Cholecystokinin (CCK), a neuro-gut peptide, occurs not only in the nervous but also in the digestive system. As a first step in elucidating whether CCK gene expression and its physiological functions co-operate in these separate organs, transgenic mice were produced using CCK promoter that directs bacterial beta-galactosidase as a reporter gene. A new transgenic vector was constructed, inserting the SV40 poly A signal 5' to the CCK promoter to impede any transcription upstream of the transgene. A 2.4 kb.p. region upstream to the transcription start site of the mouse CCK gene was used as the promoter. Transgene expression was detected first at embryonic 13.5 days in the central nervous system and increased after birth. The distribution of cells expressing beta-galactosidase transgene agreed fairly well with that of in situ hybridization. In addition, the upregulation of CCK gene expression was clearly demonstrated by expressing beta-galactosidase after injury to the brain. These results indicated that the 2.4 kb.p. of the CCK gene promoter region was sufficient to direct appropriate tissue-specific gene expression in mice.