The cephalic phase of gastric secretion occurs even before food enters the stomach, especially while it is being eaten. It results from the sight, smell, thought, or taste of food; and the greater the appetite, the more intense is the stimulation. Neurogenic signals that initiate the cephalic phase of gastric secretion originate from the cerebral cortex, and in the appetite centers of the amygdala and hypothalamus. They are transmitted through the dorsal motor nuclei of the vagi, and then through the vagus nerve to the stomach. This phase of secretion normally accounts for about 20 percent of the gastric secretion associated with eating a meal. This enhanced secretory activity brought on by the thought or sight of food is a conditioned reflex. It only occurs when we like or want food. When appetite is depressed this part of the cephalic reflex is inhibited.
Cephalic phase causes ECL cells to secrete histamine and increase HCl acid in the stomach. There will also be an influence on G cells to increase gastrin circulation.
Chain of Events—Nervous System and Hormone System:
- Thinking of food (i.e., smell, sight) stimulates the cerebral cortex.
- The cerebral cortex sends messages to hypothalamus, the medulla, and the parasympathetic nervous system via the vagus nerve, and to the stomach (gastric glands in walls of fundus and body of stomach).
- Gastric glands secrete gastric juice.
- When food enters stomach, the stomach stretches and activates stretch receptors.
- Receptors send message to the medulla, and then back to the stomach via the vagus nerve.
- Gastric glands secrete gastric juice.
- Chemical stimuli (i.e., partially digested proteins, caffeine) directly activate G-cells (enteroendocrine cells) located in the pyloric region of the stomach to secrete gastrin; this in turn stimulates gastric glands to secrete gastric juice.