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  • 11
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 50 (1981), S. 47-55 
    ISSN: 1435-1463
    Keywords: Grooming ; swim ; dopamine ; neuroleptics ; chronic ; supersensitivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Grooming induced in mice after a period of swimming was potently and dose-dependently blocked by neuroleptics. The order of potency of the neuroleptics was spiroperidol〉haloperidol〉cis-flupenthixol〉pimozide〉chlorpromazine〉thioridazine. The trans isomer of flupenthixol was inactive at 40μM/kg. Theα-adrenergic receptor antagonists, phentolamine and phenoxybenzamine, and the catecholamine synthesis inhibitor,α-methyl-p-tyrosine were essentially without effect on the grooming behaviour. Amitriptyline inhibited grooming behaviour only in doses which severely affected the animals motor function. Fluoxetine was without effect. Cisflupenthixol was less active in inhibiting grooming in animals chronically treated with haloperidol than in control animals, indicating the presence of supersensitive dopamine receptors. The data indicate that swim-induced grooming in mice is mediated via dopaminergic systems.
    Type of Medium: Electronic Resource
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  • 12
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mice, administered haloperidol 3 mg/kg/day, in their drinking water for 21 days, were tested for their responsiveness to cholinergic and anticholinergic drugs 4 days after withdrawal from haloperidol (or vehicle). Haloperidol-treated animals administered methylhyoscine (1 mg/kg i.p.) and various doses of physostigmine (5 to 1215μg/kg) displayed significantly less depression of locomotor activity than vehicle-treated animals. Atropine, 5 mg/kg, whilst ineffective in producing locomotor stimulation in vehicle-treated animals, produced marked stimulation in haloperidol-treated animals. Methylatropine (5 mg/kg) did not produce significant stimulation in either group. Dopamine receptor supersensitivity was present in these animals as haloperidol-treated mice, pretreated withα-methyl-tyrosine and reserpine, displayed a significantly greater locomotor response to apomorphine than did vehicle-treated animals. The data support the hypothesis that long-term administration of haloperidol produces an apparent hyposensitivity of central muscarinic receptors.
    Type of Medium: Electronic Resource
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  • 13
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 57 (1983), S. 13-25 
    ISSN: 1435-1463
    Keywords: Supersensitive ; noradrenaline receptor ; neuroleptics ; dopamine ; tyramine ; chronic haloperidol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rats were administered haloperidol (3–4 mg/kg/day) in their drinking water for 42 days, and experiments conducted on the seventh day of withdrawal. Anaesthetized haloperidol treated rats exhibited a similar mean blood pressure (BP) and heart rate (HR) response to control rats when challenged with phenylephrine (IV). When similarly pretreated rats were challenged with one of four possible doses of clonidine (IV), haloperidol treated rats were less sensitive than control rats to clonidine's hypertensive action, but there were no effects of treatment on the hypotensive (BP) effect of clonidine nor on its bradycardic effect. When one of six possible doses of tyramine was administered a similar mean BP response was seen in both treatment groups, but the positive HR response in the haloperidol-treated group was much less than in the vehicle-treated group. Atria isolated from haloperidol treated or control rats revealed a similar chronotropic response to noradrenaline and tyramine challenge. These data indicate that chronic haloperidol does not cause a generalized change inα-adrenergic receptor sensitivity. Nevertheless, it is clear that haloperidol has produced changes in the cardiovascular response of rats to these drugs.
    Type of Medium: Electronic Resource
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  • 14
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 62 (1985), S. 219-230 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Bromocriptine (BRC) produced neither locomotor stimulation nor stereotyped behavior in mice and rats pretreated with reserpine plus alphamethyl-p-tyrosine (AMPT). However, the blockade of locomotor stimulation in mice by AMPT could be reversed by their prior treatment with a low, behaviorally inactive dose of L-DOPA. BRC potentiated the stereotypy (rats) and locomotor stimulation (mice) produced by apomorphine in animals pretreated with reserpine plus AMPT. Moreover, BRC potentiated the stimulant effect of d-amphetamine in reserpinised mice, while nomifensine, but not fluoxetine or desipramine, potentiated the stimulant effect of BRC in mice. After direct application to the nucleus accumbens or caudate nucleus of rats, BRC was inactive. However, when BRC and DA were applied together to the nucleus accumbens, BRC enhanced the stimulant effect of DA. These data show that BRC by itself does not cause behavioral stimulation in rodents. Despite having affinity for the DA D 2-receptor, BRC is incapable of causing excitation in rats and mice unless another DA-receptor agonist such as apomorphine or DA is present. The data are discussed in relation to the published literature and the hypothesis presented that BRC affects the signal transmitted by DA-receptor agonists such as apomorphine at or beyond the postsynaptic DA-receptor.
    Type of Medium: Electronic Resource
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  • 15
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 50 (1981), S. 209-224 
    ISSN: 1435-1463
    Keywords: L-DOPA ; chronic ; dopamine receptors ; supersensitivity ; subsensitivity ; locomotor activity ; adrenergic receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mice were pretreated once daily with L-DOPA (200 mg/kg) plus benserazide (B) (50 mg/kg) for ten days and challenged with various doses of L-DOPA+B on the first, fourth or sixteenth days of withdrawal. L-DOPA+B-pretreated mice were more sensitive to the locomotor stimulant effects of L-DOPA+B challenge one and four days, but not sixteen days after withdrawal. The enhanced response was most marked on the first day of withdrawal. Other mice, pretreated once daily with B (50 mg/kg), responded one day after the tenth dose with a slightly enhanced response to L-DOPA+B challenge compared to the response of vehicle-pretreated animals. Moreover, vehicle-pretreated mice challenged with B alone, were significantly less active than those challenged with vehicle. On the first day of withdrawal, the L-DOPA+B-pretreated animals were supersensitive to the locomotor stimulant effects of apomorphine but subsensitive to dexamphetamine (Bailey et al., 1979). On the fourth day of withdrawal, there were no differences in the responses of the L-DOPA+B-pretreated mice compared to the vehicle-pretreated mice, to apomorphine or apomorphine plus clonidine, but L-DOPA+B-pretreated mice were still subsensitive to the locomotor stimulant effects of dexamphetamine. Clonidine produced a dose-dependent, but similar, degree of hypothermia in both pretreatment groups. On the first and fourth days of withdrawal L-DOPA+B-pretreated mice exhibited higher brain levels of dopamine (DA) and DOPA than vehicle-pretreated mice in response to an acute dose of L-DOPA+B. The biochemical results suggest that the enhanced locomotor response to L-DOPA+B in L-DOPA+B-pretreated mice is probably dependent on changes in the amount of L-DOPA (and DA) available in the brain. Moreover, it is not ruled out that some of the effects of L-DOPA+B pretreatment were due to the B alone. Some of the enhanced response to L-DOPA+B on the first day of withdrawal may have been dependent on the same mechanism as that underlying the apparent supersensitivity to apomorphine. The subsensitive response to dexamphetamine would appear to be independent of changes in post-synaptic DA andα-adrenergic receptor sensitivity.
    Type of Medium: Electronic Resource
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  • 16
    Electronic Resource
    Electronic Resource
    Springer
    World journal of surgery 2 (1978), S. 173-174 
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 17
    Electronic Resource
    Electronic Resource
    Springer
    Aequationes mathematicae 23 (1981), S. 6-23 
    ISSN: 1420-8903
    Keywords: Primary 05A15 ; Secondary 15A15, 15A33
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics
    Type of Medium: Electronic Resource
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  • 18
    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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  • 19
    ISSN: 1432-2072
    Keywords: Tetrahydrocannabinol ; Cannabidiol ; Cannabinol ; Ethanol ; Human ; Performance ; Cognitive ; Motor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cannabinoids (THC, 215 μ/kg; CBD, 320 μg/kg; CBN, 320 μg/kg) and ethanol (0.54 g/kg) were administered orally to human volunteers alone and in all possible combinations and performance decrements were assessed on a battery of tests (standing steadiness, simple and complex reaction times, pursuit rotor and Vienna Determination Apparatus) over a 280 min period. Blood ethanol concentrations and pulse rates were measured, an assessment was made of conjunctival hyperaemia and the subjects were asked to estimate the nature and degree of their intoxication. THC alone produced significant decrements on all the performance measures (general performance, standing steadiness, reaction speed and psychomotor performance) which were slow in onset, and were still evident at the end of the experiment. The increases in pulse rates and conjunctival hyperaemia as well as the subjects' assessment of their intoxication followed a similar time course. Ethanol also produced significant decrements in all but the psychomotor co-ordination factor which were rapid in onset with complete recovery by the end of the test period. There was no suggestion of systematic effects involving CBD or CBN, either alone or in combination with other drugs, and it was possible to describe the data in terms of a model which referred only to the effects of THC and ethanol. The combined effects of THC and ethanol were greater than those of THC alone, both in the performance measures, where virtually no recovery occurred, and in the self-assessment of intoxication and could be described in terms of an additive model with no statistical evidence for interaction. Blood ethanol levels were unaffected by cannabinoid pretreatment. There was no suggestion that the effects of THC or THC plus ethanol were further modified in any was by the inclusion of CBD and/or CBN in the cannabinoid pretreatment.
    Type of Medium: Electronic Resource
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  • 20
    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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