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  • 1
    ISSN: 1432-2072
    Keywords: 6-Hydroxydopamine ; α-Methyltyrosine ; Reserpine ; Shuttle-Box Avoidance ; T-maze Performance ; Bar Press Performance ; Norepinephrine ; Dopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of 6-hydroxydopamine treatment on behavioral performance in an operant, shuttle-box and a T-maze task were examined. In spite of marked depletions of brain catecholamines, 6-hydroxydopamine-treated rats showed no significant reductions in performance level in these tasks. However, administration of 1 mg/kg of reserpine which had no effect in control subjects was found to cause severe disruption of bar press responding on a CRF schedule in 6-hydroxydopamine-treated rats. Similarly, low doses of α-MPT which also had no observable effect in control rats produced a severe depression of performance of not only CRF responding but also responding in the shuttle-box avoidance and T-maze tasks in centrally-sympathectomized subjects. The relationship of these findings to the proposal that catecholamines are important to the maintenance of behavioral responding and to possible mechanisms involved in the behavioral effects of 6-hydroxydopamine are discussed.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: 6-Hydroxydopamine ; Brain Norepinephrine ; Brain Dopamine ; Reserpine ; α-Methyltyrosine ; U-14,624 ; Operant Behavior
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of prior catecholamine reductions produced by 6-hydroxydopamine on the behavioral depressant effects of catecholamine depleting and neuroleptic drugs were examined using a continuously reinforced bar-press response. In spite of large depletions, 6-hydroxydopamine treated rats showed no deficits in performance. Similarly, animals preferentially depleted of norepinephrine or dopamine showed no deficit in this task. When α-methyltyrosine or reserpine were administered at a dose which had minimal effect on responding in control animals, the 6-hydroxydopamine group in which both amines were reduced and the group preferentially depleted of dopamine showed severe deficits in bar-press responding. Responding in rats preferentially depleted of norepinephrine was slightly reduced but not to the extent observed in animals depleted of dopamine. Administration of the dopamine-Β-hydroxylase inhibitor, U-14,624, depressed responding but did not produce differential effects which correlated with brain norepinephrine concentration in the 6-hydroxydopamine-treated groups. Furthermore, the behavioral depression produced after treatment with chlorpromazine, haloperidol, and pimozide was not altered by any of the 6-hydroxydopamine treatments. These findings provide further evidence for the view that dopamine depletion plays a major role in the behavioral depressant effects of α-methyltyrosine and reserpine, but do not eliminate a role for brain norepinephrine.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2072
    Keywords: 6-Hydroxydopamine ; Motor Activity ; d-Amphetamine ; U-14,624 ; α-Methyltyrosine ; L-Dopa ; Stereotypy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The significance of central noradrenergic and dopaminergic neural systems for the locomotor stimulant effects of d-amphetamine were investigated in rats with depletions of norepinephrine, dopamine, or both catecholamines produced by treatment with either reserpine, L-α-methyl-tyrosine (α-MPT), 6-hydroxydopamine (6-OHDA), or the dopamine-Β-hydroxylase inhibitor 1-phenyl-3-(2-thiazolyl)-2-thiourea (U-14,624). In animals pretreated with reserpine, amphetamine-stimulated locomotor activity was blocked by Β-MPT but not by U-14,624 when amphetamine was given l h after these catecholamine synthesis inhibitors. In rats with chronic depletions of brain norepinephrine, dopamine, or both catecholamines produced by different 6-OHDA treatments, both amphetamine-stimulated motor activity and stereotyped behavior were antagonized by treatments reducing dopamine or both catecholamines but not in animals in which brain norepinephrine was reduced. Results are consistent with the view that the locomotor stimulation and stereotyped behaviors produced by d-amphetamine are dependent upon functional dopaminergic neural systems in brain.
    Type of Medium: Electronic Resource
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  • 4
    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
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