The NMDA antagonist MK-801 causes marked locomotor stimulation in monoamine-depleted mice (original) (raw)

Summary

It was shown in the present study that the selective non-competitive N-methyl-D-aspartate (NMDA) antagonist MK-801 [(+)-5-methyl-10,11-dihydroxy-5H-dibenzo(a,d)cyclohepten-5,10-imine] caused a pronounced and dose-dependent increase in locomotion in mice pretreated with a combination of reserpine and α-methyl-para-tyrosine. Haloperidol pretreatment did not antagonize the MK-801-induced stimulation of locomotion. The findings are discussed in relation to the concept of a corticostriatothalamocortical negative feedback loop serving to protect the cortex from an overload of information and hyperarousal. Such a feedback loop would encompass i.a. corticostriatal glutamatergic neurons and it would be modulated by mesencephalostriatal dopaminergic neurons.

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  1. Maria Carlsson
    Present address: Department of Pharmacology, University of Göteborg, Göteborg, Sweden

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  1. Department of Pharmacology, University of Göteborg, Göteborg, Sweden
    A. Carlsson

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  1. Maria Carlsson
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  2. A. Carlsson
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Carlsson, M., Carlsson, A. The NMDA antagonist MK-801 causes marked locomotor stimulation in monoamine-depleted mice.J. Neural Transmission 75, 221–226 (1989). https://doi.org/10.1007/BF01258633

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