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  • 1
    ISSN: 0165-1781
    Keywords: animal models of disease ; bipolar affective disease ; mesolimbic dopamine pathway ; opiate abstinence syndrome ; β-Endorphin
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: Key words Nicotine ; Locomotor activity ; Calcium antagonists ; Nimodipine ; Dopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The effects of nimodipine, an L-type calcium channel antagonist, on nicotine-induced locomotor activity were investigated in drug-naive rats. Nicotine (0.4 mg/kg IP) produced significant increases in locomotion following acute administration. However, when rats were given injections of nimodipine (5, 10, or 20 mg/kg IP) 1 h prior to the test drug, nicotine-induced locomotor activity was altered. Nimodipine 5 mg did not significantly block locomotor activity produced by nicotine. In contrast, pretreatment with 10 and 20 mg nimodipine significantly blocked nicotine-induced locomotor activity. These findings clearly indicate that nicotine-induced locomotion is altered by nimodipine in a dose-dependent fashion. Results further suggest that the effect of nicotine on locomotion is calcium-dependent.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2072
    Keywords: Attention ; d-Amphetamine ; alpha-Flupenthixol ; Mesolimbic dopamine ; Nucleus accumbens ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A test of attentional switching was devised for the rat in which it obtained sucrose reinforcement by an appropriate nose-poke response that discriminated which of two visual events terminated first, in a specially designed chamber. The effect of mesolimbic dopamine depletion (to 20% of control values) produced by infusions of 6-hydroxy-dopamine (6-OHDA) into the nucleus accumbens (N. Acc) on stable discrimination was measured alone and in the presence of a range of doses of d-amphetamine (0.4–2.3 mg/kg IP). The 6-OHDA lesion of the N. Acc impaired post-operative performance transiently by reducing choice accuracy and slowing response latency. By post-operative days 12–16, however, performance recovered to control levels and was not differentially affected by a mainpulation of task difficulty. d-Amphetamine produced dose-dependent performance impairments, which were antagonised by the 6-OHDA treatment. In a second group of N. Acc lesioned rats, the neuroleptic alpha-flupenthixol (0.1–1.0 mg/kg) led to fewer trials being completed and longer latencies than in the sham-operated control group. The results are discussed in terms of the possible attentional mechanisms underlying the d-amphetamine-induced disruption of performance mediated by the N. Acc and of the implications for psychopathology resulting from possible dysfunction of this region.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 92 (1987), S. 25-29 
    ISSN: 1432-2072
    Keywords: Nicotinic receptors ; Rats ; Behavior ; Stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Repeated exposure to nicotine increases both the number of central nicotinic receptors and the behavioral stimulant effect of nicotine. In the present experiments, the behavioral response to nicotine was examined in photocell activity cages. Groups of rats were tested using doses from 0.1 to 1.6 mg/kg both before and after all rats were exposed for 5 days to a common dose of 0.2 mg/kg/day. Prior to the 5-day exposure, there was a dose-related stimulant response to nicotine, with a maximum response seen at 0.4 mg/kg. After the 5-day exposure, the dose-effect curve was shifted upward, so that greater stimulation was produced at each test dose of nicotine. Other groups of rats were exposed for 5 days to doses of nicotine ranging from 0.01 to 0.30 mg/kg/day. On the 6th day all rats received a common test dose of 0.2 mg/kg and their response was measured in the activity cages. In animals exposed to 0.01 mg/kg/day, the test day response was not different from saline controls, but the groups exposed to higher doses showed increased stimulation in response to the common test dose. Measurements of nicotinic receptor binding using [3H]-acetylcholine found increased binding in groups receiving 0.03 mg/kg/day or more, but not in the group that received 0.01 mg/kg/day. The correspondence between the doses that increase behavioral stimulant reactions to nicotine and the doses that increase nicotinic binding suggest that increased receptor numbers may be responsible for the increased behavioral stimulation. However, rats given high doses (1.6 mg/kg, twice per day) did not show increased behavioral stimulation to a test dose of 0.2 mg/kg. In those rats, receptor binding was increased even more than in rats exposed to lower chronic doses. Several hypotheses are offered for this apparent discrepancy.
    Type of Medium: Electronic Resource
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