Objective To observe the effect of electroacupuncture(EA) at “Baihui”(GV20) and “Shenshu”(BL23) on the pathological injury of neurons in SAMP8 mice and the anti-inflammatory effect on neuron repair

providing a new experimental basis for EA prevention and treatment of Alzheimer's disease. Methods Twelve 7-month-old SAMP8 mice were randomly divided into model and EA groups

and 6 SAMR1 mice of the same age and genetic background were used as normal group. Mice in the EA group were needled at GV20 and bilateral BL23

and EA(1 mA

2 Hz) was applied to bilateral BL23 for 15 min

once daily

10 d as a course for a total of 4 courses

with an interval of 1 d. Mice in the normal and model groups were captured and fixed in the same way as the EA group. The spatial learning and memory ability was detected by Morris water maze test. Neuronal nuclear antigen(NeuN) positive expression and the number of NeuN-positive cells in dentate gyrus(DG) were detected by immunofluorescence staining. The protein expression levels of ionized calcium binding adapter molecule 1(Iba-1)

tumor necrosis factor-α(TNF-α)

interleukin(IL)-6 and IL-1β in hippocampus were detected by Western blot. The ultrastructure of nerve cells in DG was observed by transmission electron microscopy. Results Compared with the normal group

the average escape latency was prolonged(P<0.01)

the number of platform crossing was significantly reduced(P<0.01)

the average fluorescence intensity of NeuN and the number of NeuN-positive cells in hippocampus DG region decreased(P<0.05)

the expression levels of Iba-1

TNF-α

IL-6 and IL-1β in hippocampus were increased(P<0.05) in the model group.Compared with the model group

the ave-rage escape latency was shortened(P<0.01)

the number of platform crossing times was significantly increased(P<0.01)

the average fluorescence intensity of NeuN and the number of NeuN-positive cells in hippocampus DG region increased(P<0.05)

the expression levels of Iba-1

TNF-α

IL-6 and IL-1β in hippocampus were decreased(P<0.05) in the EA group. The morphology of nerve cells in the hippocampus DG region was normal

and the organelles in the cytoplasm were clear

complete and regularly distributed in the normal group. However

the morphology of nerve cells in the model group was seriously irregular

which was also irregular in EA group but somewhat relieved compared with model group. Conclusion EA at GV20 and BL23 can improve the learning and memory ability of SAMP8 mice

which may be related to inhibiting the neuroinflammatory response

increasing the number of neurons and improving the ultrastructure of the DG region of the hippocampus to play the role of neuron protection.