The satiating potency of cholecystokinin (CCK) has been well characterized, including its mediation by capsaicin-sensitive vagal primary afferents. We have previously shown that peripherally administered CCK activates the MAPK-signaling cascade in a population of nucleus of the solitary tract (NTS) neurons, and that preventing ERK1/2 phosphorylation partly attenuates CCK's satiating potency. The aim of this study was to identify the neurochemical phenotypes of the NTS neurons that exhibit CCK-induced activation of ERK1/2. Using confocal microscopy we first demonstrate that intraperitoneal CCK administration increases the number of neurons that express phosphorylated ERK1/2 (pERK1/2) in the medial and commissural subnuclei of the NTS. We also demonstrate that the percentage of tyrosine hydroxylase-immunoreactive neurons exhibit induction of ERK-phosphorylation as determined by double-labeling with a phospho-specific antibody. Using Western blotting, we then show that the robust increase in tyrosine hydroxylase phosphorylation obtained with ip CCK is significantly attenuated in rats pretreated with the ERK-pathway blocker U0126 injected into the 4^th ventricle. In addition, CCK injections increased pERK1/2 labeling in POMC neurons in the NTS. In contrast, only the rare GAD67, nNOS, and leptin responsive neuron exhibited CCK-induced pERK immunoreactivity. We conclude that activation of POMC-immunoreactive neurons and tyrosine hydroxylase activity via the ERK-signaling pathway in the NTS partly contributes to CCK's satiating effets.