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  • 2000-2004  (2)
  • 1990-1994  (3)
  • 1985-1989
  • 2001  (2)
  • 1990  (3)
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  • 2000-2004  (2)
  • 1990-1994  (3)
  • 1985-1989
Year
  • 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
    Springer
    Experimental brain research 81 (1990), S. 53-58 
    ISSN: 1432-1106
    Keywords: Vasopressin ; Oxytocin ; Adrenocorticotrophic hormone ; Emotional stress ; Opioid ; Prolactin ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of an opioid receptor antagonist, naloxone (NAL), were studied on the changes in pituitary hormone secretion induced by emotional stress. Male Wistar rats were trained with tone stimuli paired with electric footshocks and tested with the tone and environmental cue signals for emotional stress of fear acquired by learning as described previously (Onaka et al. 1988). Rats received s.c. injected NAL 30 min before testing at doses of 0, 0.2, 1.0, 5.0 and 25.0 mg/kg b.w. Half the rats were injected with 0.5 M NaCl (20 ml/kg b.w.) together with NAL. In these hypertonic rats plasma vasopressin level was slightly increased after NAL. The increment was statistically significant in control groups but not in experimental groups. However the suppression of vasopressin secretion by emotional stimuli was not changed by NAL. Plasma oxytocin levels were extremely high and not significantly different among experimental, unshocked control and untested control groups. NAL further increased the oxytocin level dose-dependently. NAL did not significantly change plasma adrenocorticotrophic hormone (ACTH) levels and hence did not modify the augmentative response in ACTH secretion to emotional stimuli. Plasma prolactin level was significantly elevated after emotional stimuli and NAL depressed the prolactin level in each of experimental and control groups. After NAL, the magnitude of the facilitatory response in prolactin secretion to emotional stimuli was decreased. Motor activity and its suppressive response to emotional stimuli were not influenced by NAL. In another half of rats under a normal osmotic condition the vasopressin response to emotional stimuli was not affected by NAL. NAL further augmented potentiation of oxytocin secretion after emotional stimuli dose-dependently. Effects of NAL on ACTH level, prolactin level and motor activity were similar to those in rats under hypertonic conditions. These results demonstrate that endogenous opioids are selectively and differentially involved in hypothalamo-hypophysial responses to fear-related emotional stress.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1793
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Determination of low molecular weight carbohydrates in marine environments indicated that 1-O-β-D-galactosylglycerol, 6-O-α-D-galactosyl-1-O-β-D-galacto-sylglycerol, sucrose, laminaribiose and laminaritriose are widely distributed in seawaters, suspended and sinking particles, and sediments in coastal as well as in deep-sea waters [e.g. Mikawa Bay and Sagami Bay, Kumano Nada (offshore Japan), and northwest North Pacific Ocean, Bering Sea and Antarctic Ocean: collections during 1978–1984]. Identification of these glycosylglycerols and oligosaccharides in algal cells such as a flagellate (Olisthodisus luteus), blue-green algae (e.g.Trichodesmium sp.) and a diatom (Reptocylindrus denicus) strongly suggests that these sugars are photosynthetically produced by algae in the euphotic zone and are then rapidly transported to the deep sea as sinking particles which can be collected by sediment-trap experiments. The rapid decay rate of low molecular weight carbohydrates by microorganisms suggests that the transported sugars provide energy substrates for microorganisms living in the deep sea.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-136X
    Keywords: Octopamine ; Juvenile hormone ; cAMP ; Cockroach ; Electrophysiology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Juvenile hormone production by the corpora allata of the adult female cockroach, Diploptera punctata, can be modulated by treatment with the biogenic amine, octopamine. Endogenous octopamine has been identified within the CA, using HPLC and electrochemical detection. Treatment with octopamine results in a sinusoidal, dose-dependent inhibition of JH biosynthesis by CA from day 2 virgin females, with maximal inhibition occurring at 10-10 M and 10-4 M. In day 4 and day 8 mated female corpora allata octopamine inhibited JH biosynthesis at 5·10-5 M. Although the elevation of either cAMP or cGMP within the CA is known to be associated with an inhibition of JH biosynthesis, treatment with high concentrations of octopamine results in an increase in the level of cAMP but not cGMP. This effect is both dose- and time-dependent. Octopamine treatment also initiates changes in the passive membrane responses of the CA. Superfusion of CA with octopamine results in a pronounced hyperpolarization of CA cells and an increase in the electrotonic potential (indicative of the degree of electrical coupling between CA cells). This effect could be blocked by the octopamine receptor blocker phentolamine. Treatment with octopamine or phentolamine also blocked the hyperpolarization of CA cells normally associated with electrical stimulation of the axon tracts innervating the CA. We hypothesize that octopamine may be a natural neuromodulator of JH production by CA, regulating ion channels in CA cells themselves as well as release of the inhibitory neuropeptide, allatostatin, from the terminals within the CA.
    Type of Medium: Electronic Resource
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