Abstract
THE interactions of amphetamines and catecholamines in the peripheral sympathetic nervous system and in the brain have been widely studied. Amphetamines have been reported to mimic catecholamines at their receptor sites1–3, inhibit monoamine oxidase4, impair reuptake mechanism for the catecholamines5 and to directly release catecholamines into the synaptic cleft6. Although the consensus of the available literature indicates that d-amphetamine indirectly stimulates catecholamine postsynaptic receptors by increasing the release and blocking the reuptake of catecholamines7,8, the question whether dopamine, noradrenaline or both, are of importance for the central actions of d-amphetamine is controversial7,8. Recently, α-adrenergic9, β-adrenergic10–13 and dopaminergic14,15 receptors in brain tissue have been successfully identified by measuring the binding of radiolabelled ligands to specific receptor sites. Availability of such methods has permitted the examination of the effects of acute and chronic administration of psychotropic drugs on the postsynaptic catecholaminergic receptors in brain tissue13,16. We report here the effects of acute and chronic administration of d-amphetamine on the postsynaptic β-adrenergic receptors in rat brain.
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BANERJEE, S., SHARMA, V., KUNG, L. et al. Amphetamine induces β-adrenergic receptor supersensitivity. Nature 271, 380–381 (1978). https://doi.org/10.1038/271380a0
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DOI: https://doi.org/10.1038/271380a0
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