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  • 3-Methoxy-4-hydroxyphenylglycol (MHPG)  (1)
  • 5-Hydroxytryptamine  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Use of 6-hydroxydopamine to deplete brain catecholamines in the rhesus monkey: effects on urinary catecholamine metabolites and behavior (1981)
    Springer
    Psychopharmacology 73 (1981), S. 1-11 
    Details
    ISSN: 1432-2072
    Keywords: 6-Hydroxydopamine ; Rhesus monkey ; 3-Methoxy-4-hydroxyphenylglycol (MHPG) ; Catecholamines ; Social behavior ; Operant performance ; Dyskinesia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The purpose of this study was to determine: 1) whether 6-hydroxydopamine (6-OHDA), previously shown to deplete brain catecholamines (CA) in rodents, depletes brain CA in rhesus monkeys; 2) whether depletion of brain CA produces changes in behavior; and, 3) whether urinary output of 3-methoxy-4-hydroxyphenylglycol (MHPG) reflects brain norepinephrine (NE) depletions. Repeated intracerebroventricular (ICV) injection of 6-OHDA (N=20; 15.5–73.3 mg/subject) produced chronic changes in social behavior and, at higher dosages, reduced output of urinary MHPG. However, 4 weeks after the last ICV 6-OHDA injection, urinary MHPG excretion returned to baseline values and whole brain CA content was not reliably different from control. A single treatment with 6-OHDA microinjected into the substantia nigra (SN) (N=12; 120–240 μg/subject) produced chronic whole brain depletions of brain CA without depleting serotonin. Reductions in brain CA were associated with a specific set of motor behaviors, aphagia, and adipsia. SN 6-OHDA produced greater brain NE depletions than ICV 6-OHDA, but urinary MHPG output was not reduced. SN 6-OHDA treated subjects showed chronic changes in social behavior and were more sensitive to the operant response rate decreasing effects of alpha-methyl-para-tyrosine (AMPT) than control subjects. Subjects with the largest depletions of brain dopamine (DA) (〉90%) were hypokinetic, rigid, and had a distal limb tremor. These results show that SN but not ICV injection of 6-OHDA can deplete brain CA in the rhesus monkey. The most prominent behavioral changes were characterized bydisturbances in motor function. Urinary MPHG output does not reflect depletions of brain NE in this species.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00431091
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Involvement of brain monoamines in the stimulant and paradoxical inhibitory effects of methylphenidate (1975)
    Springer
    Psychopharmacology 44 (1975), S. 5-10 
    Details
    ISSN: 1432-2072
    Keywords: Methylphenidate ; Locomotor Activity ; 5-Hydroxytryptamine ; Tyrosine Hydroxylase Inhibition ; Dopamine ; Β-Hydroxylase Inhibition ; p-Chlorophenylalanine ; 5,7-Dihydroxytryptamine ; 5-Hydroxytryptophan ; MAO Inhibitors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The significance of central noradrenergic, dopaminergic and serotonergic neural systems for the locomotor stimulant effects of methylphenidate was investigated in the rat. In order to study the role of brain catecholamines, rats were pretreated with reserpine (2.5 mg/kg) followed 24 hrs later by treatment with α-methyltyrosine (25 mg/kg) or U-14,624 (75 mg/kg), a dopamine-Β-hydroxylase inhibitor. In these experiments, methylphenidate stimulated motor activity was antagonized by α-methyltyrosine and enhanced after treatment with U-14,624, suggesting that release of newly synthesized dopamine is important to a locomotor stimulant action of methylphenidate. Evidence implicating brain serotonin in the actions of methylphenidate was obtained in rats pretreated with pargyline or p-chlorophenylalanine (PCPA). Administration of pargyline 1 hr prior to methylphenidate was found to reduce the locomotor activity induced by methylphenidate and this was antagonized by pretreatment with low doses of PCPA. Higher doses of PCPA caused a significant elevation of methylphenidate induced activity which could be reduced by 5-hydroxytryptophan. Destruction of serotonergic neurons with 5,7-dihydroxytryptamine also potentiated methylphenidate induced locomotion. These latter findings suggest that serotonergic fibers have an inhibitory function in brain. These results are discussed in relation to the possible mechanism by which methylphenidate may act in hyperkinesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00421175
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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