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  • 1
    ISSN: 1432-2072
    Keywords: Amphetamine ; Haloperidol ; Dopamine ; Y-Maze ; Alternation ; Rearing ; Collateral behaviour ; “Switching” ; Novelty ; Attention ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The degree of alternation of arm choice in a Y-maze was examined on 15-min tests over 4 days in rats treated (IP) with saline, amphetamine (0.5 or 2.0 mg/kg) or pretreated with haloperidol (0.08 mg/kg) in each condition prior to test. On day 1 amphetamine-treated animals chose arms at random, but from day 2–4 those receiving the higher dose perseverated their choice. Controls maintained alternation. These effects could be prevented by haloperidol pretreatment. Amphetamine treatment increased the frequency of rearing at the middle, choice-point of the maze more than at the end of an arm. The increase at the mid-point was suppressed by haloperidol pretreatment from day 1 and at the end of an arm from day 2. Amphetamine induced an increase in head-turning/“looking” that was suppressed by haloperidol from day 2. The effect of haloperidol in increasing the duration of an item of looking or rearing at the end of an arm also started later in testing. Two effects are postulated to have occurred: (i) a conflict on day 1 between novelty-controlled sensory or attentional effects that leads to an alternation of arm choice and amphetamine-induced dopaminergic activity that facilitates an alternation of behavioural responses. The result was random choice and increased rearing at the choice point. (ii) On days 2–4 the drug-induced effects on switching motor responses came to control behaviour.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: GABA ; Ventral tegmental area ; Dopamine ; Pictrotoxin ; EOS ; Enkephalin ; Locomotor activity ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The spontaneous activity of rats was measured after activation or inhibition of GABA activity in the ventral tegmental area of the midbrain (VTA). Six hours after bilateral injection of ethanolamine-o-sulphate (GABA agonist) into the VTA, the behavioural activation induced either by d-amphetamine (amph) or by bilateral VTA infusion of a long-lasting enkephalin analogue was completely blocked. Bilateral infusion of picrotoxin (GABA antagonist) into the VTA elicited a short-lived (40 min) dose-dependent behavioural activation which was not reduced either by prior specific lesion of the meso-cortico-limbic dopaminergic neurones or by administration of the opiate antagonist naloxone. Moreover, the simultaneous administration of picrotoxin and amph induced complex changes in behaviour which consisted of additive effects during the first 40 min, followed by an inhibition of the activating effect of amph. Our findings indicate that GABA-mediated inhibition involves both dopaminergic and non-dopaminergic neurones within the VTA, and possible implications for human pathology are discussed.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 84 (1984), S. 431-435 
    ISSN: 1432-2072
    Keywords: Stress ; Amphetamine ; Locomotor activity ; Dopamine ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Adult male rats submitted to mild, 20 min electric foot shock sessions for 10 days displayed an enhanced locomotor response to 0.75 mg/kg (+)amphetamine 24 h after the last shock session, when compared to non-stressed controls. This effect was still present in rats specifically deprived of their forebrain noradrenergic innervation, suggesting the involvement of a dopaminergic mechanism. Cortical and limbic dopamine turnover which increased immediately after acute and repeated foot shocks returned to normal 24 h later, at the time of the pharmacological testing. This fact indicates that a permanent modification of the basal DA activity is not responsible for the above effect apomorphine was enhanced in experimental animals, while hypoactivity resulting from the injection of 0.05 mg/kg apomorphine was similar in control and shocked rats. This latter result suggests the existence of an increased postsynaptic DA sensitivity as a result of repeated stress.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 87 (1985), S. 238-241 
    ISSN: 1432-2072
    Keywords: Conditioned taste aversion ; Vasopressin ; Vasopressin analogs ; Vasopressin antagonist ; Hypertension ; Apomorphine ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rats injected SC with arginine vasopressin (AVP) following consumption of a milk solution developed a marked aversion to the taste of this solution. An analog of vasopressin devoid of pressor activity, dDAVP, was unable to induce conditioned taste aversion. The aversive stimulus properties of AVP were blocked by the vasopressor antagonist dPTyr(Me)AVP. This antagonist did not block apomorphine-mediated conditioned taste aversion. These results demonstrate that AVP induces conditioned taste aversion by interacting with vasopressor-like receptors.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 98 (1989), S. 61-67 
    ISSN: 1432-2072
    Keywords: Rat ; Place preference ; Extinction ; Conditioning ; Naloxone ; Heroin ; Clonidine ; Pimozide ; Memory
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract These experiments examined the neurochemical mechanisms involved in the development and expression of place conditioning produced by heroin. Conditioned place preferences (CPP) lasting up to 8 weeks were obtained with doses of 50–1000 μg/kg heroin, using a regimen shown not to produce physical dependence. Naloxone pretreatment (50 μg/kg) during conditioning prevented the acquisition of heroin-induced CPP, but when given only on the test day, naloxone (50 or 1000 μg/kg) did not prevent the expression of heroin CPP. Clonidine disrupted the establishment of heroin CPP at 20 μg/kg, but disrupted its expression only at debilitating doses (100 and 200 μg/kg). Pimozide attenuated the acquisition (100 μ/kg) and expression (250 μg/kg) of heroin CPP. Together, these results support a role for opioid and catecholamine systems in the acquisition of heroin reinforcement, but they suggest that once heroin CPP is established, its expression in opiate-free subjects is not opiate receptor mediated and is relatively refractory to pharmacological treatments which disrupt acquisition. The data challenge the notion that the conditioned effects of opiates in drug-free animals are related to the release of endogenous opioids, and they also may help to explain why naloxone and clonidine are ineffective in the treatment of opiate addiction.
    Type of Medium: Electronic Resource
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