TRPV1 is a polymodel non-selective cation channel that can be activated by capsaicin, pH, heat and other noxious stimuli. In the last few years, expression of trpv1 has been certified in variety tissue and apparented different with species. However, distribution of trpv1 in the CNS is still a controversial question.Increasing evidences has demonstrated important role of TRPV1 in central system diseases, however the functions of TRPV1 in the brain are still an open question. Tom Schilling revealed that TRPV1 cation channels may provide potential therapeutic targets to reduce microglia-induced oxidative stress in Alzheimer’s disease (AD). Clinical data showed that TRPV1 mRNA and protein were up-regulated in the mesial temporal lobe epilepsy patients. Our research aims to detect the expression of TRPV1 in hippocampus and cortex on developmental brain in C57BL/6 mice and explore the potential drug therapeutic targets in the age-dependent diseases. Mice model was using differential development C57BL/6 mice: 2-week old (n=12), 4-week old (n=12), 8-week old (n=12) and 16-week old (n=12) mice, respectively corresponded to infancy, adolescence, adult stage and gerontic in human. Detecting the expression of TRPV1 mRNA and protein were respectively by qRT-PCR, western blotting and immunohistochemistry. Values are means ± S.E.M., compared by nonparametric tests. Our findings revealed that trpv1 channel express in both two brain regions in C57B/6 mouse showing age-dependent. Comparing to 2-week old mouse in hippocampus, the mRNA level of 4,8,16 weeks old mice are increased, the relative expression in those groups are enhanced separately by 1.93 fold,11.43 fold and 1.8 fold (*p<0.05). In cortex, the difference multiple of 4,8,16 weeks old mice were about 2.66 fold, 3.02 fold and 2.21 fold compared to 2 weeks old mice, respectively. In addition, protein level of 4,8,16 weeks old mice in hippocampus and cortex from western blotting and immunohitochemistry both increased comparing to 2 weeks old mouse, in keeping with mRNA level both in hippocampus and cortex. These results indicated that TRPV1 expression in developing brain showed an age-dependence pattern, thus raised the possibility that TRPV1 may play a key role related to age and developing brain diseases. Our study provides a basis for further studies of TRPV1 as a possible newly pharmacology target for age-dependent diseases such as Alzheimer’s disease, parkinson’s disease, age-dependent epileptic encephalopathy and febrile seizures.