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Govindan Dayanithi - One of the best experts on this subject based on the ideXlab platform.

  • Regulation of activity-dependent dendritic Vasopressin Release from rat supraoptic neurones.
    The Journal of physiology, 2005
    Co-Authors: Mike Ludwig, Govindan Dayanithi, Vicky A Tobin, Philip M Bull, Nancy Sabatier, Rainer Landgraf, Gareth Leng
    Abstract:

    Magnocellular neurones of the hypothalamus Release Vasopressin and oxytocin from their dendrites and soma. Using a combination of electrophysiology, microdialysis, in vitro explants, and radioimmunoassay we assessed the involvement of intracellular Ca(2+) stores in the regulation of dendritic Vasopressin Release. Thapsigargin and cyclopiazonic acid, which mobilize Ca(2+) from intracellular stores of the endoplasmic reticulum, evoked Vasopressin Release from dendrites and somata of magnocellular neurones in the supraoptic nucleus. Thapsigargin also produced a dramatic potentiation of dendritic Vasopressin Release evoked by osmotic or high potassium stimulation. This effect is long lasting, time dependent, and specific to thapsigargin as caffeine and ryanodine had no effect. Furthermore, antidromic activation of electrical activity in the cell bodies Released Vasopressin from dendrites only after thapsigargin pretreatment. Thus, exposure to Ca(2+) mobilizers such as thapsigargin or cyclopiazonic acid primes the releasable pool of Vasopressin in the dendrites, so that Release can subsequently be evoked by electrical and depolarization-dependent activation. Vasopressin itself is effective in inducing dendritic Vasopressin Release, but it is ineffective in producing priming.

  • intracellular calcium increase and somatodendritic Vasopressin Release by Vasopressin receptor agonists in the rat supraoptic nucleus involvement of multiple intracellular transduction signals
    Journal of Neuroendocrinology, 2004
    Co-Authors: Nancy Sabatier, Izumi Shibuya, Govindan Dayanithi
    Abstract:

    Vasopressin neurones of the supraoptic nucleus are autoregulated by Vasopressin Released from their soma and dendrites. Vasopressin binds to specific autoreceptors to trigger an influx of Ca(2+), and this response involves both phospholipase C (PLC) and adenylate cyclase (AC) pathways that, in the periphery, are activated by V(1) (V(1a) and V(1b))- and V(2)-type receptors. To investigate the pathways involved in the [Ca(2+)](i) response, [Ca(2+)](i) measurements were made on freshly dissociated neurones using Fura-2 microspectrofluorimetry, and Vasopressin Release was measured from isolated supraoptic nuclei. The [Ca(2+)](i) increase and Vasopressin Release induced by the V(1a) agonist were strongly inhibited by a PLC blocker, an IP(3) receptor antagonist, and a PKC blocker. An AC inhibitor did not affect the V(1a) response, while PKA inhibitors significantly reduced the V(1a)-induced [Ca(2+)](i) and Release responses. The [Ca(2+)](i) increase and Vasopressin Release elicited by the V(2) agonist were attenuated not only by AC pathway blockers, but also by PLC inhibitors. Surprisingly, the V(1b) agonist showed no [Ca(2+)](i) or Vasopressin Release response. In conclusion, the V(1a) agonist activates both PLC and AC pathway, confirming the functional expression of a V(1a) Vasopressin receptor on Vasopressin neurones. The V(2) agonist activation of both PLC and AC pathways could result from an action on the PLC-linked unknown receptor, and/or the AC-linked dual angiotensin II-Vasopressin receptor.

  • neurosteroid regulation of oxytocin and Vasopressin Release from the rat supraoptic nucleus
    The Journal of Physiology, 2003
    Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, Govindan Dayanithi
    Abstract:

    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.

  • Neurosteroid regulation of oxytocin and Vasopressin Release from the rat supraoptic nucleus.
    The Journal of physiology, 2003
    Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, Govindan Dayanithi
    Abstract:

    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.

  • The light chain of tetanus toxin inhibits calcium-dependent Vasopressin Release from permeabilized nerve endings.
    Neuroscience, 1992
    Co-Authors: Govindan Dayanithi, Ulrich Weller, Gudrun Ahnert-hilger, H. Link, J.j. Nordman, Manfred Gratzl
    Abstract:

    The effects of tetanus toxin and its light and heavy chain subunits on Vasopressin Release were investigated in digitonin-permeabilized neurosecretory nerve terminals isolated from the neural lobe of the rat pituitary gland. Exocytosis was induced by challenging the permeabilized nerve endings with micromolar calcium concentrations. Tetanus toxin inhibited Vasopressin Release only in the presence of the reducing agent dithiothreitol. This effect was irreversible. The purified light chain of tetanus toxin strongly inhibited exocytosis in a dose-dependent manner with half-maximal effect at c. 10 nM. The action of the light chain was observed after only 2.5 min of preincubation. Separated heavy chain subunit had no effect on hormone secretion. Inhibition of Vasopressin Release could be prevented by preincubating the light chain of tetanus toxin with an immune serum against tetanus toxin. The data clearly demonstrate that in mammalian neurosecretory nerve endings tetanus toxin acts at a step downstream from the activation by Ca2+ of the exocytotic machinery and that the functional domain of this toxin is confined to its light chain.

Mike Ludwig - One of the best experts on this subject based on the ideXlab platform.

  • the role of the actin cytoskeleton in oxytocin and Vasopressin Release from rat supraoptic nucleus neurons
    The Journal of Physiology, 2007
    Co-Authors: Vicky A Tobin, Mike Ludwig
    Abstract:

    Magnocellular neurons of the supraoptic nucleus (SON) can differentially control peptide Release from the somato/dendritic and axon terminal compartment. Dendritic Release can be selectively regulated through activation of intracellular calcium stores by calcium mobilizers such as thapsigargin (TG), resulting in preparation (priming) of somato/dendritic peptide pools for subsequent activity-dependent Release. As dynamic modulation of the actin cytoskeleton is implicated in secretion from synaptic terminals and from several types of neuroendocrine cells, we studied its involvement in oxytocin and Vasopressin Release from SON neurons. Confocal image analysis of the somata revealed that the normally continuous cortical band of F-actin is disrupted after high potassium (K+, 50 mm) or TG (200 nm) stimulation. The functional importance of actin remodelling was studied using cell-permeable actin polymerizing (jasplakinolide, 2 μm) or depolymerizing agents (latrunculin B, 5 μm) to treat SON and neural lobe (NL) explants in vitro and measure high K+-induced oxytocin and Vasopressin Release. Latrunculin significantly enhanced, and jasplakinolide inhibited, high-K+-evoked somato/dendritic peptide Release, while Release from axon terminals was not altered, suggesting that high-K+-evoked Release in the SON, but not the NL, requires depolymerization of the actin cytoskeleton. TG-induced priming of somato/dendritic Release was also blocked by jasplakinolide and latrunculin, suggesting that priming involves changes in actin remodelling.

  • Regulation of activity-dependent dendritic Vasopressin Release from rat supraoptic neurones.
    The Journal of physiology, 2005
    Co-Authors: Mike Ludwig, Govindan Dayanithi, Vicky A Tobin, Philip M Bull, Nancy Sabatier, Rainer Landgraf, Gareth Leng
    Abstract:

    Magnocellular neurones of the hypothalamus Release Vasopressin and oxytocin from their dendrites and soma. Using a combination of electrophysiology, microdialysis, in vitro explants, and radioimmunoassay we assessed the involvement of intracellular Ca(2+) stores in the regulation of dendritic Vasopressin Release. Thapsigargin and cyclopiazonic acid, which mobilize Ca(2+) from intracellular stores of the endoplasmic reticulum, evoked Vasopressin Release from dendrites and somata of magnocellular neurones in the supraoptic nucleus. Thapsigargin also produced a dramatic potentiation of dendritic Vasopressin Release evoked by osmotic or high potassium stimulation. This effect is long lasting, time dependent, and specific to thapsigargin as caffeine and ryanodine had no effect. Furthermore, antidromic activation of electrical activity in the cell bodies Released Vasopressin from dendrites only after thapsigargin pretreatment. Thus, exposure to Ca(2+) mobilizers such as thapsigargin or cyclopiazonic acid primes the releasable pool of Vasopressin in the dendrites, so that Release can subsequently be evoked by electrical and depolarization-dependent activation. Vasopressin itself is effective in inducing dendritic Vasopressin Release, but it is ineffective in producing priming.

  • neurosteroid regulation of oxytocin and Vasopressin Release from the rat supraoptic nucleus
    The Journal of Physiology, 2003
    Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, Govindan Dayanithi
    Abstract:

    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.

  • Neurosteroid regulation of oxytocin and Vasopressin Release from the rat supraoptic nucleus.
    The Journal of physiology, 2003
    Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, Govindan Dayanithi
    Abstract:

    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.

  • Intrahypothalamic Vasopressin Release. An inhibitor of systemic Vasopressin secretion
    Advances in Experimental Medicine and Biology, 1998
    Co-Authors: Mike Ludwig, Gareth Leng
    Abstract:

    Vasopressin and oxytocin are Released into the extracellular space of the supraoptic (SON) and paraventricular nuclei (PVN). The dendrites of these neurones contain a high density of neurosecretory granules, and exocytotic profiles have been visualised by electron microscopy. Release within the SON has been measured using microperfusion techniques; Release is tetrodotoxin-independent, calcium-dependent, and is activated by a range of physiological stimuli, including suckling, dehydration, haemorrhage and stress. Release of Vasopressin into the SON is regulated by a number of forebrain and brainstem areas. Dendritic Release does not necessarily parallel neurohypophyseal Release, and may occur semi-independently of spike activity in the soma and axons. The physiological consequences of dendritic Vasopressin Release are not clear, Vasopressin and oxytocin appear to induce further Vasopressin and oxytocin Release from the dendrites. In contrast, by combining retrodialysis and electrophysiology we have shown that, unlike oxytocin which excites oxytocin neurones, Vasopressin inhibits the electrical activity of Vasopressin neurones, and hence suppresses Vasopressin Release from the pituitary. Thus, Vasopressin Released from dendrites may act on Vasopressin neurones to regulate their phasic activity by an auto-inhibitory action within the SON. Since dendritic Vasopressin Release is increased and prolonged after various stimuli, this mechanism may act to restrain excitation of Vasopressin neurones (and hence Vasopressin secretion from the neurohypophysis) during continuing stimulation.

Gareth Leng - One of the best experts on this subject based on the ideXlab platform.

  • Regulation of activity-dependent dendritic Vasopressin Release from rat supraoptic neurones.
    The Journal of physiology, 2005
    Co-Authors: Mike Ludwig, Govindan Dayanithi, Vicky A Tobin, Philip M Bull, Nancy Sabatier, Rainer Landgraf, Gareth Leng
    Abstract:

    Magnocellular neurones of the hypothalamus Release Vasopressin and oxytocin from their dendrites and soma. Using a combination of electrophysiology, microdialysis, in vitro explants, and radioimmunoassay we assessed the involvement of intracellular Ca(2+) stores in the regulation of dendritic Vasopressin Release. Thapsigargin and cyclopiazonic acid, which mobilize Ca(2+) from intracellular stores of the endoplasmic reticulum, evoked Vasopressin Release from dendrites and somata of magnocellular neurones in the supraoptic nucleus. Thapsigargin also produced a dramatic potentiation of dendritic Vasopressin Release evoked by osmotic or high potassium stimulation. This effect is long lasting, time dependent, and specific to thapsigargin as caffeine and ryanodine had no effect. Furthermore, antidromic activation of electrical activity in the cell bodies Released Vasopressin from dendrites only after thapsigargin pretreatment. Thus, exposure to Ca(2+) mobilizers such as thapsigargin or cyclopiazonic acid primes the releasable pool of Vasopressin in the dendrites, so that Release can subsequently be evoked by electrical and depolarization-dependent activation. Vasopressin itself is effective in inducing dendritic Vasopressin Release, but it is ineffective in producing priming.

  • neurosteroid regulation of oxytocin and Vasopressin Release from the rat supraoptic nucleus
    The Journal of Physiology, 2003
    Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, Govindan Dayanithi
    Abstract:

    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.

  • Neurosteroid regulation of oxytocin and Vasopressin Release from the rat supraoptic nucleus.
    The Journal of physiology, 2003
    Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, Govindan Dayanithi
    Abstract:

    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.

  • Intrahypothalamic Vasopressin Release. An inhibitor of systemic Vasopressin secretion
    Advances in Experimental Medicine and Biology, 1998
    Co-Authors: Mike Ludwig, Gareth Leng
    Abstract:

    Vasopressin and oxytocin are Released into the extracellular space of the supraoptic (SON) and paraventricular nuclei (PVN). The dendrites of these neurones contain a high density of neurosecretory granules, and exocytotic profiles have been visualised by electron microscopy. Release within the SON has been measured using microperfusion techniques; Release is tetrodotoxin-independent, calcium-dependent, and is activated by a range of physiological stimuli, including suckling, dehydration, haemorrhage and stress. Release of Vasopressin into the SON is regulated by a number of forebrain and brainstem areas. Dendritic Release does not necessarily parallel neurohypophyseal Release, and may occur semi-independently of spike activity in the soma and axons. The physiological consequences of dendritic Vasopressin Release are not clear, Vasopressin and oxytocin appear to induce further Vasopressin and oxytocin Release from the dendrites. In contrast, by combining retrodialysis and electrophysiology we have shown that, unlike oxytocin which excites oxytocin neurones, Vasopressin inhibits the electrical activity of Vasopressin neurones, and hence suppresses Vasopressin Release from the pituitary. Thus, Vasopressin Released from dendrites may act on Vasopressin neurones to regulate their phasic activity by an auto-inhibitory action within the SON. Since dendritic Vasopressin Release is increased and prolonged after various stimuli, this mechanism may act to restrain excitation of Vasopressin neurones (and hence Vasopressin secretion from the neurohypophysis) during continuing stimulation.

Leonard Share - One of the best experts on this subject based on the ideXlab platform.

  • Evidence that nitric oxide can act centrally to stimulate Vasopressin Release.
    Neuroendocrinology, 1993
    Co-Authors: Masahiro Ota, Joan T. Crofton, Gregory T. Festavan, Leonard Share
    Abstract:

    Nitric oxide (NO) is the endothelium-derived relaxing factor, which causes relaxation of vascular smooth muscle. NO synthetase, the enzyme for the synthesis of NO from its precursor L-arginine, is also widely distributed in neurons in the brain, and it has been suggested that NO may serve as an important neuromodulator. Because NO synthetase is present in the hypothalamus in relatively high concentration, we have determined whether NO can affect the Release of Vasopressin in conscious, chronically prepared rats. The intracerebroventricular (i.c.v.) injection of S-nitroso-N-acetylpenicillamine (12.5 and 25 micrograms; SNAP), that spontaneously breaks down to form NO, caused transient dose-related increases in the plasma Vasopressin concentration of 1 and 2 microU/ml (p < 0.01), respectively. In control experiments in which N-acetylpenicillamine (25 micrograms), the precursor for the preparation of SNAP, was injected i.c.v. there was a small, 0.4 microU/ml, increase (p < 0.01) in the plasma Vasopressin level. The i.c.v. injection of L-arginine (0.5 and 1 mg), also the precursor for the biosynthesis of NO, resulted in dose-dependent increases in the plasma Vasopressin concentration similar in magnitude to those caused by SNAP. When D-arginine (1 mg), which cannot serve as a substrate for NO synthetase, was injected i.c.v., there was only a slight delayed increase in the plasma Vasopressin concentration. Thus, NO can act centrally to stimulate Vasopressin Release and may serve as a neuromodulator in the control of Vasopressin Release.

  • Effect on Vasopressin Release of microinjection of cholinergic agonists into the rat supraoptic nucleus.
    Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York N.Y.), 1992
    Co-Authors: Masahiro Ota, Joan T. Crofton, K. Toba, Leonard Share
    Abstract:

    It is likely that central cholinergic pathways to the paraventricular and supraoptic nuclei participate in the control of Vasopressin Release. We have shown previously that this is due, in part, to activation of muscarinic, but not nicotinic, receptors in the paraventricular nucleus. There is, however, reason to believe that this cholinergic effect in the supraoptic nucleus may be the result of activation of nicotinic receptors. To test this possibility, we have studied in conscious unrestrained rats the effect of microinjection of muscarinic and nicotinic agonists into the supraoptic nucleus on Vasopressin Release, mean arterial blood pressure, and heart rate. Under ether anesthesia, a stainless steel guide cannula was placed in the supraoptic nucleus 5-7 days before the experiment, and femoral, arterial, and venous catheters were implanted 1 day before the experiment. Microinjection of nicotine into the supraoptic nucleus at doses of 1 and 10 micrograms resulted in transient increases in the plasma Vasopressin concentration that were 7-fold and 11-fold greater, respectively, than control values at 3 min. There were also small transient increases in mean arterial blood pressure, but heart rate was unchanged. The microinjection of 2 and 20 ng of oxotremorine, a muscarinic agonist, into the supraoptic nucleus had no effect on the plasma Vasopressin concentration, mean arterial blood pressure, or heart rate. These doses of oxotremorine were previously shown to have potent stimulatory effects on Vasopressin Release when microinjected into the paraventricular nucleus. These findings suggest that the central cholinergic stimulation of Vasopressin Release is due, in part, to activation of muscarinic receptors in the paraventricular nucleus and nicotinic receptors in the supraoptic nucleus.

  • Interactions between brain acetylcholine and prostaglandins in control of Vasopressin Release
    American Journal of Physiology-Regulatory Integrative and Comparative Physiology, 1991
    Co-Authors: M. Inoue, Joan T. Crofton, Leonard Share
    Abstract:

    We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of Vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma Vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma Vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak Vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of Vasopressin Release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of Vasopressin Release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

  • Reversible Changes in Osmoregulation of Vasopressin Release Due to Impaired Water Excretion
    American journal of kidney diseases : the official journal of the National Kidney Foundation, 1991
    Co-Authors: Barry M. Wall, Joan T. Crofton, Leonard Share, Hugh H. Williams, Daniel N. Presley, C. Robert Cooke
    Abstract:

    Studies of renal water handling and the effects of altered hydration and posture on the osmoregulation of Vasopressin Release were performed on a chronically hyponatremic patient with complete cervical spinal cord transection at the C-5 level. Acute oral water loading studies showed marked reduction in free water clearance and urine diluting ability, despite appropriate suppression of plasma Vasopressin concentrations. Orthostatic reductions in arterial blood pressure during head-up tilting and following the assumption of sitting posture were also demonstrable, and may have contributed to, but could not fully account for, the defect in renal water excretion, which persisted in supine posture. Hypertonic sodium chloride infusion studies performed before fluid restriction showed that low preinfusion plasma osmolality was associated with a reduced osmotic threshold for Vasopressin Release, which was subsequently corrected by a period of fluid restriction that restored the patient's plasma osmolality to a normal level. This shift in osmotic threshold can be inferred from both linear regression and log-linear regression analysis of the data. These studies show that marked impairment of renal water excretion coupled with unrestricted water intake can result in altered osmoregulation of Vasopressin Release in association with persistent plasma hypo-osmolality, which can be corrected by fluid restriction.

Helene Widmer - One of the best experts on this subject based on the ideXlab platform.

  • neurosteroid regulation of oxytocin and Vasopressin Release from the rat supraoptic nucleus
    The Journal of Physiology, 2003
    Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, Govindan Dayanithi
    Abstract:

    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.

  • Neurosteroid regulation of oxytocin and Vasopressin Release from the rat supraoptic nucleus.
    The Journal of physiology, 2003
    Co-Authors: Helene Widmer, Frederic Bancel, Gareth Leng, Mike Ludwig, Govindan Dayanithi
    Abstract:

    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.