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Gareth Leng - One of the best experts on this subject based on the ideXlab platform.
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neurosteroid regulation of oxytocin and vasopressin release from the rat Supraoptic Nucleus
The Journal of Physiology, 2003Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, 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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Neurosteroid regulation of oxytocin and vasopressin release from the rat Supraoptic Nucleus.
The Journal of physiology, 2003Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, 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 17beta-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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β-Endorphin cells in the arcuate Nucleus: Projections to the Supraoptic Nucleus and changes in expression during pregnancy and parturition
Journal of neuroendocrinology, 2002Co-Authors: Alison J. Douglas, Gareth Leng, R.j. Bicknell, James A. Russell, Simone MeddleAbstract:Supraoptic Nucleus oxytocin neurone activity and secretion are inhibited in late pregnancy and parturition by endogenous opioids. Here, we investigated alterations in the projections and gene expression of β-endorphin/pro-opiomelanocortin neurones in the arcuate Nucleus in the pregnant rat. All regions of the arcuate Nucleus were found to contain cells immunoreactive for β-endorphin fluorescent microbeads retrogradely transported from the Supraoptic Nucleus, and double-labelled neurones (β-endorphin plus microbeads), showing that β-endorphin neurones throughout the arcuate Nucleus project to the Supraoptic Nucleus. There was an increase in the number of β-endorphin-immunoreactive cells in the arcuate Nucleus and an increase in the density of β-endorphin fibres within the Supraoptic Nucleus and peri-Supraoptic region in late pregnancy and parturition, suggesting enhanced expression of β-endorphin and increased β-endorphin innervation of the Supraoptic Nucleus. Pro-opiomelanocortin mRNA expression in the arcuate Nucleus increased in late compared to early pregnancy: the number of positive neurones significantly increased in the caudal region. Fos expression (an indicator of neuronal activation) in the arcuate Nucleus was colocalized in β-endorphin neurones in both proestrus and parturient rats, but the number of positive cells did not increase during parturition, suggesting lack of activation of β-endorphin neurones at birth. Thus, β-endorphin cells in the arcuate Nucleus project to the Supraoptic Nucleus and increased innervation during pregnancy may explain the enhanced endogenous opioid inhibition of oxytocin neurones.
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Local injection of pertussis toxin attenuates morphine withdrawal excitation of rat Supraoptic Nucleus neurones
Brain research bulletin, 2000Co-Authors: Colin H. Brown, Gareth Leng, Louise E. Johnstone, Niall P. Murphy, John A. RussellAbstract:Abstract Morphine inhibits oxytocin neurones via G i/o -protein-linked μ-opioid receptors. Following chronic morphine administration oxytocin cells develop dependence, shown by withdrawal excitation after administration of the opioid antagonist, naloxone. Here, inactivation of G i/o -proteins by pre-treatment of morphine-dependent rats with pertussis toxin injected into the left Supraoptic Nucleus reduced withdrawal-induced Fos protein expression within the injected Nucleus by 41 ± 10% compared to the contralateral Nucleus, indicating that functional G i/o -proteins are essential for the development and/or expression of morphine dependence by oxytocin cells in the Supraoptic Nucleus. In another group of rats, pertussis toxin did not alter the responses to either systemic cholecystokinin administration or systemic hypertonic saline administration, indicating that pertussis toxin does not prevent oxytocin cells from responding to stimuli that are not mediated by G i/o -proteins. Finally, pertussis toxin reduced acute morphine inhibition of systemic hypertonic saline-induced Fos protein expression in the Supraoptic Nucleus, confirming that pertussis toxin effectively inactivates G i/o -proteins in the Supraoptic Nucleus. Thus, the expression of morphine withdrawal excitation by Supraoptic Nucleus oxytocin cells requires the functional integrity of G i/o -proteins within the Nucleus.
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GABAergic projection from the arcuate Nucleus to the Supraoptic Nucleus in the rat.
Neuroscience Letters, 2000Co-Authors: Mike Ludwig, Gareth LengAbstract:Abstract Electrical stimulation of the neurones in the hypothalamic arcuate Nucleus results in a transient inhibition followed by a marked post-stimulus excitation of magnocellular neurones of the Supraoptic Nucleus. Microdialysis administration of the γ-aminobutyric acid agonist (GABA A ), muscimol, directly into the Supraoptic Nucleus inhibited both oxytocin and vasopressin neurones and these actions were fully reversed by the GABA A antagonist bicuculline. In addition, bicuculline administration blocked the inhibition induced by arcuate stimulation, but had no effect on the post-stimulus excitation. Thus, part of the inhibitory pathway arising from or passing through the arcuate Nucleus to the Supraoptic Nucleus is mediated by the neurotransmitter GABA. However, the post-inhibitory excitation induced by arcuate stimulation is not a rebound response, but appears to involve an independent excitatory pathway.
Mike Ludwig - One of the best experts on this subject based on the ideXlab platform.
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Activity-dependent feedback modulation of spike patterning of Supraoptic Nucleus neurons by endogenous adenosine
American journal of physiology. Regulatory integrative and comparative physiology, 2006Co-Authors: Philip M. Bull, Colin H. Brown, John A. Russell, Mike LudwigAbstract:Neuropeptide secretion from the dendrites of hypothalamic magnocellular Supraoptic Nucleus (SON) neurons contributes to the regulation of neuronal activity patterning, which ultimately determines t...
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neurosteroid regulation of oxytocin and vasopressin release from the rat Supraoptic Nucleus
The Journal of Physiology, 2003Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, 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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Neurosteroid regulation of oxytocin and vasopressin release from the rat Supraoptic Nucleus.
The Journal of physiology, 2003Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, 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 17beta-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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Vasopressin regulation of noradrenaline release within the Supraoptic Nucleus.
Journal of neuroendocrinology, 2001Co-Authors: Mike Ludwig, Tatsushi Onaka, Kinji YagiAbstract:The effect of electrically evoked dendritic vasopressin release on noradrenaline release into the hypothalamic Supraoptic Nucleus was assessed by in vivo microdialysis in conjunction with high pressure liquid chromatography and electrochemical detection. Electrical activation of magnocellular Supraoptic neurones by stimulation of their axons at the level of the neural lobe significantly increased noradrenaline release into the Nucleus (2.5-fold, P
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GABAergic projection from the arcuate Nucleus to the Supraoptic Nucleus in the rat.
Neuroscience Letters, 2000Co-Authors: Mike Ludwig, Gareth LengAbstract:Abstract Electrical stimulation of the neurones in the hypothalamic arcuate Nucleus results in a transient inhibition followed by a marked post-stimulus excitation of magnocellular neurones of the Supraoptic Nucleus. Microdialysis administration of the γ-aminobutyric acid agonist (GABA A ), muscimol, directly into the Supraoptic Nucleus inhibited both oxytocin and vasopressin neurones and these actions were fully reversed by the GABA A antagonist bicuculline. In addition, bicuculline administration blocked the inhibition induced by arcuate stimulation, but had no effect on the post-stimulus excitation. Thus, part of the inhibitory pathway arising from or passing through the arcuate Nucleus to the Supraoptic Nucleus is mediated by the neurotransmitter GABA. However, the post-inhibitory excitation induced by arcuate stimulation is not a rebound response, but appears to involve an independent excitatory pathway.
John A. Russell - One of the best experts on this subject based on the ideXlab platform.
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Activity-dependent feedback modulation of spike patterning of Supraoptic Nucleus neurons by endogenous adenosine
American journal of physiology. Regulatory integrative and comparative physiology, 2006Co-Authors: Philip M. Bull, Colin H. Brown, John A. Russell, Mike LudwigAbstract:Neuropeptide secretion from the dendrites of hypothalamic magnocellular Supraoptic Nucleus (SON) neurons contributes to the regulation of neuronal activity patterning, which ultimately determines t...
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oxytocin released within the Supraoptic Nucleus of the rat brain by positive feedback action is involved in parturition related events
Journal of Neuroendocrinology, 2003Co-Authors: Inga D. Neumann, Alison J. Douglas, John A. Russell, Quentin J. Pittman, Rainer LandgrafAbstract:Oxytocin is released within the Supraoptic Nucleus during parturition and suckling. During suckling, such release is important in positive feedback stimulation of oxytocin neurons. We have investigated whether oxytocin released within this hypothalamic Nucleus during parturition (1) acts on local receptors to further amplify its own release in a positive feedback manner and (2) is critically involved in the regulation of the delivery process. To examine the effect of the oxytocin antagonist on oxytocin release within the Supraoptic Nucleus, microdialysates were sampled before and during parturition and either vehicle or the antagonist was infused adjacent to the microdialysis probe directly into the Supraoptic Nucleus after delivery of the second pup. Intranuclear infusion of an oxytocin receptor antagonist (des-Gly-NH2d(CH2)5[Tyr(Me)2Thr4]OVT; 50 ng/0.5 microliters) significantly (P < 0.01) diminished the parturition-related rise in oxytocin release within the Supraoptic Nucleus and reduced the number of pups delivered during the first and second 30-min dialysis period compared to vehicle-treated controls. Bilateral infusion of the oxytocin receptor antagonist into the Supraoptic Nucleus after delivery of the second pup significantly slowed parturition (P < 0.05), although the parturition-related rise in plasma oxytocin concentration was unchanged. In addition, the onset of suckling was significantly affected by the antagonist as indicated by fewer liver pups and fewer surviving pups with milk in their stomachs 24 hours after parturition (P < 0.05). To seek other, periventricular sites of oxytocin action during parturition, oxytocin or the oxytocin antagonist was infused into the lateral cerebral ventricle from the birth of pup 2. Via this route, oxytocin speeded up parturition, but the antagonist was ineffective; thus it appears that periventricular oxytocin-sensitive sites are not normally active in promoting parturition, and can do so. The findings indicate a receptor-mediated positive feedback action of oxytocin on its own release within the Supraoptic Nucleus during parturition, which seems to be involved in the progress of parturition without significantly affecting circulation oxytocin levels. Oxytocin released within the Supraoptic Nucleus might be important for the coordinated activation of oxytocin neurons and for the synergistic central and peripheral oxytocin effects involved in the regulation of parturition-related events necessary for the survival of the newborn, including the onset of lactation.
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Local injection of pertussis toxin attenuates morphine withdrawal excitation of rat Supraoptic Nucleus neurones
Brain research bulletin, 2000Co-Authors: Colin H. Brown, Gareth Leng, Louise E. Johnstone, Niall P. Murphy, John A. RussellAbstract:Abstract Morphine inhibits oxytocin neurones via G i/o -protein-linked μ-opioid receptors. Following chronic morphine administration oxytocin cells develop dependence, shown by withdrawal excitation after administration of the opioid antagonist, naloxone. Here, inactivation of G i/o -proteins by pre-treatment of morphine-dependent rats with pertussis toxin injected into the left Supraoptic Nucleus reduced withdrawal-induced Fos protein expression within the injected Nucleus by 41 ± 10% compared to the contralateral Nucleus, indicating that functional G i/o -proteins are essential for the development and/or expression of morphine dependence by oxytocin cells in the Supraoptic Nucleus. In another group of rats, pertussis toxin did not alter the responses to either systemic cholecystokinin administration or systemic hypertonic saline administration, indicating that pertussis toxin does not prevent oxytocin cells from responding to stimuli that are not mediated by G i/o -proteins. Finally, pertussis toxin reduced acute morphine inhibition of systemic hypertonic saline-induced Fos protein expression in the Supraoptic Nucleus, confirming that pertussis toxin effectively inactivates G i/o -proteins in the Supraoptic Nucleus. Thus, the expression of morphine withdrawal excitation by Supraoptic Nucleus oxytocin cells requires the functional integrity of G i/o -proteins within the Nucleus.
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Direct pathways to the Supraoptic Nucleus from the brainstem and the main olfactory bulb are activated at parturition in the rat.
Neuroscience, 2000Co-Authors: Simone Meddle, Gareth Leng, R.j. Bicknell, Johann R. Selvarajah, John A. RussellAbstract:Sensory input from female reproductive structures is paramount for the co-ordination of neuroendocrine changes at parturition. Using a retrograde tracer (fluorescent latex microspheres) in combination with Fos (as an indicator of neuronal activation) and tyrosine hydroxylase (to identify catecholaminergic neurons) immunocytochemistry we identified cells within the brainstem and main olfactory bulb that project to the Supraoptic Nucleus, and which become significantly activated at parturition (compared to virgin rats and rats on the day of expected parturition). Within the A2/C2 region in the Nucleus tractus solitarii, 60% of the projecting activated cells were catecholaminergic, as were 59% of such cells in the A1/C1 region of the ventrolateral medulla. This suggests that oxytocin and vasopressin neurons within the Supraoptic Nucleus are stimulated at parturition via afferent inputs from the brainstem, but the input is not exclusively noradrenergic. Within the mitral layer of the main olfactory bulb, cells that projected to the Supraoptic Nucleus were significantly activated, suggesting that the olfactory system may regulate Supraoptic Nucleus cell firing at parturition. The preoptic area, organum vasculosum of the lamina terminalis and medial amygdala contained cells that projected to the Supraoptic Nucleus but these projections were not significantly activated at parturition, although non-projecting cells in these regions were. On the expected day of parturition, but before birth, projections from the organum vasculosum of the lamina terminalis to the Supraoptic Nucleus became significantly activated. These findings provide evidence of direct afferent pathways to the Supraoptic Nucleus from the brain stem and olfactory bulbs that are activated at parturition.
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Inhibition of rat oxytocin and vasopressin Supraoptic Nucleus neurons by nociceptin in vitro
Neuroscience, 1998Co-Authors: N. Doi, M. B. Dutia, John A. RussellAbstract:Abstract The effects of nociceptin (orphanin FQ) on the excitability of electrophysiologically-identified oxytocin and vasopressin neurons were investigated in rat hypothalamic Supraoptic Nucleus slices in vitro , using whole-cell patch-clamp recording techniques. Nociceptin inhibited the spontaneous discharge of 9/20 (45%) of Supraoptic Nucleus neurons tested, while in the remaining 11/20 neurons it inhibited firing rate and induced repetitive burst-firing. There were no differences between the effects of nociceptin on oxytocin and vasopressin neurons. When recordings were made using EGTA-containing patch pipettes, nociceptin caused inhibition in all 30 Supraoptic Nucleus neurons tested, and burst-firing was not seen. The inhibitory effects of nociceptin persisted in low Ca, Co medium, and were not antagonized by naloxone at concentrations sufficient to antagonize the inhibitory actions of morphine and U50 488. The actions of nociceptin on Supraoptic Nucleus neurons are therefore likely to be mediated by postsynaptic opioid receptor-like (ORL 1 ) receptors that are distinct from known opioid receptors. The inhibitory responses to nociceptin were also insensitive to naloxone benzoylhydrazone, which itself had no effect on the spontaneous discharge of the Supraoptic Nucleus neurons. Our findings demonstrate that endogenous nociceptin may have a functional role in regulating oxytocin and vasopressin secretion through its actions on hypothalamic Supraoptic Nucleus neurons.
Tatsushi Onaka - One of the best experts on this subject based on the ideXlab platform.
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Intermittent footshock facilitates dendritic vasopressin release but suppresses vasopressin synthesis within the rat Supraoptic Nucleus
Journal of Neuroendocrinology, 2003Co-Authors: Tatsushi Onaka, Ryota Serino, Yoichi UetaAbstract:Emotional stress inhibits vasopressin release from the pituitary but may facilitate its release from the dendrites in the hypothalamus. We examined effects of intermittently applied footshock upon the amount of vasopressin heteronuclear RNA in the hypothalamus. The footshock decreased plasma vasopressin concentration but increased its extracellular concentration within the Supraoptic Nucleus. The contents of the vasopressin heteronuclear RNA in the Supraoptic Nucleus were significantly decreased after the shock. These data suggest that intermittent footshock decreases not only vasopressin release from the axon terminals in the pituitary, but also vasopressin synthesis in the cell bodies in the hypothalamus while the stimulus facilitates vasopressin release from the dendrites in the hypothalamus. The data also suggest differential control of dendritic vasopressin release and synthesis in the hypothalamus.
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Facilitative role of endogenous oxytocin in noradrenaline release in the rat Supraoptic Nucleus
The European journal of neuroscience, 2003Co-Authors: Tatsushi Onaka, Tomoko Yamashita, Keiko Ikeda, Kazufumi HondaAbstract:Oxytocin is released not only from the axon terminals in the neurothypophysis but also from the dendrites in the hypothalamus. In the present study, we examined the role of dendritic oxytocin release in regulating presynaptic noradrenaline release within the hypothalamus. In vivo microdialysis experiments showed that local application of oxytocin augmented high-K+-induced noradrenaline release in the hypothalamic Supraoptic Nucleus. Oxytocin application to the hypothalamic synaptosomal preparation in vitro also potentiated high-K+-induced noradrenaline release. The effect of oxytocin was dose-dependent and was blocked by an oxytocin receptor antagonist. We then examined roles of oxytocin released from the dendrites using in vivo microdialysis. Local application of an oxytocin receptor antagonist impaired noradrenaline release in the Supraoptic Nucleus in response to high-K+ solution or noxious stimuli. An i.c.v. injection of an oxytocin receptor antagonist also impaired oxytocin release from the pituitary after noxious stimuli. These data suggest that dendritic oxytocin facilitates activation of oxytocin neurons, at least in part by augmentation of noradrenaline release via a presynaptic action.
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Vasopressin regulation of noradrenaline release within the Supraoptic Nucleus.
Journal of neuroendocrinology, 2001Co-Authors: Mike Ludwig, Tatsushi Onaka, Kinji YagiAbstract:The effect of electrically evoked dendritic vasopressin release on noradrenaline release into the hypothalamic Supraoptic Nucleus was assessed by in vivo microdialysis in conjunction with high pressure liquid chromatography and electrochemical detection. Electrical activation of magnocellular Supraoptic neurones by stimulation of their axons at the level of the neural lobe significantly increased noradrenaline release into the Nucleus (2.5-fold, P
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Vasopressin differentially modulates noradrenaline release in the rat Supraoptic Nucleus.
Neuroreport, 2001Co-Authors: Tomoko Yamashita, Tatsushi Onaka, Xiu Liu, Kazufumi Honda, Toshikazu Saito, Kinji YagiAbstract:Vasopressin is released not only from axon terminals in the neurohypophysis but also from soma/dendrite regions in the Supraoptic Nucleus. In order to investigate presynaptic roles of dendritically released vasopressin, we examined effects of local application of vasopressin upon noradrenaline release within the Supraoptic Nucleus by a microdialysis method. Noradrenaline release within the Supraoptic Nucleus was facilitated by local perfusion with high K+ or an NMDA receptor antagonist. Vasopressin augmented noradrenaline increase after high K+ but reduced it after an NMDA receptor antagonist, AP-5. The results suggest that dendritically released vasopressin modulates noradrenaline release within the Supraoptic Nucleus in a bimodal fashion.
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Nicotine facilitates noradrenaline release in the rat Supraoptic Nucleus.
Neuroreport, 2001Co-Authors: Xiu Liu, Tatsushi Onaka, Kinji YagiAbstract:Nicotine injected in the Supraoptic Nucleus facilitates vasopressin release from the neurohypophysis. Nicotinic acetylcholine receptors have been found not only on vasopressin-producing cell bodies but also on presynaptic nerve terminals in the Nucleus. Vasopressin cells receive excitatory synaptic inputs from noradrenergic neurones. To test whether nicotine facilitates noradrenaline release in the Supraoptic Nucleus, we perfused the Supraoptic Nucleus with nicotine through a microdialysis probe. Nicotine increased the extracellular noradrenaline concentrations in the Nucleus. A noradrenaline uptake inhibitor, desipramine, increased the extracellular noradrenaline concentrations in the Nucleus and did not block the noradrenaline increase after nicotine. The results suggest that nicotine acts within the Supraoptic Nucleus to facilitate noradrenaline release pre-synaptically. This presynaptic action may contribute, in part, to vasopressin release after nicotine.
Colin H. Brown - One of the best experts on this subject based on the ideXlab platform.
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Kisspeptin Activation of Supraoptic Nucleus Neurons in Vivo
Endocrinology, 2011Co-Authors: Victoria Scott, Colin H. BrownAbstract:Oxytocin and vasopressin are synthesized by magnocellular neurosecretory cells in the hypothalamic Supraoptic and paraventricular nuclei and are released from the posterior pituitary gland into the circulation. Intravenous administration of the ligand for the G protein-coupled receptor 54 receptor, kisspeptin-10, increases plasma oxytocin levels and intracerebroventricular kisspeptin-10 increases vasopressin levels, indicating that kisspeptin might play a role in various physiological functions via stimulation of oxytocin and vasopressin secretion. Because posterior pituitary hormone secretion is dependent on action potential (spike) discharge, we used in vivo extracellular single unit recording to determine the effects of kisspeptin-10 on Supraoptic Nucleus neurons in urethane-anaesthetized female rats. Intravenous kisspeptin-10 (100 μg) increased the firing rate of oxytocin neurons from 3.7 ± 0.8 to 4.7 ± 0.8 spikes/sec (P = 0.0004), but only a quarter of vasopressin neurons responded to iv kisspeptin-1...
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Activity-dependent feedback modulation of spike patterning of Supraoptic Nucleus neurons by endogenous adenosine
American journal of physiology. Regulatory integrative and comparative physiology, 2006Co-Authors: Philip M. Bull, Colin H. Brown, John A. Russell, Mike LudwigAbstract:Neuropeptide secretion from the dendrites of hypothalamic magnocellular Supraoptic Nucleus (SON) neurons contributes to the regulation of neuronal activity patterning, which ultimately determines t...
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Local injection of pertussis toxin attenuates morphine withdrawal excitation of rat Supraoptic Nucleus neurones
Brain research bulletin, 2000Co-Authors: Colin H. Brown, Gareth Leng, Louise E. Johnstone, Niall P. Murphy, John A. RussellAbstract:Abstract Morphine inhibits oxytocin neurones via G i/o -protein-linked μ-opioid receptors. Following chronic morphine administration oxytocin cells develop dependence, shown by withdrawal excitation after administration of the opioid antagonist, naloxone. Here, inactivation of G i/o -proteins by pre-treatment of morphine-dependent rats with pertussis toxin injected into the left Supraoptic Nucleus reduced withdrawal-induced Fos protein expression within the injected Nucleus by 41 ± 10% compared to the contralateral Nucleus, indicating that functional G i/o -proteins are essential for the development and/or expression of morphine dependence by oxytocin cells in the Supraoptic Nucleus. In another group of rats, pertussis toxin did not alter the responses to either systemic cholecystokinin administration or systemic hypertonic saline administration, indicating that pertussis toxin does not prevent oxytocin cells from responding to stimuli that are not mediated by G i/o -proteins. Finally, pertussis toxin reduced acute morphine inhibition of systemic hypertonic saline-induced Fos protein expression in the Supraoptic Nucleus, confirming that pertussis toxin effectively inactivates G i/o -proteins in the Supraoptic Nucleus. Thus, the expression of morphine withdrawal excitation by Supraoptic Nucleus oxytocin cells requires the functional integrity of G i/o -proteins within the Nucleus.
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kappa-opioid regulation of neuronal activity in the rat Supraoptic Nucleus in vivo
The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998Co-Authors: Colin H. Brown, Mike Ludwig, Gareth LengAbstract:We investigated the influence of endogenous κ-opioids on the activity of Supraoptic neurons in vivo . Administration of the κ-antagonist nor -binaltorphimine (200 μg/kg, i.v.), increased the activity of phasic (vasopressin), but not continuously active (oxytocin), Supraoptic neurons by increasing burst duration (by 69 ± 24%) and decreasing the interburst interval (by 19 ± 11%). Similarly, retrodialysis of nor -binaltorphimine onto the Supraoptic Nucleus increased the burst duration (119 ± 57% increase) of vasopressin cells but did not alter the firing rate of oxytocin cells (4 ± 8% decrease). Thus, an endogenous κ-agonist modulates vasopressin cell activity by an action within the Supraoptic Nucleus. To eliminate κ-agonist actions within the Supraoptic Nucleus, we infused the κ-agonist U50,488H (2.5 μg/hr at 0.5 μg/hr) into one Supraoptic Nucleus over 5 d to locally downregulate κ-receptor function. Such infusions reduced the spontaneous activity of vasopressin but not oxytocin cells and reduced the proportion of cells displaying spontaneous phasic activity from 26% in vehicle-infused nuclei to 3% in U50,488H-infused nuclei; this treatment also prevented acute inhibition of both vasopressin and oxytocin cells by U50,488H (1000 μg/kg, i.v.), confirming functional κ-receptor downregulation. In U50,488H-infused Supraoptic nuclei, vasopressin cell firing rate was increased by nor -binaltorphimine (100 and 200 μg/kg, i.v.) but not to beyond that found in vehicle-treated nuclei, indicating that these cells were not U50,488H-dependent. Thus, normally functioning κ-opioid mechanisms on vasopressin cells are essential for the expression of phasic firing.
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The role of afferent inputs to Supraoptic Nucleus oxytocin neurons during naloxone-precipitated morphine withdrawal in the rat
Neuroscience, 1997Co-Authors: Niall P. Murphy, Colin H. Brown, Tatsushi Onaka, Gareth LengAbstract:Abstract During prolonged exposure to morphine, oxytocin neurons of the rat Supraoptic Nucleus develop dependence, shown by hyperexcitation following morphine withdrawal. The present study investigated the role of afferent projections to the Supraoptic Nucleus in this withdrawal excitation. Rats were made morphine-dependent by continuous intracerebroventricular infusion of morphine at increasing doses (up to 50 μg/h). On the sixth day, rats were anaesthetized with pentobarbitone and morphine withdrawal was precipitated by intraperitoneal injection of naloxone (5 mg/kg). Fos-immunoreactivity in the Supraoptic Nucleus, and also in the median preoptic Nucleus, organum vasculosum of the lamina terminalis and subfornical organ, which project to the Supraoptic Nucleus, increased following morphine withdrawal. However, retrograde tracing from the Supraoptic Nucleus showed that, of the neurons in these regions which project to the Supraoptic Nucleus, only 0.4–7.1% expressed Fos in response to morphine withdrawal. Following morphine withdrawal, Fos-immunoreactivity was present in 39.2% and 19.8% of the tyrosine hydroxylase-immunoreactive neurons of the A1/C1 and A2/C2 cell groups. Of the cells in these regions identified as projecting to the Supraoptic Nucleus, 11.3% in the region of the A2 cell group and 12.7% in the region of the A1 cell group expressed Fos after morphine withdrawal. In a second study, monoamine release was measured in the Supraoptic Nucleus of urethane-anaesthetized morphine-dependent and -naive rats. Retrodialysis of naloxone (10−5 M) into the Supraoptic Nucleus induced a small increase in plasma oxytocin concentration in morphine-dependent rats (13.5±4.8 pg/ml increase) but not in naive rats (1.2±5.9 pg/ml decrease), with no significant change in monoamine release in either morphine-dependent or -naive rats. Intravenous injection of naloxone (5 mg/kg) 1 h later produced a further significant increase in plasma oxytocin concentration in morphine-dependent rats concomitant with a significant increase in noradrenaline release from the Supraoptic Nucleus. Thus, morphine-withdrawal excitation of Supraoptic oxytocin neurons occurs concurrently with a modestly increased activity of their input from the brainstem, and very little activation in other known inputs.
