Postsynaptic GluR2 Involved in Amelioration of Aβ-Induced Memory Dysfunction by KAIXIN-San Through Rescuing Hippocampal LTP in Mice.

Kaixin-San (KXS), a Chinese formula, was used to treat "amnesia," a senile dementia in the modern world. This formula was reported to improve behavioral performances in many animal models. This study was designed to explore how KXS has improved amyloid-β (Aβ)-induced memory dysfunction in mice. The mouse models were achieved through unilateral ventricle injection with Aβ42. The effects of KXS on memory improvement were evaluated by the step-down test. The electrophysiological changes induced by KXS were measured by long-term potentiation (LTP) analysis in the hippocampus in vivo. The expression of glutamate receptor 2 (GluR2) was observed through immunohistochemical staining. Behavioral experiment outcome demonstrated reduced avoidance time and increased error time during the step-down test in the mice of Aβ group. This memory impairment, however, was reversed by KXS. Electrophysiological experiment showed no significant difference between Aβ group and KXS group either in the size or the shape of field excitatory postsynaptic potentiation recorded from perforant path to dentate gyrus pathway. However, LTP in this region was reduced by Aβ and recovered by KXS administration. Moreover, immunohistochemical staining showed increased postsynaptic GluR2 expression in DG area in KXS group. These findings suggest that Aβ results in impairment to memory function of the animals, and KXS protects the animal from memory loss by rescuing LTP through postsynaptic mechanism which refers to increasing GluR2 expression.