Abstract
Histidine decarboxylase activities in the stomachs of freely feeding rats or fasted rats treated with gastrin are 3 and 2 times, respectively, greater than enzyme activity of fasted rats. Administration of gastrin produces a marked increase of gastric histidine decarboxylase in 30 min with maximal effects between 2 and 3 hr, and a decline of enzyme activity to fasting levels after 8 hr. Puromycin and cycloheximide completely prevent the rise of gastric histidine decarboxylase activity induced by gastrin, whereas actinomycin D tends to stimulate this rise in activity. When cycloheximide is administered to freely feeding rats there is an exponential fall in gastric histidine decarboxylase activity with a half-life of 2.1 hr. Cycloheximide treatment accelerates the decline of gastric histidine decarboxylase activity after enhancement by gastrin.
ACKNOWLEDGMENT This research was supported by USPHS grants TO 1-MH-11267 and 1 RO1 NB 07275. Solomon H. Snyder is a recipient of NIMH Research Career Development Award 5 KO3-MH-33128.
- Copyright ©, 1968, by Academic Press Inc.
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