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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 322 (1983), S. 322-324 
    ISSN: 1432-1912
    Keywords: Corpus striatum ; (+)-Amphetamine ; Acetylcholine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The electrically evoked, calcium-dependent release of 3H-acetylcholine from slices of rat striatum was inhibited in a concentration-dependent manner by (+)-amphetamine (0.2–20 μM). This inhibitory effect of (+)-amphetamine was unaffected by depletion of the endogenous stores, of dopamine by pretreatment with rescrpine (5 mg/kg, 24h). However, the combined treatment of reserpine with α-methyl-p-tyrosine (300 mg/kg) or NSD 1015 (100 mg/kg) reduced significantly these inhibitory effects of (+)-amphetamine. Similar results were obtained after chronic 6-hydroxydopamine lesions of the corpus striatum. The inhibition of 3H-acetylcholine release by (+)-amphetamine in rats pretreated with reserpine was potentiated in the presence of 10 μM pargyline. These results support the view that the inhibitory effects of (+)-amphetamine on the electrically-evoked release of 3H-acetylcholine are mediated by dopamine released from a special pool of newly synthetized transmitter rather than through a direct action on an amphetamine recognition site or receptor.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 329 (1985), S. 123-127 
    ISSN: 1432-1912
    Keywords: Amphetamine ; Corpus striatum ; Endogenous dopamine ; Dopamine release ; Reserpine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The release of endogenous dopamine evoked by electrical stimulation or by exposure to (+)-amphetamine (10 μM) was determined in superfused striatal slices of the rat. The spontaneous and the electrically-evoked release of dopamine were significantly increased in the presence of nomifensine (10 μM). After reserpine pretreatment (5 mg/kg, s.c., 24 h), the striatal dopamine content was reduced by about 90%. Exposure to 10 μM (+)-amphetamine during 2 min released similar amounts of dopamine from striatal slices of untreated or reserpine pretreated rats. Similar results were obtained when monoamine oxidase activity was inhibited in vivo with pargyline. Pretreatment with reserpine does not modify the (+)-amphetamine-induced release of dopamine, in spite of the marked reduction of the striatal dopamine content. These results provide direct evidence for the view that (+)-amphetamine releases dopamine from a special, reserpine-resistant pool of newly synthetized transmitter.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1912
    Keywords: Monoamine oxidase inhibition Dopamine release ; Amphetamine ; Potassium depolarization ; Corpus striatum ; Substantia nigra
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of monoamine oxidase inhibition on the release of 3H-dopamine induced by exposure to amphetamine or to potassium were studied in the corpus striatum and in the substantia nigra of the rat using identical in vitro experimental conditions. Marked differences between the two areas of the dopaminergic neurone were found. In the corpus striatum, release of 3H-dopamine was observed during exposure to low concentrations of amphetamine, while considerably higher concentrations of amphetamine were required to elicit 3H-dopamine release from the substantia nigra. The difference in the effects of amphetamine on the release of 3H-dopamine from the substantia nigra and the rat corpus striatum was observed independently of whether monoamine oxidase activity was intact or inhibited by pargyline. Exposure to potassium was also more effective in inducing 3H-dopamine release from the striatum than from the substantia nigra, but the difference was less pronounced than that observed for amphetamine. Since inhibition of monoamine oxidase by pargyline results in changes in the proportions of vesicular and axoplasmic dopamine, conclusions about the in vivo effects of amphetamine on dopaminergic neurotrans-mission should not be based on in vitro studies in which the enzyme is inhibited. In addition, in vitro studies on dopamine release by nerve depolarization should be carried out under the physiological conditions in which monoamine oxidase is not inhibited by drugs.
    Type of Medium: Electronic Resource
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