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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 97 (1989), S. 432-435 
    ISSN: 1432-2072
    Keywords: Metamphetamine ; Behavioral deficits ; Dopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The functional consequences following methamphetamine-induced neuronal damage were evaluated under several different conditions known to affect the magnitude of the lesion. It was found that methamphetamine (6.25 mg/kg administered SC, four times at 2-h intervals) caused long-lasting depletions of striatal dopamine and serotonin and that pretreatment with the antioxidant, ascorbic acid (100 mg/kg), attenuated these depletions, whereas pretreatment with the superoxide dismutase inhibitor diethyldithiocarbamate (200 mg/kg) exacerbated these depletions. The dopamine depletions resulting from the repeated administration of methamphetamine under these various conditions did not result in any alteration in the consumption of a sweetened-condensed milk solution under baseline conditions. However, when these lesioned animals were challenged with acutely administered methamphetamine, it was observed that there was an altered sensitivity to the milk intake decreasing effects of this compound. That is, the degree to which the acutely administered methamphetamine reduced the intake of sweetened-condensed milk was highly correlated with the magnitude of the methamphetamine-induced dopamine and serotonin depletions. These observations support the hypothesis that methamphetamine-induced neuronal damage is mediated by free radical formation and indicate that behavioral measures may be employed to assess neuronal damage.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 88 (1986), S. 401-402 
    ISSN: 1432-2072
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; MPTP ; Dopamine ; Avoidance behavior
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The behavioral and neurochemical consequences of the intrastriatal administration of 1-methyl-4-phenylpyridinium ion (MPP+), the toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), were evaluated using the shuttlebox avoidance paradigm. MPP+ caused a significant depletion of striatal dopamine and significant disruption of shuttlebox performance. L-Dopa administration reversed both the dopamine depletion and the behavioral deficits. These observations are discussed in reference to the rodent-MPTP model of Parkinson's disease.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
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