Abstract
Very young rats were fed a simple diet which contained enough galactose io cause marked signs of galactose toxicity. After 8-10 weeks, the amounts of serotonin required to cause half-maximal contractions of isolated strips of their stomachs were determined quantitatively. The amount required was much larger than that needed for tissues from control animals (ie, those fed similar amounts of glucose instead of galactose). This was interpreted to mean that the galactose-fed animals had a deficiency of serotonin receptors in their stomachs. By contrast, the responsiveness to acetylcholine was normal. Responsiveness of the galactose stomachs to serotonin could be resotred partially by treatment in vitro with the purified lipids which were found by other tests to have activity expected of the serotonin receptor. In contrast to the findings with stomachs, the isolated uteri of galactose-fed rats were normal in responsiveness to both serotonin and acetylcholine. The suggestion was made that clinical galactose mia of the kind resulting from hereditary lack of the transferase enzyme may be marked by a similar defect in serotonin receptors, and that this defect may help to understand the mental failure found in the disease.