Effect of electroacupuncture on expression of CREB and its ability to bind to synaptic proteins in amygdala and hippocampus of rats with post-traumatic stress disorder

Abstract

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. 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. 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). 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.