Monoamine mediation of the morphine‐induced activation of mice

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Abstract
Summary: . The dose‐response relationship for hyperactivity in grouped mice following the injection of morphine sulphate has been established. . The activation response can be modified by drugs which affect either catecholamines or indoleamines. . The monoamine precursors l‐DOPA and 5‐hydroxytryptophan potentiate the response. . The monoamine synthesis inhibitors α‐methyl‐p‐tyrosine and p‐chlorophenylalanine reduce the response. . Inhibition of monoamine oxidase activity by pargyline caused a great increase in the response. The simultaneous administration of reserpine resulted in a further potentiation. . Reserpine blocked the response whenever it was given alone, either before, with or after the injection of morphine. . Blockade of α‐adrenoceptors with phentolamine or phenoxybenzamine reduced the response. . Blockade of tryptaminergic receptors with methysergide or cinanserin also antagonized the response. . The major tranquillizers haloperidol and chlorpromazine reduced the response. Haloperidol was especially effective in this regard. . The tricyclic antidepressant drug imipramine potentiated the response. . The morphine antagonist nalorphine completely prevented the response. . The anticholinergic agent atropine and the antihistaminic drug mepyramine did not affect the response. . We conclude that dopamine, noradrenaline and 5‐hydroxytryptamine are all involved in the normal activation response of grouped mice to morphine, with dopaminergic mechanisms being of primary importance.