Objective To observe the effect of electroacupuncture(EA) on the expression of cAMP-response element binding protein(CREB

a key protein for BDNF-TrkB signaling) and it's blinding ability to synaptic key protein in the amygdala and hippocampus of rats with post-traumatic stress disorder(PTSD)

so as to lay a foundation for further study of the interaction mechanism between BDNF-TrkB signaling and synaptic plasticity. Methods Twenty-four male SD rats were randomly divided into blank

model and electroacupuncture(EA) groups

with 8 rats in each group. The PTSD model was established by psychological stress(bondage) and physiological stress(forced swimming and anesthesia). After modeling

EA(2 Hz/100 Hz

1 mA) was applied to "Baihui"(GV20) "Shenting"(GB24) and bilateral "Shenshu"(BL23) for 20 min

once daily for 21 days. The behavioral changes(spontaneous locomotor within 30 min and contextual fear conditioning tests in 7 days) were detected by using a spontaneous locomotor detection box

and a conditioned fear response test chamber

respectively. The expression of CREB was detected by immunohistochemistry and Western blot

separately. The binding abilities of CREB to synaptic proteins(post synaptic density 95 [PSD95]

synaptophysin [SYN] and growth-associated protein 43 [GAP43]) were verified by chromatin-immunoprecipitation(CHIP) technique. Results After modeling

the spontaneous locomotor distance

the expression levels of CREB and the binding ability of CREB to PSD95 protein in the amygdala and hippocampus were significantly decreased(P<0.01)

and the percentage of freezing time significantly increased in the model group relevant to the blank group(P<0.01). Following the intervention

the spontaneous locomotor distance

and the expression levels of CREB and the binding ability of CREB to PSD95 protein were considerably increased in the EA group relevant to the model group(P<0.05

P<0.01). No significant changes were found in the binding abilities of CREB to SYN and GAP43 after modeling and after EA intervention(P>0.05). Conclusion EA can improve the motor activity in PTSD rats

which may be associated with its effect in increasing the binding ability of CREB to the synaptic key protein PSD95 to regulate the interaction between the synaptic plasticity and BDNF-TrkB signaling pathway of the amygdala and hippocampus.