It has been reported1that children with Mongolism demonstrate an idiosyncrasy to atropine with a significantly increased rate of pupillary dilatation after conjunctival instillation. One possible explanation of this hypersensitivity may be that in Mongolism there is a diminished availability of some natural antagonist to atropine. Now one such substance is serotonin which has been shown to have an action in pharmacological opposition to atropine in rabbit intestine2and guinea pig ileum.3Moreover, we have found that in Mongolism there is a decreased urinary excretion of 5-hydroxyindoleacetic acid,4the end-product of serotonin. The mean seven-hour excretion of 5-HIAA after an oral dose of 250 mg/kg.dl-tryptophan was 47μg/kg. for 16 children with Mongolism as opposed to 66.0μg/kg. for 13 normal controls. While these differences are probably not significant by the Aspin Welch Test5(p= <0.1 and >0.05), a similar trend was shown in another
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Donough OʼBrien (1960) studied this question.
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