Gastrin‐immunoreactive cells were fairly numerous in the pancreas and upper duodenum of the rat at about the time of birth. A minor population of these cells stained with antibodies directed against the N‐terminal region of gastrin‐34 as well as with antibodies directed against the C‐terminal region. The remainder of the cells stained with the C‐terminally directed antibodies only. Within a fortnight after birth all gastrin‐immunoreactive cells disappeared from the pancreas and were greatly reduced in number in the duodenum; those that remained were probably CCK cells. Gastrin cells were rare in the antrum at birth and remained rare during the first days after birth. They increased in number, slowly until after weaning (15–20 days of age) and then more rapidly, until 25–30 days of age when the gastrin cell density reached that in adult rats. At the time of birth the gastrin concentration in serum was low; the subsequent increase during the first 2 weeks paralleled the development of the antral gastrin cell system. Adult postprandial serum gastrin concentrations were reached 12 days after birth. Somatostatin cells were rare in both the antral and oxyntic mucosa at birth. They increased gradually in number until about a month after birth when the cell density reached that seen in adult rats. In the oxyntic mucosa the ECL and A‐like cells are the predominant endocrine (argyrophíl) cell types. They were not detected until about 4 days after birth. Their number increased slowly until about 30 days of age. They did not stain argyrophil until about 2–4 weeks after birth. Parietal cells were few at birth; ultrastructurally they appeared to be in an active state and histochemically they were shown to contain carbonic anhydrase. The pH of the gastric content of newborn rats was close to 5; 15–17 days after birth the pH was about 4 in freely fed rats. In fasted rats shortly after birth the pH was about 4. Two weeks later it was around 2, which is the pH measured in older rats. Hence, the full capacity for acid secretion is probably not established until weaning. Fasting greatly lowers the serum gastrin concentration and the histidine decarboxylase activity of the ECL cells in adult rats. Before weaning, fasting produced these effects only to a minor degree. We suggest that acid inhibition of gastrin release does not come into play until the parietal cells secrete sufficient amounts of hydrochloric acid to lower the pH below 3, which appears to be the threshold value. This mechanism seems to be fully developed only after weaning. We propose the following sequence of events: circulating gastrin induces maturation of the oxyntic glands (0–20 days), which makes weaning (15–20 days) possible. The change in ingestive behaviour associated with weaning causes an accelerated increase in the gastrin cell density. As a consequence of the progressive maturation of the oxyntic glands, the pH of the gastric content drops, introducing the mechanism for acid inhibition of gastrin release (18‐19th day).