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  • 1
    ISSN: 1432-2072
    Keywords: Ethanol ; Acute tolerance ; α-Adrenergic receptors ; Noradrenaline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The percentage of mice able to remain on a rolling drum for 45 s was recorded at 1.25 min and 30 min after administration of ethanol (2.4 g/kg). Though there was no significant difference in brain ethanol levels at the two test times, performance was markedly different with significantly fewer mice able to remain on the drum at 1.25 min than at 30 min. This phenomenon, known as acute tolerance, was antagonised by pretreating mice with haloperidol (0.4 mg/kg), FLA-63 (25 mg/kg), diethyldithiocarbamate (400 mg/kg), phenoxybenzamine (40 mg/kg), phentolamine (20 mg/kg), yohimbine (3 mg/kg) and clozapine (1 mg/kg), but not by spiperone (0.16 mg/kg), α-methyl-p-tyrosine (300 mg/kg) or phenobarbitone (10 mg/kg). The relative potencies of the effective blocking agents suggest that α2-receptors may play an important role in mediating acute ethanol tolerance.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 66 (1979), S. 55-61 
    ISSN: 1432-2072
    Keywords: l-Dopa ; Chronic ; Apomorphine ; Dexamphetamine ; Subsensitivity ; Supersensitivity ; Dopamine ; Noradrenaline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of acute and repeated treatments with l-Dopa in oral doses of 200 mg/kg plus benserazide (50 mg/kg) was studied using locomotor activity in mice as a model of central catecholaminergic function. Mice pretreated with l-Dopa once daily for 1, 4 or 10 days responded to a challenge dose of l-Dopa (same dose as above) 1 day later with a more pronounced increase in motor activity than vehiclepretreated animals. Dexamphetamine-induced (0.5, 1.0 or 2.0 mg/kg) stimulation was found not to be significantly different in the two pretreatment groups when mice were challenged 1 day after one or four pretreatment doses of l-Dopa. However, a reduced response to dexamphetamine was observed in l-Dopa-pretreated mice (compared to vehicle-treated mice) on withdrawal of the mice from a 10-day l-Dopa pretreatment schedule. One day after one l-Dopa dose, with or without premedication with α-methyl-p-tyrosine (200 mg/kg) plus reserpine (10 mg/kg), mice responded to apomorphine (1.0 mg/kg) with significantly less activity than vehicle-pretreated mice. In contrast, 1 day after ten doses of l-Dopa, there was a shift to the left of the dose-response curve to apomorphine, which did not, however, occur 4 days after withdrawal. Hence, marked dopamine receptor sensitivity changes seem not to be of primary importance for l-Dopa hyperactivity in l-Dopa-pretreated mice. The present study also suggests that dopaminergic changes are not of consequence in the activity induced by dexamphetamine in l-Dopa-pretreated animals.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2072
    Keywords: Amphetamine ; Apomorphine ; Chronic treatment ; Dopamine ; Locomotor activity ; Noradrenaline ; Supersensitive receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mice administered dexamphetamine (4 mg/kg i.p.) once daily for 20 days displayed an enhanced locomotor response (compared to that of vehicletreated mice) to dexamphetamine when challenged 4 to 16 days but not when challenged 32 days after withdrawal. In the experiments described a 20-day dexamphetamine administration followed by an 8-day withdrawal period was used. Pimozide or haloperidol not only completely antagonised the enhanced response to dexamphetamine (2 mg/kg i.p.) in dexamphetamine-treated mice, but also antagonised all dexamphetamine-induced stimulation. Reserpine, in contrast, preferentially blocked the difference in the response to dexamphetamine of dexamphetamine-and vehicle-treated mice, without antagonising all the dexamphetamine-induced locomotion. The stimulation produced in dexamphetamine-(but not in vehicle-) treated mice by dexamphetamine was partially blocked by phentolamine, phenoxybenzamine, and propranolol. FLA-63 did not significantly influence the response to dexamphetamine in either group. That a dopaminergic mechanism plays a major role in the enhanced response to dexamphetamine was shown by the significantly greater response in dexamphetamine-treated mice to apomorphine challenge. The treatment of mice with apomorphine (10 mg/kg/day i.p. for 20 days), produced a greater response to apomorphine challenge in the apomorphine-treated mice than in vehicle-treated mice 8 days after withdrawal. The data show that with long-term administration both dexamphetamine and apomorphine are able to produce in mice what appear to be supersensitive dopamine receptors. Moreover, the enhanced response to dexamphetamine after withdrawal from long-term dexamphetamine treatment appears to require the presence of reserpine-sensitive amine stores and, to a lesser extent, the presence of unblocked α-adrenergic receptors.
    Type of Medium: Electronic Resource
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