Abstract: Objective :To use all-trans-retinoic (ATRA) to induce the expression of TrkB in neuroblastoma cell line- SH- SYSY(SYSY), to add BDNF to causes autophosphorylation of TrkB (p-TrkB)and activate TrkB/BDNF signal transudation, than to observe the change of NB cells' sensibility to chemotherapy drug, i.e. cisplatin (CDDP) before and after the blocking of TrkB receptor pathway by specific tyrosin kinase inhibitor K252a, which can block TrkB receptor pathway. Methods :ATRA was used to induce the expression of TrkB of SYSY cells, and the addition of BDNF, CDDP, and K252a;MTT assay was performed to examination the channg of cell survival rate. Apoptosis rate was measured by flow cytometry CM). Immunohistochemistry was employed to measure the expression of the autophosphorylating TrkB. Results :The expression of TrkB could specially be induced by ATRA and TrkB- BDNF signal pathway could be activated. TrkB was autophosphorylated after the addition of BD-NF. The autophosphorylation of TrkB and TrkB/BDNF signal pathway could be blocked by K252a, the survival rate of SYSY after treating with CDDP was decreased and the apoptosis rate was increased. Conclusions : The blockage of TrkB/BDNF signal pathway can increase the sensibility of chemotherapyin co- expressing TrkB and BDNF NB. Therefore treatment with inhibitors of TrkB receptors may provide potential novel therapeutic options in NB.