Objective Brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin-related kinase receptor B (TrkB), play a critical role in activity-dependent plasticity processes such as long-term potentiation, learning, and memory.It has been shown that BDNF exerts different or even opposite effects on behavior depending on the neural circuit.However, the detailed role of BDNF in memory process on the basis of its location has not been fully understood.Here, we aim to investigate the regional specific involvement of BDNF/TrkB in hippocampal-independent conditioned taste aversion (CTA) memory processes.Methods Real time PCR and ELISA were respectively used to detect the BDNF mRNA and protein changes at various time points after CTA learning.TrkB phosphorylation levels normalized to total TrkB were measured by immunoprecipitation and immunoblotting.Microinjection was used to detect role of endogenous BDNF on CTA memory formation.Results We found region-specific changes in BDNF expression during CTA learning, CTA conditioning induced increased BDNF levels in the central nuclei of amygdala (CeA) and insular cortex, but not in the basolateral amygdala (BLA) and ventromedial prefrontal cortex.Interestingly, we found that the enhanced TrkB phosphorylation occurred at the time point before the increased BDNF expression, suggesting rapid induction of activity-dependent BDNF secretion by CTA learning.Moreover, targeted infusion of BDNF antibodies or BDNF antisense oligonucleotides revealed that activity-dependent BDNF secretion and synthesis in the CeA, but not the BLA, was respectively involved in the short-and long-term memory formation of CTA.Finally, we found that infusion of exogenous BDNF into the CeA could enhance CTA learning.Conclusion These data suggest that region-specific BDNF release and synthesis temporally regulate different CTA memory phases through activation of TrkB receptors.