Tenascin (TN), an extracellular matrix glycoprotein, exhibits various functions in the developmental stage of the mammalian brain. TN-gene deficient mice show abnormal behavior such as hyperlocomotion and poor swimming ability, and this abnormal behavior may derive from a low level of dopamine transmission in the striatum or hippocampus of the TN-gene disrupted mouse brain. We assayed preprotachykinin A (PPT) and cholecystokinin (CCK) mRNAs in the terminal fields of the dopamine neuron. The levels of PPT mRNA were significantly higher in the striatum, and the expression of CCK mRNA was markedly augmented in the hippocampus of the TN-knockout mice, compared to the wild or heterozygous mice. One possible explanation of the changes of PPT and CCK mRNA expressions is functional compensation against the low level of dopamine turnover rate in the TN-knockout mouse brain.