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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 59 (1978), S. 41-45 
    ISSN: 1432-2072
    Keywords: Lithium ; Amphetamine ; Apomorphine ; Clonidine ; Locomotor activity ; Central catecholamine mechanisms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A behavioural study was performed to investigate how lithium interacts with monoamine mechanisms. Acute lithium pretreatment partially antagonized amphetamine-induced locomotor stimulation in mice. A rather small dose of l-dopa, which had no stimulant effect on locomotor activity of its own, caused a dose-dependent antagonism of the lithium-induced suppression of the amphetamine-induced locomotor stimulation. Additionally, acute lithium pretreatment had no effect on the apomorphine-clonidine-induced locomotor stimulation after elimination of presynaptic activity by means of pretreatment with reserpine and α-MT. Our interpretation of these results is that the inhibitory effect on amphetamine-induced locomotor stimulation is likely to be mediated via presynaptic mechanisms (i.e., decreased release of catecholamines or inhibition of catecholamine synthesis or a combination of both mechanisms) and, further, lithium seems to have no effect at or beyond the catecholamine receptors. However, the possibility that lithium may increase the activity in neuronal systems antagonizing the catecholamine neurons cannot be excluded.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 52 (1977), S. 145-149 
    ISSN: 1432-2072
    Keywords: TRH ; GABA ; Sleep ; Locomotor activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Administration of 10 mg/kg TRH to mice was found to reduce the sleep and hypothermia induced by 4.7 g/kg ethanol. However, TRH did not reduce the sleep of mice that were given γ-hydroxybutyric acid (GHBA), baclophen, or aminooxyacetic acid (AOAA) in combination with 3 g/kg ethanol. TRH also failed to reverse the hypothermia induced by the combination of ethanol and baclophen or GHBA, and the characteristic neurological effects of TRH e.g. tremor, increased muscle tone, and increased respiratory rate were reduced. In addition, TRH-induced locomotor stimulation was prevented by pretreatment with small doses of the GABA-ergic agents, and while 30 mg/kg TRH reduced the hypothermia produced by large doses of the GABA-ergic drugs, it did not antagonize the locomotor retardation produced by baclophen or GHBA. A hypothesis that the analeptic effects of TRH may be mediated via an inhibition of GABA systems is discussed.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 78 (1982), S. 71-75 
    ISSN: 1432-2072
    Keywords: Ethanol ; GABA agonists and antagonists ; Locomotor activity ; Ethanol-induced sleep ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The interaction between ethanol and various GABAergic drugs (muscimol, bicuculline, picrotoxin) with regard to their effects on locomotor activity, drug-induced sleep, body temperature, and convulsions was studied. It was demonstrated that the GABA receptor agonist muscimol potentiated the sedative properties of ethanol, while the opposite effect, a reduction of ethanol-produced sedation, was seen upon administration of the GABA receptor blocking agent picrotoxin. Consequently, the results from the present series of experiments indicate that ethanol enhances central GABAergic activity.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 295 (1976), S. 203-209 
    ISSN: 1432-1912
    Keywords: Ethanol ; Locomotor activity ; Dopamine ; GABA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ethanol (2.4 g/kg) was given intraperitoneally to mice and was found to cause a marked increase in spontaneous locomotor activity. When mice were pretreated with low doses of agents which mimic or augment the action of GABA (γ-hydroxybutyric acid, baclophen, or aminooxyacetic acid) the ethanol-induced locomotor stimulation was completely eliminated. Baclophen (10 mg/kg) was found to cause an initial increase followed by a later decrease in synthesis of catecholamines, as measured by the accumulation of dopa after inhibition of central aromatic l-amino acid decarboxylase, in dopamine-rich areas of rat brain. These data are consistent with previous findings that baclophen, as well as other agents which enhance the activity of GABA systems, reduce the firing of dopamine neurons, thus causing enhanced synthesis of dopamine via feedback mechanisms. These findings also indicate a potential interaction between GABA-like drugs and alcohol in man, and may be of heuristic value in the treatment of chronic alcoholism. The possibility that the mechanism of the inhibition of ethanol-induced locomotor stimulation by GABA-like drugs may be due to a selective interference with ethanol-induced dopamine release is discussed.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-2072
    Keywords: Beta-adrenoceptors ; Locomotor activity ; Propranolol ; Apomorphine ; Clonidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was undertaken in order to clarify the possible involvement of a central betaadrenoceptor mediated action on the stimulation of locomotor activity by the dopamine agonist apomorphine and the noradrenergic agonist clonidine. The effect of pretreatment with various doses of d-and dl-propranolol on apomorphine- and apomorphine plus clonidine-induced locomotor stimulation in reserpinized mice was measured in photocell activity chambers. Pretreatment with dl-propranolol prolonged the duration of apomorphine-induced locomotor stimulation without affecting the maximal level of activity. A similar tendency was seen after pretreatment with the d-form of propranolol, which has a much lower beta-receptor blocking activity. The potentiation by clonidine of the apomorphine-induced locomotor stimulation in reserpinized mice was dose-dependently reduced by pretreatment with dl-propranolol whereas d-propranolol was found to be ineffective. The results indicate that central beta-receptor mechanisms might be involved in the apomorphine plus clonidine-induced locomotor stimulation of reserpinized mice.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-2072
    Keywords: Chronic penfluridol treatment ; Locomotor activity ; Dopamine receptor supersensitivity ; Intracerebral dopamine application ; Nucleus accumbens ; Corpus striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of local application of dopamine to the nucleus accumbens or corpus striatum on locomotor activity was studied in rats 4 days after withdrawal from a 6 weeks term of penfluridol medication. The bilateral application of dopamine into the nucleus accumbens of penfluridol-treated rats produced a very marked increase in coordinated locomotor activity which was 3–5 times higher than that of rats not treated with penfluridol. This effect of dopamine in both penfluridol-treated and control rats was antagonized by intraperitoneally administered haloperidol. The bilateral application of dopamine into the corpus striatum of penfluridol-treated animals produced a marked stereotyped behavioural syndrome in all rats studied, whereas no signs of stereotyped behaviour were observed in any of the rats not treated with penfluridol. The results indicate that long-term treatment of rats with the dopamine receptor blocking agent penfluridol produces an increase in the sensitivity of the dopamine receptors in the nucleus accumbens and corpus striatum and that the nucleus accumbens may play a role in locomotor activity.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-2072
    Keywords: Key words Nicotine ; Behavioral sensitization ; Locomotor activity ; Elevated plus-maze ; Serotonin ; Citalopram
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study investigated the effects of repeated nicotine treatment on locomotor activity and behavioral inhibition, and the influence of citalopram on the behavioral effects obtained. Male rats received daily subcutaneous injections of vehicle + vehicle (veh + veh), citalopram (5.0 mg/kg) + vehicle (cit + veh), vehicle + nicotine (1.0 mg/kg; veh + nic) or citalopram+nicotine (cit + nic). Acutely, nicotine stimulated locomotor activity, and repeated daily nicotine injections sensitized veh+nic rats to the nicotine-induced locomotor stimulation after 5, 10 and 15 treatment days, whereas in cit+nic rats, the enhancement of nicotine-induced locomotion was suppressed. However, when challenged with nicotine after citalopram withdrawal (−36 h), the cit + nic treated animals were also observed to be sensitized. In the elevated plus-maze, repeated nicotine treatment produced behavioral disinhibition, measured as an increase of time spent in and entries made into open arms (%), and chronic citalopram treatment attenuated the expression of behavioral disinhibition. Moreover, the degree of nicotine sensitization correlated to the behavioral disinhibition observed. In summary, these findings suggest that behavioral sensitization to nicotine is associated with behavioral disinhibition and that chronic citalopram treatment counteracts the expression of both phenomena. Since citalopram is a highly selective serotonin reuptake inhibitor, the effects of citalopram may be due to a facilitation of serotonin neurotransmission caused by the chronic citalopram treatment.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-2072
    Keywords: Benzodiazepines ; Brain reward systems ; Dependence-producing drugs ; Diazepam ; Dopamine ; Locomotor activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It is well known that benzodiazepines produce dependence in humans and locomotor stimulation in experimental animals. In this study the possible involvement of catecholamines in the diazepam-induced locomotor stimulation in mice were investigated. Diazepam was found to have a biphasic effect; increasing locomotor activity at a low dose (0.25 mg/kg), while decreasing it at higher doses (〉0.5 mg/kg). The locomotor stimulating effect of diazepam was effectively blocked by pretreatment with the benzodiazepine receptor antagonist flumazenil, as well as with the catecholamine synthesis inhibitor α-methyltyrosine and the dopamine receptor antagonists haloperidol, spiperone and SCH 23390. Taken together, these data indicate that the locomotor stimulating effect observed after low doses of diazepam is due to activation of brain dopaminergic systems involved in locomotor activity. The observations are discussed in relation to the hypothesis that dependence-producing drugs activate specific brain reward systems.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-2072
    Keywords: Locomotor activity ; Tyrosine hydroxylation ; Catecholamines ; Ontogenesis ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A combined biochemical and behavioral study was performed postnatally on albino rats. An almost linear increase in total motor activity was observed from 1 to 15 days of age followed by a pronounced decrease in motor activity between days 15 and 18. The in vivo rate of tyrosine hydroxylase activity in whole brain was estimated by means of measuring accumulation of L-3,4-dihydroxyphenylalanine (Dopa) after administration of an inhibitor of aromatic amino acid decarboxylase NSD 1015. Additionally, Dopa accumulation was studied in regional brain areas in 10 and 14-day-old animals. A slight gradual increase in the amount of Dopa accumulation in whole brain was observed from 1 to 10 days of age, followed by a pronounced increase between 10 and 14 days. Regional studies revealed that the increase in Dopa accumulation was primarily located to striatum. The data suggest an involvement of central catecholamine neurons possibly dopaminergic, terminating in striatum. The decrease in motor activity observed after 15 days of age is interpreted as involvement of maturing inhibitory pathways of noncatecholaminergic origin.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 49 (1976), S. 253-257 
    ISSN: 1432-2072
    Keywords: Chronic ethanol administration ; Locomotor activity ; Dopamine receptor supersensitivity ; Intracerebral dopamine application ; Nucleus accumbens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of local application of dopamine into the nucleus accumbens on locomotor activity was studied in rats during and after withdrawal of long-term ethanol treatment. The bilateral application of dopamine into the nucleus accumbens of both the ethanol and withdrawal rats produced a pronounced increase in coordinated locomotor activity, which was 8–10 times higher than that of untreated water control rats. This effect of dopamine was antagonized by intraperitoneally administered haloperidol indicating a specific effect on dopamine receptors. It is concluded that prolonged ethanol administration may produce an increased sensitivity of the dopamine receptors in the nucleus accumbens and further support the contention that central catecholamine mechanisms are involved in the mediation of the withdrawal syndrome observed after longterm treatment with ethanol.
    Type of Medium: Electronic Resource
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