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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Anaesthesia 28 (1973), S. 0 
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Anaesthesia 58 (2003), S. 0 
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Anaesthesia 58 (2003), S. 0 
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 150 (1968), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Anaesthesia 49 (1994), S. 0 
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 4 (1977), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Mice were given haloperidol (approximately 3 mg.kg−1 day−1) or vehicle for 21 days and then withdrawn from the drug. All tests were performed 4 days after withdrawal.2. Haloperidol treated mice (premedicated with reserpine plus a-methyl-p-tyrosine) displayed an increased locomotor response to apomorphine and to apomorphine plus clonidine, but neither haloperidol- or vehicle-treated animals revealed any stimulant response to clonidine.3. In mice which had not been pretreated with reserpine plus a-methyl-p-tyrosine, clonidine produced a significant stimulation of locomotor activity in animals withdrawn from haloperidol but not in those withdrawn from the vehicle. Phen-oxybenzamine blocked the locomotor stimulant difference between these two groups, but did not completely antagonize the stimulant effect of clonidine in mice withdrawn from haloperidol. Pimozide was largely effective in blocking the clonidine-induced stimulation. Co-administration of phenoxybenzamine and pimozide was completely effective in blocking the stimulant effect of clonidine in mice withdrawn from haloperidol.4. The evidence for a change in catecholamine receptor sensitivity was supported by the increased stimulant effect of dexamphetamine in the haloperidol-treated, compared to the vehicle-treated animals.5. The data suggest that there is a change in the functional responsiveness of both adrenergic and dopaminergic receptors after withdrawal from long term haloperidol treatment.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-2072
    Keywords: Conditioned avoidance response ; α-Methyl-p-tyrosine ; Suppression ; Dopamine ; Reversal ; Nucleus accumbens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract These experiments sought to determine whether dopamine (DA) could reverse the depressive effects of α-methyl-p-tyrosine (AMPT) on a conditioned avoidance response (CAR). Rats were randomly allocated to shocked groups (CAR-trained) and non-shocked (CAR-naive) groups. The CAR-trained rats, conditioned to avoid an electric shock, were administered AMPT (150 mg/kg at-24 h and 50 mg/kg at-1 h, both IP), nialamide (80 mg/kg IP at-1 h) and saline (1 μl) or DA (5 or 10 μg/μl, dissolved in 1 μl saline, at time 0) directly into the nucleus accumbens. The rats were then tested for CAR at 0.5, 1, 2, 3, 4, 8, 12, 24 and 48 h. The CAR-naive rats, conditioned to the behavioural environment without electric shock being presented, were administered AMPT, nialamide and DA or saline as above. Both doses of DA antagonised the AMPT-induced suppression of the CAR in the CAR-trained rats, reaching a maximum 2–4 h after its local application. In the CAR-naive rats, DA produced a ‘pseudo-CAR’ that lasted about 4 h, but which completely disappeared at 8 h when the DA effect had worn off. These CAR-naive rats did not learn a CAR under the influence of DA. In a third group of rats, DA produced locomotor activation which, in its time course, resembled the effect of DA on CAR. It is concluded that the ability of DA to antagonise AMPT-induced depression of CAR is, in all likelihood, dependent upon DA-induced locomotor excitation, rather than upon an effect of DA on associative learning.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 83 (1984), S. 70-75 
    ISSN: 1432-2072
    Keywords: Dopamine ; Locomotor activity ; Nucleus accumbens ; Passive avoidance ; State-dependent learning ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The acquisition of a one-trial step-through passive avoidance task was examined in rats following the administration of nialamide IP and dopamine (DA) or saline into the nucleus accumbens. DA-treated rats displayed impaired learning of the task as evidenced by their lower step-through latencies on a retest trial 7 days later. The specificity of this impairment was studied in a 2×2 design involving intracerebral injections prior to both training and testing trials. It was found that DA treatment prior to the training trial disrupted learning or memorization of the task but that DA did not affect performance or retrieval and did not induce state-dependent learning. These findings suggest that DA applied to the nucleus accumbens does not facilitate learning per se.
    Type of Medium: Electronic Resource
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  • 9
    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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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 68 (1980), S. 77-83 
    ISSN: 1432-2072
    Keywords: l-DOPA ; Supersensitivity ; Subsensitivity ; Dopamine ; Locomotor activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mice, pretreated orally with l-DOPA (200 mg/kg) plus benserazide (50 mg/kg) (l-DOPA-B) responded when challenged 24h later with the same drug combination, with significantly greater locomotor stimulation than animals pretreated with the vehicle. The enhanced response was not due to an intrinsic effect of benserazide. Nor was it dependent on a change in central dopamine (DA) receptor sensitivity, because the two pretreatment groups (l-DOPA-B and vehicle) did not differ in their locomotor response to a range of apomorphine doses (300–3,000 μg/kg, IP). The enhanced response was, however, due to DA receptor stimulation because it was antagonised by premedication of the mice with haloperidol or pimozide. Moreover, the enhanced response to l-DOPA-B challenge was also produced when mice were pretreated (24h earlier) with a high dose of l-DOPA alone (without benserazide) (1,200 mg/kg, orally). Animals which had been pretreated with l-DOPA-B had significantly higher brain levels of l-DOPA and DA after a subsequent challenge dose of l-DOPA-B administered 24h later. Thus the enhanced response to l-DOPA-B observed in the present experiment appears to be dependent on some mechanism which produces higher concentrations of l-DOPA (and consequently DA) in the brain.
    Type of Medium: Electronic Resource
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