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Molecular Pharmacology, Vol 4, 187-195, Copyright © 1968 by the American Society for Pharmacology and Experimental Therapeutics
1 Departments of Pharmacology and Experimental Therapeutics and Psychiatry and
Behavioral Sciences, The Johns Hopkins University School of Medicine,
Baltimore, Maryland 21205
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.
Note:
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.