within the brain a dynamic concept of multiple and variable modes of neuropeptide communication
Frontiers in Neuroendocrinology, 2004Co-Authors: Rainer Landgraf, Inga D NeumannAbstract:Abstract As exemplified particularly with vasopressin and Oxytocin, Release of neuropeptides within the brain occurs from dendrites, somata, and axons of neurosecretory neurons; mechanisms include activation of intracellular Ca 2+ stores, changed strength of synaptic input and altered interaction between transcription factors and gene promoters. Upon demand, both diffuse spread of neuropeptides in the extracellular fluid following dendritic Release and focal Release from axonal terminals may contribute to regionally and temporally varying combinations of neuromodulator and neurotransmitter actions, thus providing a theoretically unlimited variability in interneuronal signaling. Thus, instead of favoring volume or synaptic transmission following central neuropeptide Release, a more dynamic concept is presented with multiple and variable modes of Release and communication. This concept considers neuropeptides in the extracellular fluid of the brain rather than those in the cerebrospinal fluid or plasma as primary signals, triggering a variety of receptor-mediated effects, including those underlying behavioral and neuroendocrine regulation and psychopathology.
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endogenous opioid regulation of stress induced Oxytocin Release within the hypothalamic paraventricular nucleus is reversed in late pregnancy a microdialysis study
Neuroscience, 2002Co-Authors: A Wigger, Inga D NeumannAbstract:Oxytocin secretion into blood in response to swim stress is differentially regulated by endogenous opioids in virgin and pregnant rats. Here, the influence of endogenous opioids on Oxytocin Release within the hypothalamic paraventricular and supraoptic nuclei was investigated using microdialysis in virgin and pregnant (day 19–21) rats. Rats fitted with a U-shaped microdialysis probe 3 days before testing were injected with naloxone (5 mg/kg body weight, s.c.) or vehicle (sterile saline) and, 3 min later, were forced to swim (10 min at 19°C). Within the paraventricular nucleus, basal and stimulated Oxytocin Release did not significantly differ between vehicle-treated virgin and pregnant rats. After naloxone, local Oxytocin Release in response to swimming was lowered in virgin rats (P<0.01), whereas it was further increased in pregnant rats (P<0.01). Within the supraoptic nucleus, basal Oxytocin Release was significantly lower in pregnant compared to virgin rats (P<0.01). Forced swimming induced a similar rise in intranuclear Oxytocin Release in both vehicle-treated virgin and pregnant rats, but peak levels were still higher in the virgin controls. In contrast to the paraventricular nucleus, naloxone did not alter swim-induced Oxytocin Release within the supraoptic nucleus either in virgin or pregnant rats. Vasopressin Release in the paraventricular nucleus was also increased by forced swimming but there was no effect of pregnancy or naloxone on it. In summary, in pregnancy, basal and stress-induced Oxytocin Release within the paraventricular nucleus was not changed, whereas it was blunted within the supraoptic nucleus. Further, within the paraventricular nucleus the excitatory effect of endogenous opioids on local Oxytocin Release seen in virgins was switched into an inhibitory action in pregnancy. In contrast, endogenous opioids were evidently not involved in the regulation of swim-induced Oxytocin Release within the supraoptic nucleus either in virgin or pregnant rats. Thus, pregnancy-related neuroendocrine plasticity also includes site-specific functional alterations in opioid receptor-mediated actions in the hypothalamus.
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Endogenous opioid regulation of stress-induced Oxytocin Release within the hypothalamic paraventricular nucleus is reversed in late pregnancy: a microdialysis study.
Neuroscience, 2002Co-Authors: A Wigger, Inga D NeumannAbstract:Oxytocin secretion into blood in response to swim stress is differentially regulated by endogenous opioids in virgin and pregnant rats. Here, the influence of endogenous opioids on Oxytocin Release within the hypothalamic paraventricular and supraoptic nuclei was investigated using microdialysis in virgin and pregnant (day 19–21) rats. Rats fitted with a U-shaped microdialysis probe 3 days before testing were injected with naloxone (5 mg/kg body weight, s.c.) or vehicle (sterile saline) and, 3 min later, were forced to swim (10 min at 19°C). Within the paraventricular nucleus, basal and stimulated Oxytocin Release did not significantly differ between vehicle-treated virgin and pregnant rats. After naloxone, local Oxytocin Release in response to swimming was lowered in virgin rats (P
R M Bruckmaier - One of the best experts on this subject based on the ideXlab platform.
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Oxytocin Release and milk removal in machine-milked mares
Milchwissenschaft-milk Science International, 2020Co-Authors: Alen Dzidic, L. Knopf, R M BruckmaierAbstract:In this work Oxytocin Release and milking characteristics during machine milking of mares were investigated. Two experiments were performed twice each in all animals. In experiment 1 mares were milked twice subsequently and residual milk was collected after milking 2 with injection of Oxytocin (10 i.u. i.v.). In experiment 2 mares were also milked twice, but residual milk was collected already after milking 1. Oxytocin concentrations peaked during pre-stimulation and decreased after the teat cups were attached. Total milk yield was 1.1 +/- 0.1 kg during milking 1 and 0.5 +/- 0.1 kg during milking 2 in experiment 1. Residual milk obtained after second milking was 0.7 +/- 0.1 kg. Total milk yield during milking 1 in experiment 2 was also 1.0 +/- 0.1 kg. Residual milk obtained after milking 1 was 0.9 +/- 0.1.kg. As expected there was scarcely milk left in experiment 2 after the residual milk was collected. A short peak without plateau phase characterizes milk flow curves in both experiments. Obviously Oxytocin Release during machine milking was insufficient for complete udder emptying.
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Naloxone cannot abolish the lack of Oxytocin Release during unexperienced suckling of dairy cows
Applied Animal Behaviour Science, 2001Co-Authors: Wolf-dieter Kraetzl, Dieter Schams, V. Tancin, R M BruckmaierAbstract:Abstract To evaluate the role of opioids for the regulation of Oxytocin Release in response to teat stimulation, 10 brown-Swiss dairy cows were randomized to two experiments during mid of lactation. In the first experiment, four cows without previous suckling experience were suckled by an alien calf between two normal milkings. Before and during milking or suckling, frequent blood samples were collected via a jugular cannula for determination of Oxytocin and β-endorphin. In the second experiment, six cows were treated with naloxone or saline, 10 min before the start of the first or second suckling, respectively. The collected blood samples were assayed for Oxytocin. In the first experiment, the plasma levels of β-endorphin were elevated during and after the unexperienced suckling in three cows, but not in the fourth cow, and the Release of Oxytocin during suckling was markedly reduced, suggesting no Release of alveolar milk. In the second experiment, the Release of Oxytocin during suckling was again significantly reduced. Pretreatment with naloxone before suckling did not completely abolish the adverse effect of suckling and the Oxytocin plasma level did not increase to levels comparable with control milking. In emotional stress situations, the Release of Oxytocin from the pituitary is inhibited with simultaneously elevated β-endorphin plasma levels. Although there is some evidence for a regulatory role of opioids for the Release of Oxytocin, other mediators are suggested to be more potent in regulating Oxytocin under stress conditions.
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Oxytocin Release and milk removal in ruminants
Journal of Dairy Science, 1998Co-Authors: R M Bruckmaier, J W BlumAbstract:Abstract Before milking, less than 20% of the milk yielded by dairy cows is stored within the cistern, where it is immediately available for removal. Most of the milk is available for the milking machine only after milk ejection, which occurs in response to tactile teat stimulation and Oxytocin Release. For complete milk removal, milk ejection is necessary throughout the entire milking process. The continuation of stimulatory effect of the milking machine until the end of milking is, therefore, essential. Premilking teat stimulation causes induction of alveolar milk ejection before the start of milking. Thus, bimodal milk flow curves (i.e., interruption of milk flow after removal of the cisternal milk) are avoided. Continual ejection of milk is dependent on the presence of elevated Oxytocin concentrations during the entire milking. Any interruption of the milk ejection process can disturb milk removal. Disruption of milk removal can be caused by peripheral inhibition of Oxytocin effects on the mammary gland or by inhibition of Oxytocin Release by the central nervous system. Peripheral inhibition is induced by elevated concentrations of catecholamines through stimulation of α -adrenergic receptors in the mammary gland, likely via changes in ductal resistance. Inhibition of Oxytocin Release by the central nervous system has been observed in primiparous cows immediately after parturition, during peak estrus, and during milking in unfamiliar surroundings; concentrations of β -endorphin and cortisol are elevated in this situation. However, the role of endogenous opioid peptides in the inhibition of Oxytocin Release in cows remains unclear. In conclusion, during machine-milking, the physiological requirements of the cows need to be considered, and, most importantly, stressors must be minimized.
