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  • 1
    Electronic Resource
    Electronic Resource
    Sensitization phenomena after repeated administration of cocaine or D-amphetamine in rats: associative and non-associative mechnisms and the role of dopamine in the striatum (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 355 (1997), S. 531-537 
    Details
    ISSN: 1432-1912
    Keywords: Key words Cocaine ; D-Amphetamine ; Dopamine release ; Sensitization ; Conditioning mechanisms ; Non-associative mechanisms ; Locomotor activity ; Stereotyped behaviour
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In parallel studies, the contribution of non-associative and associative mechanisms to the development of sensitization to the effects of cocaine and D-am-phetamine on locomotor activity and stereotyped behaviour were tested. Rats were pretreated with cocaine, 10mg/kg s.c. twice, D-amphetamine 1.5mg/kg s.c. once or with saline. During the pretreatment period, one group of rats was administered the drug in positive temporal association with conditional stimuli (CS) (‘associative’), another group in negative temporal association with the CS (‘non-associative’), a saline pretreated control group was exposed to the CS but administered the drug only during the test (‘naive’). On the test day, 7 days after the last drug administration, in the cocaine-sensitized group, cocaine produced the largest locomotor stimulation and the highest scores of stereotypies (mainly sniffing) in the ‘associative’ group, significantly smaller effects in the ‘non-associative’ group, and the smallest effects in the ‘naive’ group. The stereoypies (mainly licking) produced by D-amphetamine in the amphetamine-sensitized group on the test day, 7 days after the last drug administration, were also most pronounced in the ‘associative’ group, less pronounced in the ‘non-associative’ group and least in the ‘naive’ group, whereas the opposite sequences of intensities were found with regard to locomotor activation. The observations in D-amphetamine-treated groups suggest that there is a negative correlation between locomotor activity and stereotyped licking. Estimation of the extracellular dopamine using microdialysis in the striatum showed no significant differences between the three cocaine groups in the moderate increases. In contrast, after D-amphetamine treatment, the strong increases in dopamine were most pronounced in the ‘associative’ group, significantly less in the ‘non-associative’ group and even less in the ‘naive’ group. The biochemical findings in the D-amphetamine-pretreated animals are apparently related to the pronounced stereotyped licking observed in these animals which is probably induced in the striatum, whereas locomotor activation and sniffing are probably mediated elsewhere and therefore are not reflected biochemically in the striatum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00004979
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  • 2
    Electronic Resource
    Electronic Resource
    Is morphine-induced akinesia related to inhibition of reflex activation of flexor α-motoneurones? (1982)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 320 (1982), S. 101-104 
    Details
    ISSN: 1432-1912
    Keywords: Morphine ; Nucleus accumbens ; Locomotor activity ; Catalepsy ; Akinesia ; Flexor α-motoneurones
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Unilateral injections of morphine (5–15 μg) into the nucleus accumbens of non-anesthetized rats produces a decrease of locomotor activity and a catalepsy. In a similar dose-response relationship, injections of morphine into this area inhibited the reflex activation of α-motoneurones by mild tetanic stimulation of the ipsilateral peroneal nerve (flexor α-motoneurones) in halothane-anesthetized rats. All these effects were antagonized by systemic administration of naloxone. Our results suggest that a reduction in reflex activation of flexor α-motoneurones by proprioceptive stimuli seems to be relevant for the development and/or mediation of akinesia and catalepsy, and that the nucleus accumbens plays a key role in these effects produced by morphine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00506308
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  • 3
    Electronic Resource
    Electronic Resource
    Locomotor activity of rats after injection of various opiods into the nucleus accumbens and the septum mediale (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 331 (1985), S. 175-180 
    Details
    ISSN: 1432-1912
    Keywords: Locomotor activity ; Opioids ; Nucleus accumbens ; Septum mediale
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possible role of the nucleus accumbens (ACB) and, in some experiments, the septum mediale (SM) in mediating alterations in locomotor activity, produced by various opioids, was evaluated in the rat, the drug being injected either into the left central part of the ACB or into the left SM. Morphine, predominantly acting at the mu-type receptors, given in larger doses (13 or 40 nmol into the ACB) produced depression of locomotor activity and catalepsy, whereas 2.5 nmol were ineffective. Co-administration of naloxone into the ACB suppressed the effects of morphine.d-ala2,d-leu5-enkephalin (DADL), a preferential delta-type receptor agonist, produced a biphasic effect on locomotor activity, namely an inhibition of it and a catalepsy, followed by a locomotor activation. This effect was observed after 4 or 13 nmol; 1 nmol produced a delayed locomotor activation without any previous inhibition, whereas 0.4 or 0.1 nmol were ineffective. Equimolar doses of naloxone, when coadministered with DADL, only partially antagonized these effects of DADL. In contrast, co-administration of a small dose of DADL and an excess dose of naloxone into the ACB produced an immediate increase in locomotor activity. Injections of a predominant kappa type receptor agonist, MR 2033-Cl, were ineffective. Injection of DADL, either alone or combined with naloxone into the SM (1 nmol) produced an immediate stimulation of locomotor activity. The results suggest that locomotor depression and catalepsy may be mediated by opioid receptors of the mutype in the ACB, whereas locomotor stimulation is due to an action on delta type receptors, an effect which may be masked by simultaneous stimulation of mu-type receptors under certain conditions. Kappa-type receptors apparently are not involved in any of these effects. In addition, a diffusion of DADL to the adjacent SM may contribute to locomotor stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00634235
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of cocaine on the EEG power spectrum of rats are significantly altered after its repeated administration: do they reflect sensitization phenomena? (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 353 (1996), S. 545-551 
    Details
    ISSN: 1432-1912
    Keywords: Key words Cocaine ; Locomotor activity ; Sensitization ; EEG ; Dopamine receptors ; Locomotoractivity ; Conditioned place preference
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  It was previously shown that a moderate dose of cocaine (10 mg/kg i.p.) produces a pattern in the EEG power spectrum which indicates a preferential activation of dopamine D1-like receptors, namely a decrease of power in most of the frequency bands. In contrast, a large dose of cocaine (30 mg/kg i.p.) produces a decrease of power in most of the frequency bands as well, but a selective increase in the alpha-1 band, characteristic for an additional activation of dopamine D2-like receptors. In the present experiments, it was studied in rats, if in the course of sensitization, a shift from D1-like to additional D2-like receptor activation will occur or not. For this study, the animals were treated 10 times with cocaine (either 10 or 20 mg/kg) and, after a drug free interval of 4 days, tested with the same dose administered previously. Acute administration of 10 mg/kg of cocaine increased the locomotor activity slightly and its effect tended to be enhanced after repeated administration. Twenty mg/kg cocaine increased the locomotor activity more than the 10 mg/kg dose and its effect was significantly enhanced after repeated treatment. In addition, it was shown that the dose of 10 mg/kg of cocaine which activates D1- but not D2-like receptors is sufficient to elicit conditioned place preference. Ten mg/kg of cocaine produced a decrease of power in most of the frequency bands and this effect was slightly more pronounced after repeated treatment. Twenty mg/kg of cocaine acutely also produced a decrease in power in most of the frequency bands, but did not decrease the power in the alpha-1 band, being just at the threshold of activating D2-like receptors as well. Repeated administration led to a significant increase in power in the alpha-1 band and a less pronounced one in the alpha-2 band. This observation demonstrates that sensitization to cocaine can be manifest in the EEG and that after a certain dosage, a shift from an activation of D1-like dopamine receptors to an additional activation of D2-like receptors becomes obvious.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169174
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of cocaine on the EEG power spectrum of rats are significantly altered after its repeated administration: do they reflect sensitization phenomena? (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 353 (1996), S. 545-551 
    Details
    ISSN: 1432-1912
    Keywords: Cocaine ; Locomotor activity ; Sensitization ; EEG ; Dopamine receptors ; Locomotor activity ; Conditioned place preference
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It was previously shown that a moderate dose of cocaine (10 mg/kg i.p.) produces a pattern in the EEG power spectrum which indicates a preferential activation of dopamine D1-like receptors, namely a decrease of power in most of the frequency bands. In contrast, a large dose of cocaine (30 mg/kg i.p.) produces a decrease of power in most of the frequency bands as well, but a selective increase in the alpha-1 band, characteristic for an additional activation of dopamine D2-like receptors. In the present experiments, it was studied in rats, if in the course of sensitization, a shift from D1-like to additional D2-like receptor activation will occur or not. For this study, the animals were treated 10 times with cocaine (either 10 or 20 mg/kg) and, after a drug free interval of 4 days, tested with the same dose administered previously. Acute administration of 10 mg/kg of cocaine increased the Locomotor activity slightly and its effect tended to be enhanced after repeated administration. Twenty mg/kg cocaine increased the locomotor activity more than the 10 mg/kg dose and its effect was significantly enhanced after repeated treatment. In addition, it was shown that the dose of 10 mg/kg of cocaine which activates D1- but not D2-like receptors is sufficient to elicit conditioned place preference. Ten mg/kg of cocaine produced a decrease of power in most of the frequency bands and this effect was slightly more pronounced after repeated treatment. Twenty mg/kg of cocaine acutely also produced a decrease in power in most of the frequency bands, but did not decrease the power in the alpha-1 band, being just at the threshold of activating D2-like receptors as well. Repeated administration led to a significant increase in power in the alpha-1 band and a less pronounced one in the alpha-2 band. This observation demonstrates that sensitization to cocaine can be manifest in the EEG and that after a certain dosage, a shift from an activation of D1-like dopamine receptors to an additional activation of D2-like receptors becomes obvious.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169174
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    Paper (German National Licenses)
    Fulltext
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