Supraoptic Nucleus (supraoptic + nucleus)

Distribution by Scientific Domains

Terms modified by Supraoptic Nucleus

  • supraoptic nucleus neurone

  • Selected Abstracts


    The Adaptive Brain: Glenn Hatton and the Supraoptic Nucleus

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2010
    G. Leng
    In December 2009, Glenn Hatton died, and neuroendocrinology lost a pioneer who had done much to forge our present understanding of the hypothalamus and whose productivity had not faded with the passing years. Glenn, an expert in both functional morphology and electrophysiology, was driven by a will to understand the significance of his observations in the context of the living, behaving organism. He also had the wit to generate bold and challenging hypotheses, the wherewithal to expose them to critical and elegant experimental testing, and a way with words that gave his papers and lectures clarity and eloquence. The hypothalamo-neurohypophysial system offered a host of opportunities for understanding how physiological functions are fulfilled by the electrical activity of neurones, how neuronal behaviour changes with changing physiological states, and how morphological changes contribute to the physiological response. In the vision that Glenn developed over 35 years, the neuroendocrine brain is as dynamic in structure as it is adaptable in function. Its adaptability is reflected not only by mere synaptic plasticity, but also by changes in neuronal morphology and in the morphology of the glial cells. Astrocytes, in Glenn's view, were intimate partners of the neurones, partners with an essential role in adaptation to changing physiological demands. [source]


    Electrophysiological Identification of the Functional Presynaptic Nerve Terminals on an Isolated Single Vasopressin Neurone of the Rat Supraoptic Nucleus

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2010
    T. Ohbuchi
    Release of arginine vasopressin (AVP) and oxytocin from magnocellular neurosecretory cells (MNCs) of the supraoptic nucleus (SON) is under the control of glutamate-dependent excitation and GABA-dependent inhibition. The possible role of the synaptic terminals attached to SON neurones has been investigated using whole-cell patch-clamp recording in in vitro rat brain slice preparations. Recent evidence has provided new insights into the repercussions of glial environment modifications on the physiology of MNCs at the synaptic level in the SON. In the present study, excitatory glutamatergic and inhibitory GABAergic synaptic inputs were recorded from an isolated single SON neurone cultured for 12 h, using the whole-cell patch clamp technique. Neurones expressed an AVP-enhanced green fluorescent protein (eGFP) fusion gene in MNCs. In addition, native synaptic terminals attached to a dissociated AVP-eGFP neurone were visualised with synaptic vesicle markers. These results suggest that the function of presynaptic nerve terminals may be evaluated directly in a single AVP-eGFP neurone. These preparations would be helpful in future studies aiming to electrophysiologically distinguish between the functions of synaptic terminals and glial modifications in the SON neurones. [source]


    Glial Limitans Elasticity Subjacent to the Supraoptic Nucleus

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2004
    A. K. Salm
    Abstract Two previous studies from our laboratory have indicated that the ventral glial limitans subjacent to the hypothalamic supraoptic nucleus (SON-VGL) undergoes a reversible thinning upon chronic activation of the magnocellular neuroendocrine cells (MNCs) of the supraoptic nucleus (SON). Numerous other studies have shown that MNC somata hypertrophy with activation. One aim of the current study was to understand better how SON-VGL thinning occurs. A second aim was to quantify overall changes of the MNC somata region due to cellular hypertrophy to compare relative changes in dimensions. Here, we undertook a light microscopic stereological investigation of the SON and the subjacent SON-VGL of Nissl stained material under basal and activated conditions. Astrocyte numbers in the underlying SON-VGL remained stable across hydration state as did the overall volume of the SON-VGL and dendritic zone reference area. How these data are consistent with our earlier observations of SON-VGL thinning was resolved by the finding of a highly significant, 30% increase in the mediolateral dimension of the SON-VGL in dehydrated rats. These observations fit well with previous work from our laboratory that demonstrates a reorientation of SON-VGL astrocytes, from vertical to horizontal, which occurs in the activated SON-VGL. We found a significant, approximately 54%, increase in the overall volume of the MNC region of the SON. No significant rostrocaudal lengthening of the SON was detected, although a trend was evident. All the observed changes reversed with rehydration. These data indicate that elasticity of the SON-VGL acts to accommodate the volume expansion of the MNCs and enables the SON-VGL to continue as an interface between the underlying cerebrospinal fluid in the subarachnoid space and the expanded SON above. [source]


    Plasma Vasopressin Concentrations and Fos Protein Expression in the Supraoptic Nucleus Following Osmotic Stimulation or Hypovolaemia in the Ovariectomized Rat: Effect of Oestradiol Replacement

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2004
    D. E. Hartley
    Abstract The set points for vasopressin release in response to increasing plasma osmolality and hypovolaemia alter with reproductive status. Here, we studied stimulated vasopressin release following ovariectomy and oestrogen replacement, neuronal activity being measured in terms of immediate early gene expression. Observations were carried out on three groups of female Sprague-Dawley rats. The first group were ovariectomized. The second group were given a subcutaneous oestrogen implant (20 g/ml oestradiol-17,) at the time of ovariectomy. The final group were left intact and observations performed at oestrus. Two weeks after ovariectomy, vascular cannulae were implanted under anaesthesia and at least 48 h allowed for recovery before hormone release was stimulated by infusion of 1.5 m NaCl for 90 min, or hypovolaemia induced by the removal of 10 mg/kg body weight taken in 1-ml aliquots. Blood pressure was monitored, and blood samples were taken for determination of packed cell volume and plasma vasopressin and osmolality. After a minimum of 48 h, the challenge was repeated, the rats anaesthetized, and perfused with 4% paraformaldehyde. Brain sections were processed for immunocytochemical detection of Fos protein. Vasopressin release in response to both stimuli was reduced in ovariectomized compared to intact rats and the response could be substantially restored by oestradiol replacement. The number of Fos positive cells in the supraoptic nucleus of oestrogen-replaced rats was significantly higher than in the ovariectomized group and not statistically different from the intact group. [source]


    Intermittent Footshock Facilitates Dendritic Vasopressin Release but Suppresses Vasopressin Synthesis within the Rat Supraoptic Nucleus

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 7 2003
    T. Onaka
    Abstract 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. [source]


    ,-Endorphin Cells in the Arcuate Nucleus: Projections to the Supraoptic Nucleus and Changes in Expression During Pregnancy and Parturition

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 10 2002
    A. J. Douglas
    Abstract 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 ,-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 ,-endorphin fluorescent microbeads retrogradely transported from the supraoptic nucleus, and double-labelled neurones (,-endorphin plus microbeads), showing that ,-endorphin neurones throughout the arcuate nucleus project to the supraoptic nucleus. There was an increase in the number of ,-endorphin-immunoreactive cells in the arcuate nucleus and an increase in the density of ,-endorphin fibres within the supraoptic nucleus and peri-supraoptic region in late pregnancy and parturition, suggesting enhanced expression of ,-endorphin and increased ,-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 ,-endorphin neurones in both proestrus and parturient rats, but the number of positive cells did not increase during parturition, suggesting lack of activation of ,-endorphin neurones at birth. Thus, ,-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. [source]


    Vasopressin Regulation of Noradrenaline Release Within the Supraoptic Nucleus

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2000
    M. Ludwig
    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<0.03). This increase was completely blocked by administration of a nonpeptide vasopressin V1a receptor antagonist via the microdialysis probe. These data suggest that dendritically released vasopressin facilitates noradrenaline release into the hypothalamic nucleus. [source]


    Vasopressin Synthesis by the Magnocellular Neurons is Different in the Supraoptic Nucleus and in the Paraventricular Nucleus in Human and Experimental Septic Shock

    BRAIN PATHOLOGY, Issue 3 2010
    Romain Sonneville MD
    Abstract Impaired arginine vasopressin (AVP) synthesis and release by the neurohypophyseal system, which includes the neurohypophysis and magnocellular neurons of the paraventricular and supraoptic nuclei, have been postulated in septic shock, but changes in this system have never been assessed in human septic shock, and only partially experimentally. We investigated AVP synthesis and release by the neurohypophyseal system in 9 patients who died from septic shock and 10 controls, and in 20 rats with fecal peritonitis-induced sepsis and 8 sham-operation controls. Ten rats died spontaneously from septic shock, and the others were sacrificed. In patients with septic shock, as in rats that died spontaneously following sepsis induction, AVP immunohistochemical expression was decreased in the neurohypophysis and supraoptic magnocellular neurons, whereas it was increased in the paraventricular magnocellular neurons. No significant change was observed in AVP messenger RiboNucleic Acid (mRNA) expression assessed by in situ hybridization in either paraventricular or supraoptic magnocellular cells. This study shows that both in human and experimental septic shock, AVP posttranscriptional synthesis and transport are differently modified in the magnocellular neurons of the supraoptic and paraventricular nuclei. This may account for the inappropriate AVP release in septic shock and suggests that distinct pathogenic mechanisms operate in these nuclei. [source]


    Impact of Sim1 gene dosage on the development of the paraventricular and supraoptic nuclei of the hypothalamus

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2009
    Sabine Michalle Duplan
    Abstract The bHLH-PAS transcription SIM1 is required for the development of all neurons of the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus. Mice with a loss of Sim1 die within a few days of birth, presumably because of the lack of a PVN and SON. In contrast, mice with a decrease of Sim1 survive, are hyperphagic and become obese. The mechanism by which Sim1 controls food intake remains unclear. Here we show that the development of specific PVN and SON cell types is sensitive to Sim1 gene dosage. Sim1 haploinsufficiency reduces the number of vasopressin (AVP)- and oxytocin-producing cells in the PVN by about 50 and 80%, respectively, but does not affect the development of Crh, Trh and Ss neurons. A decrease of AVP-producing cells increases the sensitivity of Sim1 heterozygous mice to chronic dehydration. Moreover, retrograde labelling showed a 70% reduction of PVN neurons projecting to the dorsal vagal complex, raising the possibility that a decrease of these axons contributes to the hyperphagia of Sim1+/, mice. Sim1 haploinsufficiency is thus associated with a decrease of several PVN/SON cell types, which has the potential of affecting distinct homeostatic processes. [source]


    Behavioural and neurobiological effects of colostrum ingestion in the newborn lamb associated with filial bonding

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2009
    David Val-Laillet
    Abstract In sheep, the onset of filial bonding relies on early intake of colostrum. The aim of our work was to describe in the newborn lamb housed with its mother the immediate post-ingestive effects of colostrum intake, in terms of behaviour and brain activity. In Experiment 1, lambs received five nasogastric infusions of colostrum, or saline, or sham intubations during the first 6 h after birth. Mother,young interactions were recorded before and after the first, third and fifth infusions. The activity of the dam and of the young, which diminished over time in all groups, was temporarily increased in both partners just after each intubation procedure. The number of high-pitched bleats was significantly lower in lambs that received colostrum than in the sham group, suggesting soothing or satiating properties of colostrum. In Experiment 2, newborn lambs received a single nasogastric infusion of colostrum or saline 4.5 h after birth, or were sham intubated. Neuronal activation was investigated 1.5 h later for maximum c-Fos activity. Infusion of colostrum and saline induced different patterns of c-Fos-like immunoreactivity in the paraventricular and supraoptic nuclei of the hypothalamus as compared with the sham group. A specific oxytocinergic/vasopressinergic (OT/VSP) cell population in the paraventricular nucleus was activated following colostrum and saline infusion, but not sham intubation. Only colostrum induced the activation of the cortical amygdala and insular cortex, two structures involved in learning, associative processes, reward and emotion. We hypothesize that filial bonding may be triggered through colostrum-rewarded learning/calming processes and that the OT/VSP system may play a role. [source]


    Human brain aminopeptidase A: biochemical properties and distribution in brain nuclei

    JOURNAL OF NEUROCHEMISTRY, Issue 1 2008
    Nadia De Mota
    Abstract Aminopeptidase A (APA) generated brain angiotensin III, one of the main effector peptides of the brain renin angiotensin system, exerting a tonic stimulatory effect on the control of blood pressure in hypertensive rats. The distribution of APA in human brain has not been yet studied. We first biochemically characterized human brain APA (apparent molecular mass of 165 and 130 kDa) and we showed that the human enzyme exhibited similar enzymatic characteristics to recombinant mouse APA. Both enzymes had similar sensitivity to Ca2+. Kinetic studies showed that the Km (190 ,mol/L) of the human enzyme for the synthetic substrate- l -glutamyl-,-naphthylamide was close from that of the mouse enzyme (256 ,mol/L). Moreover, various classes of inhibitors including the specific and selective APA inhibitor, (S)-3-amino-4-mercapto-butyl sulfonic acid, had similar inhibitory potencies toward both enzymes. Using (S)-3-amino-4-mercapto-butyl sulfonic acid, we then specifically measured the activity of APA in 40 microdissected areas of the adult human brain. Significant heterogeneity was found in the activity of APA in the various analyzed regions. The highest activity was measured in the choroids plexus and the pineal gland. High activity was also detected in the dorsomedial medulla oblongata, in the septum, the prefrontal cortex, the olfactory bulb, the nucleus accumbens, and the hypothalamus, especially in the paraventricular and supraoptic nuclei. Immunostaining of human brain sections at the level of the medulla oblongata strengthened these data, showing for the first time a high density of immunoreactive neuronal cell bodies and fibers in the motor hypoglossal nucleus, the dorsal motor nucleus of the vagus, the nucleus of the solitary tract, the Roller nucleus, the ambiguus nucleus, the inferior olivary complex, and in the external cuneate nucleus. APA immunoreactivity was also visualized in vessels and capillaries in the dorsal motor nucleus of the vagus and the inferior olivary complex. The presence of APA in several human brain nuclei sensitive to angiotensins and involved in blood pressure regulation suggests that APA in humans is an integral component of the brain renin angiotensin system and strengthens the idea that APA inhibitors could be clinically tested as an additional therapy for the treatment of certain forms of hypertension. [source]


    Metabotropic Glutamate Receptors: Gatekeepers of Homeostasis

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 7 2010
    J. B. Kuzmiski
    The capacity to appropriately respond to physiological challenges or perturbations in homeostasis is a requisite for survival. It is becoming increasingly clear that long-lasting alterations in synaptic efficacy are a fundamental mechanism for modifying neuroendocrine and autonomic output. We review recent advances in our understanding of plasticity at glutamate synapses onto magnocellular neurones (MNCs) in the paraventricular and supraoptic nuclei of the hypothalamus, with a focus on the contributions of metabotropic glutamate receptors (mGluRs) to long-lasting modifications in synaptic efficacy. Special attention is paid to the role of presynaptic mGluRs as gatekeepers for metaplasticity and regulation of body fluid homeostasis. The work highlighted here provides insight into the synaptic mechanisms that couple MNC activity to physiological states. [source]


    Morphological Substrate of the Catecholaminergic Input of the Vasopressin Neuronal System in Humans

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 12 2006
    B. Duds
    It has been postulated that the stress response is associated with water balance via regulating vasopressin release. Nausea, surgical stress and insulin-induced hypoglycaemia were shown to stimulate vasopressin secretion in humans. Increased vasopressin release in turn induces water resorption through the kidneys. Although the mechanism of the stress-mediated vasopressin release is not entirely understood, it is generally accepted that catecholamines play a crucial role in influencing water balance by modulating the secretion of vasopressin. However, the morphological substrate of this modulation has not yet been established. The present study utilised double-label immunohistochemistry to reveal putative juxtapositions between tyrosine hydroxylase (TH)-immunoreactive (IR) catecholaminergic system and the vasopressin systems in the human hypothalamus. In the paraventricular and supraoptic nuclei, numerous vasopressin-IR neurones received TH-IR axon varicosities. Analysis of these juxtapositions with high magnification combined with oil immersion did not reveal any gaps between the contacted elements. In conclusion, the intimate associations between the TH-IR and vasopressin-IR elements may be functional synapses and may represent the morphological basis of vasopressin release modulated by stressors. Because certain vasopressin-IR perikarya receive no detectable TH innervations, it is possible that additional mechanisms may participate in the stress-influenced vasopressin release. [source]


    Vasopressin Synthesis by the Magnocellular Neurons is Different in the Supraoptic Nucleus and in the Paraventricular Nucleus in Human and Experimental Septic Shock

    BRAIN PATHOLOGY, Issue 3 2010
    Romain Sonneville MD
    Abstract Impaired arginine vasopressin (AVP) synthesis and release by the neurohypophyseal system, which includes the neurohypophysis and magnocellular neurons of the paraventricular and supraoptic nuclei, have been postulated in septic shock, but changes in this system have never been assessed in human septic shock, and only partially experimentally. We investigated AVP synthesis and release by the neurohypophyseal system in 9 patients who died from septic shock and 10 controls, and in 20 rats with fecal peritonitis-induced sepsis and 8 sham-operation controls. Ten rats died spontaneously from septic shock, and the others were sacrificed. In patients with septic shock, as in rats that died spontaneously following sepsis induction, AVP immunohistochemical expression was decreased in the neurohypophysis and supraoptic magnocellular neurons, whereas it was increased in the paraventricular magnocellular neurons. No significant change was observed in AVP messenger RiboNucleic Acid (mRNA) expression assessed by in situ hybridization in either paraventricular or supraoptic magnocellular cells. This study shows that both in human and experimental septic shock, AVP posttranscriptional synthesis and transport are differently modified in the magnocellular neurons of the supraoptic and paraventricular nuclei. This may account for the inappropriate AVP release in septic shock and suggests that distinct pathogenic mechanisms operate in these nuclei. [source]


    Impact of Sim1 gene dosage on the development of the paraventricular and supraoptic nuclei of the hypothalamus

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2009
    Sabine Michalle Duplan
    Abstract The bHLH-PAS transcription SIM1 is required for the development of all neurons of the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus. Mice with a loss of Sim1 die within a few days of birth, presumably because of the lack of a PVN and SON. In contrast, mice with a decrease of Sim1 survive, are hyperphagic and become obese. The mechanism by which Sim1 controls food intake remains unclear. Here we show that the development of specific PVN and SON cell types is sensitive to Sim1 gene dosage. Sim1 haploinsufficiency reduces the number of vasopressin (AVP)- and oxytocin-producing cells in the PVN by about 50 and 80%, respectively, but does not affect the development of Crh, Trh and Ss neurons. A decrease of AVP-producing cells increases the sensitivity of Sim1 heterozygous mice to chronic dehydration. Moreover, retrograde labelling showed a 70% reduction of PVN neurons projecting to the dorsal vagal complex, raising the possibility that a decrease of these axons contributes to the hyperphagia of Sim1+/, mice. Sim1 haploinsufficiency is thus associated with a decrease of several PVN/SON cell types, which has the potential of affecting distinct homeostatic processes. [source]


    GABA selectively controls the secretory activity of oxytocin neurons in the rat supraoptic nucleus

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2004
    Mario Engelmann
    Abstract Recently we reported that a single social defeat experience triggers the release of oxytocin (OXT) from somata and dendrites, but not axon terminals, of neurons of the hypothalamic,neurohypophysial system. To further investigate the regulatory mechanisms underlying this dissociated release, we exposed male Wistar rats to a 30-min social defeat and monitored release of the inhibitory amino acids gamma amino butyric acid (GABA) and taurine within the hypothalamic supraoptic nucleus (SON) using microdialysis. Social defeat caused a significant increase in the release of both GABA and taurine within the SON (up to 480%; P < 0.01 vs. prestress release). To reveal the physiological significance of centrally released GABA, the specific GABAA -receptor antagonist bicuculline (0.02 mm) was administered into the SON via retrodialysis. This approach caused a significant increase in the release of OXT both within the SON and into the blood under basal conditions and during stress (up to 300 and 200%, respectively; P < 0.05 vs. basal values), without affecting plasma vasopressin. Electrophysiological studies confirmed the selective action of bicuculline on the firing activity of OXT neurons in the SON. Taken together, our data demonstrate that GABA is released within the SON during emotional stress to act as a selective inhibitor of both central and peripheral OXT secretion. [source]


    Induction of rapid, activity-dependent neuronal,glial remodelling in the adult rat hypothalamus in vitro

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2003
    Sarah L. Langle
    Abstract The hypothalamic oxytocinergic system offers a remarkable model of morphological plasticity in the adult because its neurons and astrocytes undergo mutual remodelling in relation to differing physiological conditions. Among various factors involved in such plasticity, oxytocin (OT) itself appears of primary importance as its central administration resulted in morphological changes similar to those brought on by physiological stimuli. In the present study, we applied OT on acute hypothalamic slices from adult rats that included the supraoptic nucleus. Using ultrastructural morphometric analyses, we found that it induced a significant reduction of astrocytic coverage of OT neurons, leaving their surfaces directly juxtaposed, to an extent similar to that detected in vivo under conditions like lactation. These neuronal,glial changes were rapid and reversible, occurring within a few hours, and specifically mediated via OT receptors. They were potentiated by oestrogen and depended on calcium mobilization and de novo protein synthesis. Moreover, they depended on concurrent neuronal activation brought on by hyperosmotic stimulation or blockade of inhibitory GABAergic neurotransmission; they were inhibited by blockade of glutamatergic receptors. Taken together, our observations show that intrahypothalamic release of OT affects not only neuronal activation of the OT system but its morphological plasticity as well. Moreover, the activity dependence of the OT-induced changes strongly suggests that astrocytes can sense the level of activity of adjacent neurons and/or afferent input and this can subsequently act as a signal to bring on the neuronal and glial conformational changes. [source]


    The effects of nitric oxide on magnocellular neurons could involve multiple indirect cyclic GMP-dependent pathways

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2003
    C. M. Vacher
    Abstract Nitric oxide (NO) is known to regulate the release of arginine-vasopressin (AVP) and oxytocin (OT) by the paraventricular nucleus (PVN) and the supraoptic nucleus (SON). The aim of the current study was to identify in these nuclei the NO-producing neurons and the NO-receptive cells in mice. The determination of NO-synthesizing neurons was performed by double immunohistochemistry for the neuronal form of NO synthase (NOS), and AVP or OT. Besides, we visualized the NO-receptive cells by detecting cyclic GMP (cGMP), the major second messenger for NO, by immunohistochemistry on hypothalamus slices. Neuronal NOS was exclusively colocalized with OT in the PVN and the SON, suggesting that NO is mainly synthesized by oxytocinergic neurons in mice. By contrast, cGMP was not observed in magnocellular neurons, but in GABA-, tyrosine hydroxylase- and glutamate-positive fibers, as well as in GFAP-stained cells. The cGMP-immunostaining was abolished by incubating brain slices with a NOS inhibitor (L-NAME). Consequently, we provide the first evidence that NO could regulate the release of AVP and OT indirectly by modulating the activity of the main afferents to magnocellular neurons rather than by acting directly on magnocellular neurons. Moreover, both the NADPH-diaphorase activity and the mean intensity of cGMP-immunofluorescence were increased in monoamine oxidase A knock-out mice (Tg8) compared to control mice (C3H) in both nuclei. This suggests that monoamines could enhance the production of NO, contributing by this way to the fine regulation of AVP and OT release and synthesis. [source]


    Taurine selectively modulates the secretory activity of vasopressin neurons in conscious rats

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2001
    Mario Engelmann
    Abstract Previous experiments have shown that a 10-min forced swimming session triggers the release of vasopressin from somata and dendrites, but not axon terminals, of neurons of the hypothalamic,neurohypophysial system. To further investigate regulatory mechanisms underlying this dissociated release, we forced male Wistar rats to swim in warm (20 C) water and monitored release of the potentially inhibitory amino acids gamma amino butyric acid (GABA) and taurine into the hypothalamic supraoptic nucleus using microdialysis. Forced swimming caused a significant increase in the release of taurine (up to 350%; P < 0.05 vs. prestress release), but not GABA. To reveal the physiological significance of centrally released taurine, the specific taurine antagonist 6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide was administered into the supraoptic nucleus via retrodialysis. Administration of this antagonist caused a significant increase in the release of vasopressin within the supraoptic nucleus and into the blood both under basal conditions and during stress (up to 800%; P < 0.05 vs. basal values), without affecting hypothalamic or plasma oxytocin. Local administration of the GABAA receptor antagonist bicuculline, in contrast, failed to influence vasopressin secretion at either time point. In a separate series of in vivo electrophysiological experiments, administration of the same dosage of the taurine antagonist into the supraoptic nucleus via microdialysis resulted in an increased electrical activity of identified vasopressinergic, but not oxytocinergic, neurons. Taken together our data demonstrate that taurine is released within the supraoptic nucleus during physical/emotional stress. Furthermore, at the level of the supraoptic nucleus, taurine inhibits not only the electrical activity of vasopressin neurons but also acts as an inhibitor of both central and peripheral vasopressin secretion during different physiological states. [source]


    The role of steroid hormones in the regulation of vasopressin and oxytocin release and mRNA expression in hypothalamo neurohypophysial explants from the rat

    EXPERIMENTAL PHYSIOLOGY, Issue 2000
    Celia D. Sladek
    Vasopressin and oxytocin release from the neural lobe, and the vasopressin and oxytocin mRNA contents of the supraoptic and paraventricular nuclei are increased by hypertonicity of the extracellular fluid. The factors regulating these parameters can be conveniently studied in perifused explants of the hypothalamo-neurohypophysial system that include the supraoptic nucleus (but not the paraventricular nucleus) with its axonal projections to the neural lobe. Vasopressin and oxytocin release and the mRNA content of these explants respond appropriately to increases in the osmolality of the perifusate. This requires synaptic input from the region of the organum vasculosum of the lamina terminalis. Glutamate is a likely candidate for transmitting osmotic information from the organum vasculosum of the lamina terminalis to the magnocellular neurones, because agonists for excitatory amino acid receptors stimulate vasopressin and oxytocin release, and because increased vasopressin release and mRNA content induced in hypothalamo-neurohypophysial explants by a ramp increase in osmolality are blocked by antagonists of both NMDA (N -methyl-D-aspartate) and non-NMDA glutamate receptors. Osmotically stimulated vasopressin release is also blocked by testosterone, dihydrotestosterone, oestradiol and corticosterone. Both oestrogen and dihydrotestosterone block NMDA stimulation of vasopressin release, and in preliminary studies oestradiol blocked AMPA stimulation of vasopressin release. Thus, steroid inhibition of osmotically stimulated vasopressin secretion may reflect inhibition of mechanisms mediated by excitatory amino acids. Recent studies have demonstrated numerous mechanisms by which steroid hormones may impact upon neuronal function. Therefore, additional work is warranted to understand these effects of the steroid hormones on vasopressin and oxytocin secretion and to elucidate the potential contribution of these mechanisms to regulation of hormone release in vivo. [source]


    Electrophysiological Identification of the Functional Presynaptic Nerve Terminals on an Isolated Single Vasopressin Neurone of the Rat Supraoptic Nucleus

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2010
    T. Ohbuchi
    Release of arginine vasopressin (AVP) and oxytocin from magnocellular neurosecretory cells (MNCs) of the supraoptic nucleus (SON) is under the control of glutamate-dependent excitation and GABA-dependent inhibition. The possible role of the synaptic terminals attached to SON neurones has been investigated using whole-cell patch-clamp recording in in vitro rat brain slice preparations. Recent evidence has provided new insights into the repercussions of glial environment modifications on the physiology of MNCs at the synaptic level in the SON. In the present study, excitatory glutamatergic and inhibitory GABAergic synaptic inputs were recorded from an isolated single SON neurone cultured for 12 h, using the whole-cell patch clamp technique. Neurones expressed an AVP-enhanced green fluorescent protein (eGFP) fusion gene in MNCs. In addition, native synaptic terminals attached to a dissociated AVP-eGFP neurone were visualised with synaptic vesicle markers. These results suggest that the function of presynaptic nerve terminals may be evaluated directly in a single AVP-eGFP neurone. These preparations would be helpful in future studies aiming to electrophysiologically distinguish between the functions of synaptic terminals and glial modifications in the SON neurones. [source]


    Interleukin-1, Release in the Supraoptic Nucleus Area During Osmotic Stimulation Requires Neural Function

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 11 2008
    J. Y. Summy-Long
    Interleukin (IL)-1, is present throughout the magnocellular neuroendocrine system and co-depletes with oxytocin and vasopressin from the neural lobe during salt-loading. To examine whether IL-1, is released from the dendrites/soma of magnocellular neurones during osmotic stimulation, microdialysis adjacent to the supraoptic nucleus (SON) in conscious rats was combined with immunocapillary electrophoresis and laser-induced fluorescence detection to quantify cytokine in 5-min dialysates collected before (0,180 min; basal), and after (180,240 min), hypertonic saline injected s.c. (1.5 m NaCl). Osmotic release of IL-1, was compared after inhibiting local voltage-gated channels for Na+ (tetrodotoxin) and Ca2+ (cadmium and nickel) or by reducing intracellular Ca2+ stores (thapsigargin). Immunohistochemistry combined with microdialysis was used to localise cytokine sources (IL-1,+) and microglia (OX-42+). Under conditions of microdialysis, the basal release of IL-1,+ in the SON area was measurable and stable (pg/ml; mean SEM) from 0,60 min (2.2 0.06), 60,120 min (2.32 0.05) and 120,180 min (2.33 0.06), likely originating locally from activated microglia (OX42+; IL-1,+; ameboid, hypertrophied) and magnocellular neurones expressing IL-1,. In response to osmotic stimulation, IL-1, increased progressively in dialysates of the SON area by a mechanism dependent on intracellular Ca2+ stores sensitive to thapsigargin and, similar to dendritic secretion of oxytocin and vasopressin, required local voltage-gated Na+ and Ca2+ channels for activation by osmoregulatory pathways from the forebrain. During osmotic stimulation, neurally dependent release of IL-1, in the SON area likely upregulates osmosensitive cation currents on magnocellular neurones (observed in vitro by others), to facilitate dendritic release of neurohypophysial hormones. [source]


    Glial Limitans Elasticity Subjacent to the Supraoptic Nucleus

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2004
    A. K. Salm
    Abstract Two previous studies from our laboratory have indicated that the ventral glial limitans subjacent to the hypothalamic supraoptic nucleus (SON-VGL) undergoes a reversible thinning upon chronic activation of the magnocellular neuroendocrine cells (MNCs) of the supraoptic nucleus (SON). Numerous other studies have shown that MNC somata hypertrophy with activation. One aim of the current study was to understand better how SON-VGL thinning occurs. A second aim was to quantify overall changes of the MNC somata region due to cellular hypertrophy to compare relative changes in dimensions. Here, we undertook a light microscopic stereological investigation of the SON and the subjacent SON-VGL of Nissl stained material under basal and activated conditions. Astrocyte numbers in the underlying SON-VGL remained stable across hydration state as did the overall volume of the SON-VGL and dendritic zone reference area. How these data are consistent with our earlier observations of SON-VGL thinning was resolved by the finding of a highly significant, 30% increase in the mediolateral dimension of the SON-VGL in dehydrated rats. These observations fit well with previous work from our laboratory that demonstrates a reorientation of SON-VGL astrocytes, from vertical to horizontal, which occurs in the activated SON-VGL. We found a significant, approximately 54%, increase in the overall volume of the MNC region of the SON. No significant rostrocaudal lengthening of the SON was detected, although a trend was evident. All the observed changes reversed with rehydration. These data indicate that elasticity of the SON-VGL acts to accommodate the volume expansion of the MNCs and enables the SON-VGL to continue as an interface between the underlying cerebrospinal fluid in the subarachnoid space and the expanded SON above. [source]


    Localization of Transforming Growth Factors, TGF,1 and TGF,3, in Hypothalamic Magnocellular Neurones and the Neurohypophysis

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 7 2004
    M. Fvre-Montange
    Abstract The distribution of transforming growth factor beta (TGF,) in the rat and human hypothalamus and neurohypophysis was investigated by immunocytochemical techniques using rabbit polyclonal antisera against TGF,1 and TGF,3. Colocalization of TGF,1 or TGF,3 and arginine vasopressin (AVP) in the rat hypothalamus was studied by double immunolabelling in light microscopy, while their subcellular localization in the rat neurohypophysis was investigated by immunoelectron microscopy. TGF,1 and TGF,3 immunoreactivity was demonstrated in the cell bodies and processes of neurones in the supraoptic nucleus (SON) and paraventricular nucleus (PVN). The TGF,-immunoreactive cells were more numerous in the SON compared to the PVN. TGF,/AVP double-labelled cells were seen in both nuclei, but some neurones in the SON were labelled for TGF,1 or TGF,3, although not for AVP. In the rat and human neurohypophysis, TGF,3 immunolabelling was more diffuse and stronger than TGF,1 immunolabelling. TGF,1 expression was seen in axonal vesicles and in neurosecretory granules of the axonal endings, while TGF,3 was observed in axonal fibres. Colocalization of TGF,3 or TGF,1 and AVP was observed in some neurosecretory granules, but many were either single-labelled for TGF, or AVP or unlabelled. Our results demonstrate, for the first time, the colocalization of TGF, and neurohypophysial hormones in magnocellular neurones. We suggest that TGF, secreted by the neurohypophysis regulates the proliferation and secretion of certain anterior pituitary cells. [source]


    Ageing and the Diurnal Expression of the mRNAs for Vasopressin and for the V1a and V1b Vasopressin Receptors in the Suprachiasmatic Nucleus of Male Rats

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2004
    T. Kalamatianos
    Abstract Changes in the function of neuropeptide synthesizing cells within the suprachiasmatic nucleus (SCN), the site of the predominant circadian pacemaker, may underlie the disturbance of rhythms observed during ageing. Arginine vasopressin (AVP) is synthesized by nearly one-third of SCN neurones in the rat. This peptide has predominantly excitatory actions within the SCN mediated by V1 -type receptors; the extent to which the V1a and/or V1b receptor subtypes are involved in SCN functions remains to be determined. The present study used isotopic in situ hybridization histochemistry to examine the effects of ageing on expression of mRNAs for AVP and V1a in the SCN and for V1b in the SCN and supraoptic nucleus (SON) of male rats kept under a 12 : 12 h light/dark cycle. Analysis of film autoradiographs from young adult (2,3-month-old; n = 40) or aged (19,20-month-old; n = 40) animals, at eight time points across the light/dark cycle, revealed an equivalent pattern and amplitude for the diurnal rhythm of AVP mRNA in the SCN of the young adult and aged groups. Both groups also displayed a significant diurnal rhythm in the expression of V1a receptor mRNA; however, the amplitude of this rhythm was reduced in the aged group, due to increased levels during the light phase and early part of night. Although the expression of V1b mRNA did not display a significant diurnal rhythm within the SCN or SON, persistently elevated levels for V1b mRNA were observed in the aged group at both sites. [source]


    Plasma Vasopressin Concentrations and Fos Protein Expression in the Supraoptic Nucleus Following Osmotic Stimulation or Hypovolaemia in the Ovariectomized Rat: Effect of Oestradiol Replacement

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2004
    D. E. Hartley
    Abstract The set points for vasopressin release in response to increasing plasma osmolality and hypovolaemia alter with reproductive status. Here, we studied stimulated vasopressin release following ovariectomy and oestrogen replacement, neuronal activity being measured in terms of immediate early gene expression. Observations were carried out on three groups of female Sprague-Dawley rats. The first group were ovariectomized. The second group were given a subcutaneous oestrogen implant (20 g/ml oestradiol-17,) at the time of ovariectomy. The final group were left intact and observations performed at oestrus. Two weeks after ovariectomy, vascular cannulae were implanted under anaesthesia and at least 48 h allowed for recovery before hormone release was stimulated by infusion of 1.5 m NaCl for 90 min, or hypovolaemia induced by the removal of 10 mg/kg body weight taken in 1-ml aliquots. Blood pressure was monitored, and blood samples were taken for determination of packed cell volume and plasma vasopressin and osmolality. After a minimum of 48 h, the challenge was repeated, the rats anaesthetized, and perfused with 4% paraformaldehyde. Brain sections were processed for immunocytochemical detection of Fos protein. Vasopressin release in response to both stimuli was reduced in ovariectomized compared to intact rats and the response could be substantially restored by oestradiol replacement. The number of Fos positive cells in the supraoptic nucleus of oestrogen-replaced rats was significantly higher than in the ovariectomized group and not statistically different from the intact group. [source]


    Circulating Angiotensin II Activates Neurones in Circumventricular Organs of the Lamina Terminalis That Project to the Bed Nucleus of the Stria Terminalis

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2003
    N. Sunn
    Abstract The aim of this study was to determine, in conscious rats, whether elevated concentrations of circulating angiotensin II activate neurones in both the subfornical organ and organum vasculosum of the lamina terminalis (OVLT) that project to the bed nucleus of the stria terminalis (BNST). The strategy employed was to colocalize retrogradely transported cholera toxin B subunit (CTB) from the BNST, with elevated levels of Fos protein in response to angiotensin II. Circulating angiotensin II concentrations were increased by either intravenous infusion of angiotensin II or subcutaneous injection of isoproterenol. Neurones exhibiting Fos in response to angiotensin II were present in the subfornical organ, predominantly in its central core but with some also seen in its peripheral aspect, the dorsal and lateral margins of the OVLT, the supraoptic nucleus and the parvo- and magnocellular divisions of the paraventricular nucleus. Fos-labelling was not apparent in control rats infused with isotonic saline intravenously or injected with either CTB or CTB conjugated to gold particles (CTB-gold) only. Of the neurones in the subfornical organ that were shown by retrograde labelling to project to BNST, approximately 50% expressed Fos in response to isoproterenol. This stimulus also increased Fos in 33% of neurones in the OVLT that project to BNST. Double-labelled neurones were concentrated in the central core of the subfornical organ and lateral margins of the OVLT in response to increased circulating angiotensin II resulting from isoproterenol treatment. These data support a role for circulating angiotensin II acting either directly or indirectly on neurones in subfornical organ and OVLT that project to the BNST and provide further evidence of functional regionalization within the subfornical organ and the OVLT. The function of these pathways is yet to be determined; however, a role in body fluid homeostasis is possible. [source]


    Presynaptic Noradrenergic Regulation of Glutamate Inputs to Hypothalamic Magnocellular Neurones

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2003
    C. Boudaba
    Abstract Glutamate and norepinephrine transmitter systems play critical roles in the synaptic control of hypothalamic magnocellular neurones. We recently reported on a norepinephrine-sensitive glutamate circuit within the paraventricular nucleus (PVN) that projects to magnocellular neurones. Here, we present evidence for norepinephrine regulation of glutamate release in the PVN and supraoptic nucleus (SON) via actions on presynaptic terminals. Whole-cell synaptic currents were recorded in magnocellular neurones of the SON and PVN in an acute slice preparation. Bath application of norepinephrine (100 m) caused a robust, reversible increase in the frequency of spontaneous glutamatergic excitatory postsynaptic currents in 100% of SON neurones (246%) and in 88% of PVN magnocellular neurones (259%). The norepinephrine-induced increase in glutamate release was mediated by activation of both presynaptic ,1 receptors and ,2 receptors, but the ,1 -receptor component was the predominant component of the response. The presynaptic actions of norepinephrine were predominantly, although not completely, resistant to blockade of Na-dependent spikes, implicating a presynaptic terminal locus of action. Interestingly, the spike-dependent component of the response was greater in PVN than in SON magnocellular neurones. This robust presynaptic facilitation of glutamate release by norepinephrine, combined with the known excitatory postsynaptic actions of norepinephrine, activational effects on local glutamate circuits, and inhibitory effects on ,-aminobutyric acid release, indicate a strong excitatory role of norepinephrine in the regulation of oxytocin and vasopressin release during physiological stimulation. [source]


    Intermittent Footshock Facilitates Dendritic Vasopressin Release but Suppresses Vasopressin Synthesis within the Rat Supraoptic Nucleus

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 7 2003
    T. Onaka
    Abstract 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. [source]


    ,-Endorphin Cells in the Arcuate Nucleus: Projections to the Supraoptic Nucleus and Changes in Expression During Pregnancy and Parturition

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 10 2002
    A. J. Douglas
    Abstract 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 ,-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 ,-endorphin fluorescent microbeads retrogradely transported from the supraoptic nucleus, and double-labelled neurones (,-endorphin plus microbeads), showing that ,-endorphin neurones throughout the arcuate nucleus project to the supraoptic nucleus. There was an increase in the number of ,-endorphin-immunoreactive cells in the arcuate nucleus and an increase in the density of ,-endorphin fibres within the supraoptic nucleus and peri-supraoptic region in late pregnancy and parturition, suggesting enhanced expression of ,-endorphin and increased ,-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 ,-endorphin neurones in both proestrus and parturient rats, but the number of positive cells did not increase during parturition, suggesting lack of activation of ,-endorphin neurones at birth. Thus, ,-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. [source]