Objective To investigate the effects of electroacupuncture(EA) on the expression of related proteins in the brain-derived neurotrophic factor(BDNF)/mammalian target of rapamycin complex 1(mTORC1) signaling pathway and synapse-associated proteins and the density of dendrite spines in the prefrontal cortex(PFC) of depression model rats

and to reveal the underlying mechanism by which EA regulates the synaptic plasticity to improve depressive symptoms. Methods Thirty-six healthy male Sprague-Dawley(SD) rats were randomly divided into normal group

model group

EA group

and scopolamine(SCOP) group

with 9 in each group. The depression model was established by exposing rats to chronic unpredictable mild stress(CUMS) combined with isolated feeding. Rats in the EA group were treated with EA(2 Hz/100 Hz

1-1.2 mA) at “Baihui”(GV20)

“Yintang”(EX-HN3)

“Hegu”(LI4)

and “Taichong”(LR3)

20 min each time

once per day

for 14 d

while those in the SCOP group treated with intraperitoneal injection of 25 μg/kg SCOP

once every 16 h

for 14 d. The sucrose preference and feeding latency of rats in each group were observed in the sucrose preference test(SPT) and novelty-suppressed feeding test. The expression levels of proteins in the BDNF/mTORC1 signaling pathway and synapse-associated proteins PSD95

Synapsin Ⅰ

and GluR1 were assayed by Western blot. Golgi-Cox staining was conducted for exploring the total density of dendritic spines on the apical dendrites of layer Ⅴ pyramidal neurons in PFC as well as the densities of mature

immature

and filopodial-like dendritic spines. Results Compared with the normal group

the model group exhibited significantly decreased sucrose preference(P<0.001)

prolonged feeding latency(P<0.001)

down-regulated BDNF

mTORC1

phosphorylated mTORC1(p-mTORC1)

PSD95

Synapsin Ⅰ

and GluR1 expression(P<0.001

P<0.01)

and diminished total

mature

and immature spine dendritic densities(P<0.001). Compared with the model group

both EA and SCOP remarkably increased the sucrose preference(P<0.001)

shortened the feeding latency(P<0.001)

up-regulated the BDNF

mTORC1

p-mTORC1

PSD95

Synapsin Ⅰ

and GluR1 expression in PFC(P<0.05

P<0.01

P<0.001)

and elevated the total and immature spine dendritic densities(P<0.001

P<0.01). The density of filopodial-like dendritic spine in the EA group was obviously enhanced(P<0.01)

whereas the mature dendritic spine density in the SCOP group rose sharply(P<0.001). However

there were no significant differences between the EA group and SCOP group(P>0.05). Conclusion EA alleviates the depressive symptoms of CUMS model rats possibly by up-regulating the expression of proteins in the BDNF/mTORC1 signaling pathway and synapse-asso-ciated proteins PSD95

Synapsin Ⅰ

and GluR1

increasing the dendritic spine density

and enhancing the synaptic plasticity in PFC.