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  • 1990-1994  (1)
  • 1985-1989  (1)
  • 1955-1959
  • L-gulono-γ-lactone oxidase  (1)
  • Opioid  (1)
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  • 1990-1994  (1)
  • 1985-1989  (1)
  • 1955-1959
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 45 (1989), S. 126-129 
    ISSN: 1420-9071
    Keywords: L-gulono-γ-lactone oxidase ; ascorbic acid deficiency ; enzyme defect ; rat ; nuclei acid hybridization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary A mutant strain of Wistar rats with L-gulono-γ-lactone oxidase deficiency has recently been established. To investigate this deficiency by DNA and RNA blot hybridization analyses, a fragment of a previously cloned cDNA encoding rat L-gulono-γ-lactone oxidase was used as a probe. When genomic DNA of the mutant rat was digested with several restriction enzymes, the probe hybridized to fragments of the same sizes as those produced from DNA of normal rats. Poly(A)+RNA from the liver of the mutant rat was found to contain an L-gulono-γ-lactone oxidase-specific mRNA of a normal size at a comparable level to that of normal rats. An in vitro translation experiment revealed that the mRNA programmed the synthesis of an enzyme protein which had the same molecular weight as that of the translational product of the normal mRNA, although the amount synthesized was markedly reduced as compared with that synthesized with the normal mRNA. In accordance with this observation, a very low but definite degree of L-gulono-γ-lactone oxidase activity was detected in the microsomes of the mutant rat by a newly developed, highly sensitive method.
    Type of Medium: Electronic Resource
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  • 2
    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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