Food intake suppression induced by fourth ventricular CCK and MTII but not oxytocin and bombesin is partially mediated by activation of the ERK intracellular signaling cascade

• Published in: Appetite 2007-07, Vol.49 (1), p.335-335
• Main Authors: Townsend, R.L., Zheng, H., Patterson, L.M., Berthoud, H.-R.
• Format: Article
• Language: English
• ISSN: 0195-6663; 1095-8304
• DOI: 10.1016/j.appet.2007.03.202

Our previous work suggests that the caudal brainstem mechanisms of food satiation may involve signaling through the mitogen-activated protein kinase ERK1/2 cascade in a population of nucleus of the solitary tract (NTS) neurons. Peripheral administration of CCK and fourth ventricular injection of the stable MC4-receptor agonist MTII led to rapid phosphorylation of ERK1/2 in specific neurons, and CCK as well as MTII-induced suppression of food intake in fasted rats was significantly attenuated by fourth ventricular administration of U0126, a blocker of ERK-phosphorylation. Here, we tested the ability of U0126 to attenuate the satiating effects of oxytocin and bombesin/GRP two other natural ligands that may suppress food intake in the dorsal vagal complex through their hypothalamus-NTS projections. Both, oxytocin (2ìg in 4 V) and bombesin (25 ng in 4 V) suppressed food intake similarly in vehicle and U0126-pretreated rats (30 min intake oxytocin: −2.1 and −2.9 g; bombesin: −2.05 and −2.9 g, respectively; all decreases significant, p