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  • 2000-2004  (6)
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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 13 (2001), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We examined the role of N-methyl-d-aspartate (NMDA) receptors in the control of noradrenaline release in the supraoptic nucleus (SON) using a microdialysis method in urethane-anaesthetized rats. Local application of 0.5 mm NMDA into the SON by retrodialysis decreased noradrenaline content in the dialysate from the SON. On the other hand, MK-801, a channel blocker of NMDA receptors, or D(–)2-amino-5-phosphonopentanoic acid (AP-5), a competitive NMDA receptor antagonist, increased the basal noradrenaline content. Tetrodotoxin did not completely block the noradrenaline increase after NMDA antagonists. Infusion of Ca2+-free solution containing Ni2+ and Cd2+, or a mixture of ω-agatoxin IVA and ω-conotoxin GVIA, voltage-sensitive Ca2+ channels blockers, did not block noradrenaline increase after AP-5, but blocked noradrenaline increase after high K+. Infusion of intracellular Ca2+ blockers, thapsigargin or TMB-8, impaired noradrenaline increase after AP-5 but not that after high K+. These data are consistent with the hypothesis that activation of an NMDA receptor inhibits an intracellular Ca2+ store-dependent noradrenaline release from nerve terminals in the SON.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 13 (2001), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The present study aimed to examine roles of N-methyl-D-aspartic acid (NMDA) receptors in oxytocin and vasopressin release after osmotic stimuli. A noncompetitive NMDA receptor antagonist, MK-801 (0.2 mg/kg body weight, i.p.), significantly decreased plasma concentrations of oxytocin and vasopressin after hypertonic saline injection (0.3 or 0.6 M NaCl, i.p., 20 ml/kg). By contrast, oxytocin release induced by injection of cholecystokinin octapeptide (20 µg/kg, i.p.) was not significantly changed by MK-801. Hypertonic saline injection increased the number of cells expressing Fos in the supraoptic nucleus and in the regions anterior and ventral to the third ventricle (AV3V) regions [the organum vasculosum of the lamina terminalis (OVLT) and median preoptic nucleus]. MK-801 decreased the number of cells expressing protein in these areas after hypertonic saline injection. A microdialysis method showed that a hypertonic saline injection (0.6 M NaCl, 20 ml/kg, i.p.) facilitated glutamic acid release in and near the OVLT. The results support the view that NMDA receptor in the AV3V region modulates in a facilitative fashion the AV3V inputs to the supraoptic neurosecretory neurones.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neuroendocrinology 16 (2004), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Oxytocin is released from the pituitary gland in response to a variety of stressful stimuli, including noxious stimuli, conditioned fear and exposure to novel environments. These responses are believed to be mediated, at least in part, by noradrenergic projections from the medulla oblongata, and some of these noradrenergic neurones also contain prolactin-releasing peptide (PrRP). Central administration of either PrRP or noradrenaline stimulates oxytocin secretion into the circulation. Stressful stimuli activate PrRP-containing noradrenergic neurones in the medulla oblongata, and it is thus possible that PrRP/noradrenergic projections to the hypothalamus mediate oxytocin responses to stressful stimuli. Here, the roles of brainstem PrRP/noradrenergic projections to the hypothalamus in oxytocin responses to different kinds of stressful stimuli are reviewed, with a particular emphasis on conditioned fear. Roles of dendritic oxytocin release during stress and metabolic factors affecting stress pathways are also discussed.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 15 (2003), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: This study investigated the effects of novelty stress on neuroendocrine activities and running performance in Thoroughbred horses. First, to examine the neuroendocrine responses to novelty stress, we exposed horses to two types of novel environmental stimuli (audiovisual or novel field stimuli). After the stimuli, plasma concentrations of vasopressin, catecholamines and adrenocorticotropin (ACTH), as well as heart rates, were significantly increased in each experiment. Second, we investigated neuroendocrine activities during incremental exercise. Plasma concentrations of vasopressin, catecholamines, ACTH and blood lactate increased as the exercise load increased. Finally, we investigated the effects of novelty stimuli on neuroendocrine activities and running performance during supra-maximal exercise (110% VHRmax). When the novelty stimuli were presented to horses, the increases in plasma vasopressin and catecholamines due to exercise load were significantly smaller than those in the control experiments. Blood lactate during supra-maximal exercise was also significantly lower and total run time until exhaustion was prolonged in the novel environmental stimuli compared to the control. These results suggest that novelty stimuli facilitate vasopressin release from the posterior pituitary in addition to activating the sympatho-adrenomedullary and the hypothalamic-pituitary-adrenocortical axes in thoroughbred horses, and increase exercise capacity, resulting in improvement of running performance during supra-maximal exercise.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 15 (2003), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neuroendocrinology 12 (2000), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
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