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  • 1
    ISSN: 1432-2072
    Keywords: d-Amphetamine ; Supersensitivity ; Nucleus accumbens ; Apomorphine ; Chronic
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Treatment of rats with d-amphetamine (5 mg/kg) once daily for 25 days did not change locomotor responses, on day 7 of withdrawal, to dopamine (DA) or d-amphetamine into the nucleus accumbens. Nor was there a change in 3H-spiperone binding of caudate nucleus membranes. There was no effect of treatment on the locomotor response of rats to 1.0, 1.5 or 2.0 mg/kg d-amphetamine IP. However, d-amphetamine-treated rats were significantly less sensitive to 0.5 mg d-amphetamine. Although 1, 2 or 3 mg/kg apomorphine produced the same degree of stereotypy in both treatment groups, there was a significant difference in the response of the two groups to 0.5 mg apomorphine, d-amphetamine-treated animals being less sensitive than vehicle-treated animals. No change was found in brain DA levels with or without synthesis inhibition. The present data do not support the hypothesis that chronic treatment of rats with d-amphetamine can produce supersensitive post-synaptic DA receptors.
    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
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    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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