Neuromedin C microinjected into the amygdala inhibits feeding

Abstract Bombesin-like peptides including gastrin releasing peptide and neuromedin C are known to inhibit feeding. Bombesin receptors have been found in moderate to high densities in the amygdaloid body, which is essentially involved in the regulation of feeding and body weight. In the present experiments neuromedin C (15, 30, and 60 ng), a carboxyterminal decapeptid fragment of gastrin releasing peptide, was bilaterally microinjected into the central part of the amygdala in ad libitum fed male CFY rats. Food intake was measured every 5 min for 30 min and also 60 min following neuromedin C or vehicle microinjections. Fifteen nanograms neuromedin C significantly suppressed liquid food consumption for 5 min and 30 ng for 25 min. However, 60 ng was not effective. Neuromedin C effects were blocked by prior application of the bombesin receptor antagonist [Leu13 -ψ(CH2 NH)-Leu14 ]-bombesin. Neuromedin C treatment increased latency to feeding, decreased food intake, decreased the time spent feeding and their ratio, the number and the duration of feeding episodes during the first 5 min, without modifying body temperature or stereotype activity. Results indicate that neuromedin C may decrease the efficiency of feeding and that activation of bombesin receptors in the central amygdala may reduce appetite.