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Catecholamines in the Brain as Mediators of Amphetamine Psychosis

Solomon H. Snyder

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Abstract

Amphetamine psychosis appears to be a fruitful experimental model of paranoid schizophrenia or paranoid state. A variety of animal and human studies suggest that neurochemical mediation of certain behavioral effects of amphetamine in animals may reflect such mechanisms in human amphetamine psychosis. Specifically, locomotor stimulation appears attributable to central norepinephrine and stereotyped behavior to dopamine, while experiments with amphetamine isomers in man suggest a dopamine mediation of human amphetamine psychosis. Pharmacological and stereochemical evidence suggests that clinical efficacy of phenothiazine drugs in the treatment of schizophrenia may be related to blockade of dopamine receptors. Taken together, these findings provoke the speculation that specific and distinct effects of amphetamines on dopamine and norepinephrine neurons may combine to account for major symptoms of amphetamine psychosis.

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What this paper is about

Amphetamine psychosis appears to be a fruitful experimental model of paranoid schizophrenia or paranoid state. A variety of animal and human studies suggest that neurochemical mediation of certain behavioral effects of amphetamine in animals may reflect such mechanisms in human amphetamine psychosis. Specifically, locomotor stimulation appears attributable to central norepinephrine and stereotyped behavior to dopamine, while experiments with amphetamine isomers in man suggest a dopamine mediation of human amphetamine psychosis. Pharmacological and stereochemical evidence suggests that clinical efficacy of phenothiazine drugs in the treatment of schizophrenia may be related to blockade of dopamine receptors. Taken together, these findings provoke the speculation that specific and distinct effects of amphetamines on dopamine and norepinephrine neurons may combine to account for major symptoms of amphetamine psychosis.

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Available abstract

Amphetamine psychosis appears to be a fruitful experimental model of paranoid schizophrenia or paranoid state. A variety of animal and human studies suggest that neurochemical mediation of certain behavioral effects of amphetamine in animals may reflect such mechanisms in human amphetamine psychosis. Specifically, locomotor stimulation appears attributable to central norepinephrine and stereotyped behavior to dopamine, while experiments with amphetamine isomers in man suggest a dopamine mediation of human amphetamine psychosis. Pharmacological and stereochemical evidence suggests that clinical efficacy of phenothiazine drugs in the treatment of schizophrenia may be related to blockade of dopamine receptors. Taken together, these findings provoke the speculation that specific and distinct effects of amphetamines on dopamine and norepinephrine neurons may combine to account for major symptoms of amphetamine psychosis.

Key concepts: Amphetamine, Dopamine hypothesis of schizophrenia, Neurochemical, Psychosis, Dopamine, Psychology, Schizophrenia (object-oriented programming), Neuroscience

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