The Experts below are selected from a list of 27 Experts worldwide ranked by ideXlab platform
Colin H Brown - One of the best experts on this subject based on the ideXlab platform.
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physiological regulation of MagnoCellular Neurosecretory Cell activity integration of intrinsic local and afferent mechanisms
Journal of Neuroendocrinology, 2013Co-Authors: Colin H Brown, Mike Ludwig, Jaideep S Bains, Javier E SternAbstract:The hypothalamic supraoptic and paraventricular nuclei contain MagnoCellular Neurosecretory Cells (MNCs) that project to the posterior pituitary gland where they secrete either oxytocin or vasopressin (the antidiuretic hormone) into the circulation. Oxytocin is important for delivery at birth and is essential for milk ejection during suckling. Vasopressin primarily promotes water reabsorption in the kidney to maintain body fluid balance, but also increases vasoconstriction. The profile of oxytocin and vasopressin secretion is principally determined by the pattern of action potentials initiated at the Cell bodies. Although it has long been known that the activity of MNCs depends upon afferent inputs that relay information on reproductive, osmotic and cardiovascular status, it has recently become clear that activity depends critically on local regulation by glial Cells, as well as intrinsic regulation by the MNCs themselves. Here, we provide an overview of recent advances in our understanding of how intrinsic and local extrinsic mechanisms integrate with afferent inputs to generate appropriate physiological regulation of oxytocin and vasopressin MNC activity.
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Autocrine feedback inhibition of plateau potentials terminates phasic bursts in MagnoCellular Neurosecretory Cells of the rat supraoptic nucleus
The Journal of Physiology, 2004Co-Authors: Colin H Brown, Charles W. BourqueAbstract:Phasic activity in MagnoCellular Neurosecretory Cells is characterized by alternating periods of activity (bursts) and silence. During phasic bursts, action potentials are superimposed on plateau potentials that are generated by summation of depolarizing after-potentials. Dynorphin is copackaged in vasopressin Neurosecretory vesicles that are exocytosed from MagnoCellular Neurosecretory Cell dendrites and terminals, and both peptides have been implicated in the generation of phasic activity. Here we show that somato-dendritic dynorphin release terminates phasic bursts by autocrine inhibition of plateau potentials in MagnoCellular Neurosecretory Cells recorded intraCellularly from hypothalamic explants using sharp electrodes. Conditioning spike trains caused an activity-dependent reduction of depolarizing after-potential amplitude that was partially reversed by α-latrotoxin (which depletes Neurosecretory vesicles) and by nor-binaltorphimine (κ-opioid receptor antagonist), but not by an oxytocin/vasopressin receptor antagonist or a μ-opioid receptor antagonist, indicating that activity-dependent inhibition of depolarizing after-potentials requires exocytosis of an endogenous κ-opioid peptide. κ-Opioid inhibition of depolarizing after-potentials was not mediated by actions on evoked after-hyperpolarizations since these were not affected by κ-opioid receptor agonists or antagonists. Evoked bursts were prolonged by antagonism of κ-opioid receptors with nor-binaltorphimine and by depletion of Neurosecretory vesicles by α-latrotoxin, becoming everlasting in ∼50% of Cells. Finally, spontaneously active neurones exposed to nor-binaltorphimine switched from phasic to continuous firing as plateau potentials became non-inactivating. Thus, dynorphin coreleased with vasopressin generates phasic activity through activity-dependent feedback inhibition of plateau potentials in MagnoCellular Neurosecretory Cells.
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Autocrine feedback inhibition of plateau potentials terminates phasic bursts in MagnoCellular Neurosecretory Cells of the rat supraoptic nucleus.
The Journal of physiology, 2004Co-Authors: Colin H Brown, Charles W. BourqueAbstract:Phasic activity in MagnoCellular Neurosecretory Cells is characterized by alternating periods of activity (bursts) and silence. During phasic bursts, action potentials are superimposed on plateau potentials that are generated by summation of depolarizing after-potentials. Dynorphin is copackaged in vasopressin Neurosecretory vesicles that are exocytosed from MagnoCellular Neurosecretory Cell dendrites and terminals, and both peptides have been implicated in the generation of phasic activity. Here we show that somato-dendritic dynorphin release terminates phasic bursts by autocrine inhibition of plateau potentials in MagnoCellular Neurosecretory Cells recorded intraCellularly from hypothalamic explants using sharp electrodes. Conditioning spike trains caused an activity-dependent reduction of depolarizing after-potential amplitude that was partially reversed by alpha-latrotoxin (which depletes Neurosecretory vesicles) and by nor-binaltorphimine (kappa-opioid receptor antagonist), but not by an oxytocin/vasopressin receptor antagonist or a micro-opioid receptor antagonist, indicating that activity-dependent inhibition of depolarizing after-potentials requires exocytosis of an endogenous kappa-opioid peptide. kappa-Opioid inhibition of depolarizing after-potentials was not mediated by actions on evoked after-hyperpolarizations since these were not affected by kappa-opioid receptor agonists or antagonists. Evoked bursts were prolonged by antagonism of kappa-opioid receptors with nor-binaltorphimine and by depletion of Neurosecretory vesicles by alpha-latrotoxin, becoming everlasting in approximately 50% of Cells. Finally, spontaneously active neurones exposed to nor-binaltorphimine switched from phasic to continuous firing as plateau potentials became non-inactivating. Thus, dynorphin coreleased with vasopressin generates phasic activity through activity-dependent feedback inhibition of plateau potentials in MagnoCellular Neurosecretory Cells.
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opioid modulation of MagnoCellular Neurosecretory Cell activity
Neuroscience Research, 2000Co-Authors: Colin H Brown, John A Russell, Gareth LengAbstract:MagnoCellular Neurosecretory Cells of the hypothalamic supraoptic and paraventricular nuclei secrete the hormones, oxytocin and vasopressin, into the systemic circulation from the posterior pituitary gland. Oxytocin is important for parturition and is essential for lactation. Vasopressin regulates body fluid homeostasis. The secretion of these hormones is altered in response to peripheral stimuli that are conveyed via projections from other parts of the brain. Endogenous opioid peptide systems interact with the MagnoCellular Neurosecretory system at several levels to restrain the basal secretion of these hormones as well as their secretory responses to various physiological stimuli. The inhibition of basal secretion can occur at the level of the Neurosecretory terminals where endogenous opioids inhibit the release of oxytocin, and at the Cell bodies of MagnoCellular Cells to modulate the activity pattern of vasopressin Cells. The responses of the MagnoCellular Neurosecretory system to physiological stimuli are also regulated by these mechanisms but in addition probably also by pre-synaptic inhibition of afferent inputs to MagnoCellular Cells as well as direct effects on the Cell bodies of afferent input Cells to modulate their activity. Here, we review the mechanisms and functional consequences of opioid interactions with oxytocin and vasopressin Cells.
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review article opioid modulation of MagnoCellular Neurosecretory Cell activity
2000Co-Authors: Colin H Brown, John A Russell, Gareth LengAbstract:MagnoCellular Neurosecretory Cells of the hypothalamic supraoptic and paraventricular nuclei secrete the hormones, oxytocin and vasopressin, into the systemic circulation from the posterior pituitary gland. Oxytocin is important for parturition and is essential for lactation. Vasopressin regulates body fluid homeostasis. The secretion of these hormones is altered in response to peripheral stimuli that are conveyed via projections from other parts of the brain. Endogenous opioid peptide systems interact with the MagnoCellular Neurosecretory system at several levels to restrain the basal secretion of these hormones as well as their secretory responses to various physiological stimuli. The inhibition of basal secretion can occur at the level of the Neurosecretory terminals where endogenous opioids inhibit the release of oxytocin, and at the Cell bodies of MagnoCellular Cells to modulate the activity pattern of vasopressin Cells. The responses of the MagnoCellular Neurosecretory system to physiological stimuli are also regulated by these mechanisms but in addition probably also by pre-synaptic inhibition of afferent inputs to MagnoCellular Cells as well as direct effects on the Cell bodies of afferent input Cells to modulate their activity. Here, we review the mechanisms and functional consequences of opioid interactions with oxytocin and vasopressin Cells. © 2000 Elsevier Science Ireland Ltd. All rights reserved.
Gareth Leng - One of the best experts on this subject based on the ideXlab platform.
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the active role of dendrites in the regulation of MagnoCellular Neurosecretory Cell behavior
Progress in Brain Research, 2002Co-Authors: Mike Ludwig, John A Russell, Nancy Sabatier, Govindan Dayanithi, Gareth LengAbstract:Abstract The interactions of the dendritically released neuropeptides vasopressin and oxytocin with co-released neuroactive substances such as opioids and nitric oxide are reviewed. Endogenous opioids regulate MagnoCellular neurons at the level of the supraoptic nucleus and the relationship of dendritically released peptides and co-released opioids seems to be dependent on the stimulus given and the physiological state of the animal. Nitric oxide has a prominent inhibitory action on supraoptic neurons and these actions are predominantly mediated indirectly by GABA inputs. The role of these co-released neuroactive substances in differentially regulated release of neuropeptides from dendrites versus distant axon terminals has to be determined in more detail. A picture emerges in which release of vasopressin and oxytocin from different anatomical compartments of a single neuron may arise from different intraCellular secretory pools and their preparation before release.
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opioid modulation of MagnoCellular Neurosecretory Cell activity
Neuroscience Research, 2000Co-Authors: Colin H Brown, John A Russell, Gareth LengAbstract:MagnoCellular Neurosecretory Cells of the hypothalamic supraoptic and paraventricular nuclei secrete the hormones, oxytocin and vasopressin, into the systemic circulation from the posterior pituitary gland. Oxytocin is important for parturition and is essential for lactation. Vasopressin regulates body fluid homeostasis. The secretion of these hormones is altered in response to peripheral stimuli that are conveyed via projections from other parts of the brain. Endogenous opioid peptide systems interact with the MagnoCellular Neurosecretory system at several levels to restrain the basal secretion of these hormones as well as their secretory responses to various physiological stimuli. The inhibition of basal secretion can occur at the level of the Neurosecretory terminals where endogenous opioids inhibit the release of oxytocin, and at the Cell bodies of MagnoCellular Cells to modulate the activity pattern of vasopressin Cells. The responses of the MagnoCellular Neurosecretory system to physiological stimuli are also regulated by these mechanisms but in addition probably also by pre-synaptic inhibition of afferent inputs to MagnoCellular Cells as well as direct effects on the Cell bodies of afferent input Cells to modulate their activity. Here, we review the mechanisms and functional consequences of opioid interactions with oxytocin and vasopressin Cells.
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review article opioid modulation of MagnoCellular Neurosecretory Cell activity
2000Co-Authors: Colin H Brown, John A Russell, Gareth LengAbstract:MagnoCellular Neurosecretory Cells of the hypothalamic supraoptic and paraventricular nuclei secrete the hormones, oxytocin and vasopressin, into the systemic circulation from the posterior pituitary gland. Oxytocin is important for parturition and is essential for lactation. Vasopressin regulates body fluid homeostasis. The secretion of these hormones is altered in response to peripheral stimuli that are conveyed via projections from other parts of the brain. Endogenous opioid peptide systems interact with the MagnoCellular Neurosecretory system at several levels to restrain the basal secretion of these hormones as well as their secretory responses to various physiological stimuli. The inhibition of basal secretion can occur at the level of the Neurosecretory terminals where endogenous opioids inhibit the release of oxytocin, and at the Cell bodies of MagnoCellular Cells to modulate the activity pattern of vasopressin Cells. The responses of the MagnoCellular Neurosecretory system to physiological stimuli are also regulated by these mechanisms but in addition probably also by pre-synaptic inhibition of afferent inputs to MagnoCellular Cells as well as direct effects on the Cell bodies of afferent input Cells to modulate their activity. Here, we review the mechanisms and functional consequences of opioid interactions with oxytocin and vasopressin Cells. © 2000 Elsevier Science Ireland Ltd. All rights reserved.
John A Russell - One of the best experts on this subject based on the ideXlab platform.
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the active role of dendrites in the regulation of MagnoCellular Neurosecretory Cell behavior
Progress in Brain Research, 2002Co-Authors: Mike Ludwig, John A Russell, Nancy Sabatier, Govindan Dayanithi, Gareth LengAbstract:Abstract The interactions of the dendritically released neuropeptides vasopressin and oxytocin with co-released neuroactive substances such as opioids and nitric oxide are reviewed. Endogenous opioids regulate MagnoCellular neurons at the level of the supraoptic nucleus and the relationship of dendritically released peptides and co-released opioids seems to be dependent on the stimulus given and the physiological state of the animal. Nitric oxide has a prominent inhibitory action on supraoptic neurons and these actions are predominantly mediated indirectly by GABA inputs. The role of these co-released neuroactive substances in differentially regulated release of neuropeptides from dendrites versus distant axon terminals has to be determined in more detail. A picture emerges in which release of vasopressin and oxytocin from different anatomical compartments of a single neuron may arise from different intraCellular secretory pools and their preparation before release.
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opioid modulation of MagnoCellular Neurosecretory Cell activity
Neuroscience Research, 2000Co-Authors: Colin H Brown, John A Russell, Gareth LengAbstract:MagnoCellular Neurosecretory Cells of the hypothalamic supraoptic and paraventricular nuclei secrete the hormones, oxytocin and vasopressin, into the systemic circulation from the posterior pituitary gland. Oxytocin is important for parturition and is essential for lactation. Vasopressin regulates body fluid homeostasis. The secretion of these hormones is altered in response to peripheral stimuli that are conveyed via projections from other parts of the brain. Endogenous opioid peptide systems interact with the MagnoCellular Neurosecretory system at several levels to restrain the basal secretion of these hormones as well as their secretory responses to various physiological stimuli. The inhibition of basal secretion can occur at the level of the Neurosecretory terminals where endogenous opioids inhibit the release of oxytocin, and at the Cell bodies of MagnoCellular Cells to modulate the activity pattern of vasopressin Cells. The responses of the MagnoCellular Neurosecretory system to physiological stimuli are also regulated by these mechanisms but in addition probably also by pre-synaptic inhibition of afferent inputs to MagnoCellular Cells as well as direct effects on the Cell bodies of afferent input Cells to modulate their activity. Here, we review the mechanisms and functional consequences of opioid interactions with oxytocin and vasopressin Cells.
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review article opioid modulation of MagnoCellular Neurosecretory Cell activity
2000Co-Authors: Colin H Brown, John A Russell, Gareth LengAbstract:MagnoCellular Neurosecretory Cells of the hypothalamic supraoptic and paraventricular nuclei secrete the hormones, oxytocin and vasopressin, into the systemic circulation from the posterior pituitary gland. Oxytocin is important for parturition and is essential for lactation. Vasopressin regulates body fluid homeostasis. The secretion of these hormones is altered in response to peripheral stimuli that are conveyed via projections from other parts of the brain. Endogenous opioid peptide systems interact with the MagnoCellular Neurosecretory system at several levels to restrain the basal secretion of these hormones as well as their secretory responses to various physiological stimuli. The inhibition of basal secretion can occur at the level of the Neurosecretory terminals where endogenous opioids inhibit the release of oxytocin, and at the Cell bodies of MagnoCellular Cells to modulate the activity pattern of vasopressin Cells. The responses of the MagnoCellular Neurosecretory system to physiological stimuli are also regulated by these mechanisms but in addition probably also by pre-synaptic inhibition of afferent inputs to MagnoCellular Cells as well as direct effects on the Cell bodies of afferent input Cells to modulate their activity. Here, we review the mechanisms and functional consequences of opioid interactions with oxytocin and vasopressin Cells. © 2000 Elsevier Science Ireland Ltd. All rights reserved.
Charles W. Bourque - One of the best experts on this subject based on the ideXlab platform.
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Autocrine feedback inhibition of plateau potentials terminates phasic bursts in MagnoCellular Neurosecretory Cells of the rat supraoptic nucleus
The Journal of Physiology, 2004Co-Authors: Colin H Brown, Charles W. BourqueAbstract:Phasic activity in MagnoCellular Neurosecretory Cells is characterized by alternating periods of activity (bursts) and silence. During phasic bursts, action potentials are superimposed on plateau potentials that are generated by summation of depolarizing after-potentials. Dynorphin is copackaged in vasopressin Neurosecretory vesicles that are exocytosed from MagnoCellular Neurosecretory Cell dendrites and terminals, and both peptides have been implicated in the generation of phasic activity. Here we show that somato-dendritic dynorphin release terminates phasic bursts by autocrine inhibition of plateau potentials in MagnoCellular Neurosecretory Cells recorded intraCellularly from hypothalamic explants using sharp electrodes. Conditioning spike trains caused an activity-dependent reduction of depolarizing after-potential amplitude that was partially reversed by α-latrotoxin (which depletes Neurosecretory vesicles) and by nor-binaltorphimine (κ-opioid receptor antagonist), but not by an oxytocin/vasopressin receptor antagonist or a μ-opioid receptor antagonist, indicating that activity-dependent inhibition of depolarizing after-potentials requires exocytosis of an endogenous κ-opioid peptide. κ-Opioid inhibition of depolarizing after-potentials was not mediated by actions on evoked after-hyperpolarizations since these were not affected by κ-opioid receptor agonists or antagonists. Evoked bursts were prolonged by antagonism of κ-opioid receptors with nor-binaltorphimine and by depletion of Neurosecretory vesicles by α-latrotoxin, becoming everlasting in ∼50% of Cells. Finally, spontaneously active neurones exposed to nor-binaltorphimine switched from phasic to continuous firing as plateau potentials became non-inactivating. Thus, dynorphin coreleased with vasopressin generates phasic activity through activity-dependent feedback inhibition of plateau potentials in MagnoCellular Neurosecretory Cells.
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Autocrine feedback inhibition of plateau potentials terminates phasic bursts in MagnoCellular Neurosecretory Cells of the rat supraoptic nucleus.
The Journal of physiology, 2004Co-Authors: Colin H Brown, Charles W. BourqueAbstract:Phasic activity in MagnoCellular Neurosecretory Cells is characterized by alternating periods of activity (bursts) and silence. During phasic bursts, action potentials are superimposed on plateau potentials that are generated by summation of depolarizing after-potentials. Dynorphin is copackaged in vasopressin Neurosecretory vesicles that are exocytosed from MagnoCellular Neurosecretory Cell dendrites and terminals, and both peptides have been implicated in the generation of phasic activity. Here we show that somato-dendritic dynorphin release terminates phasic bursts by autocrine inhibition of plateau potentials in MagnoCellular Neurosecretory Cells recorded intraCellularly from hypothalamic explants using sharp electrodes. Conditioning spike trains caused an activity-dependent reduction of depolarizing after-potential amplitude that was partially reversed by alpha-latrotoxin (which depletes Neurosecretory vesicles) and by nor-binaltorphimine (kappa-opioid receptor antagonist), but not by an oxytocin/vasopressin receptor antagonist or a micro-opioid receptor antagonist, indicating that activity-dependent inhibition of depolarizing after-potentials requires exocytosis of an endogenous kappa-opioid peptide. kappa-Opioid inhibition of depolarizing after-potentials was not mediated by actions on evoked after-hyperpolarizations since these were not affected by kappa-opioid receptor agonists or antagonists. Evoked bursts were prolonged by antagonism of kappa-opioid receptors with nor-binaltorphimine and by depletion of Neurosecretory vesicles by alpha-latrotoxin, becoming everlasting in approximately 50% of Cells. Finally, spontaneously active neurones exposed to nor-binaltorphimine switched from phasic to continuous firing as plateau potentials became non-inactivating. Thus, dynorphin coreleased with vasopressin generates phasic activity through activity-dependent feedback inhibition of plateau potentials in MagnoCellular Neurosecretory Cells.
Mike Ludwig - One of the best experts on this subject based on the ideXlab platform.
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physiological regulation of MagnoCellular Neurosecretory Cell activity integration of intrinsic local and afferent mechanisms
Journal of Neuroendocrinology, 2013Co-Authors: Colin H Brown, Mike Ludwig, Jaideep S Bains, Javier E SternAbstract:The hypothalamic supraoptic and paraventricular nuclei contain MagnoCellular Neurosecretory Cells (MNCs) that project to the posterior pituitary gland where they secrete either oxytocin or vasopressin (the antidiuretic hormone) into the circulation. Oxytocin is important for delivery at birth and is essential for milk ejection during suckling. Vasopressin primarily promotes water reabsorption in the kidney to maintain body fluid balance, but also increases vasoconstriction. The profile of oxytocin and vasopressin secretion is principally determined by the pattern of action potentials initiated at the Cell bodies. Although it has long been known that the activity of MNCs depends upon afferent inputs that relay information on reproductive, osmotic and cardiovascular status, it has recently become clear that activity depends critically on local regulation by glial Cells, as well as intrinsic regulation by the MNCs themselves. Here, we provide an overview of recent advances in our understanding of how intrinsic and local extrinsic mechanisms integrate with afferent inputs to generate appropriate physiological regulation of oxytocin and vasopressin MNC activity.
-
the active role of dendrites in the regulation of MagnoCellular Neurosecretory Cell behavior
Progress in Brain Research, 2002Co-Authors: Mike Ludwig, John A Russell, Nancy Sabatier, Govindan Dayanithi, Gareth LengAbstract:Abstract The interactions of the dendritically released neuropeptides vasopressin and oxytocin with co-released neuroactive substances such as opioids and nitric oxide are reviewed. Endogenous opioids regulate MagnoCellular neurons at the level of the supraoptic nucleus and the relationship of dendritically released peptides and co-released opioids seems to be dependent on the stimulus given and the physiological state of the animal. Nitric oxide has a prominent inhibitory action on supraoptic neurons and these actions are predominantly mediated indirectly by GABA inputs. The role of these co-released neuroactive substances in differentially regulated release of neuropeptides from dendrites versus distant axon terminals has to be determined in more detail. A picture emerges in which release of vasopressin and oxytocin from different anatomical compartments of a single neuron may arise from different intraCellular secretory pools and their preparation before release.