Cholecystokinin (CCK) is an important satiety factor, acting via the vagus nerve to influence: central feeding centers. CCK binding sites have been demonstrated in the vagal sensory nodose ganglion and within the nerve proper. Using in situ hybridization, expression of the CCKA and (B) receptors (Rs), as well as of CCK itself, was studied in the normal nodose ganglion (NG), and after vagotomy, starvation and high-fat diet. CCKA-R mRNA expression in dorsal root ganglia (DRGs) was also explored. In the NG, 33% of the neuron profiles (NPs) contained CCKA-R mRNA and in 9% we observed CCKB-R mRNA. CCK mRNA was not found in normal NGs. Peripheral vagotomy decreased the number of CCKA-R mRNA-expressing NPs, dramatically increased the number of CCKB-R mRNA, and induced CCK mRNA and preproCCK-like immunoreactivity in nodose NPs. No significant differences in the number of NPs labelled for either mRNA species were detected following 48 h food deprivation or in rats fed a high-fat content diet. In DRGs, 10% of the NPs expressed CCKA-R mRNA, a number that was not affected by either axotomy or inflammation. This cell population was distinct from neurons expressing calcitonin gene-related peptide mRNA. These results demonstrate that the CCKA-R is expressed by both viscero- and somatosensory primary sensory neurons, supporting a role for this receptor as a mediator both of CCK-induced satiety and in sensory processing at the spinal level. The stimulation of CCK and CCKB-R gene expression following vagotomy suggests a possible involvement in the response to injury for these molecules. (C) 2001 Elsevier Science B.V. All rights reserved.