Objective:AFM1-BSA and AFM1-OVA were synthesized and then identified in this experiment.Methods: Using oximation method ,AFM1 was transformed to oxime compounds while the reaction process was monitored via TLC method aiming to identify the compounds.Coupled with carrier protein BSA and OVA respectively , we obtained AFM1-BSA and AFM1-OVA, then identified synthetic antigen via UV spectrophotometry and SDS-PAGE.Antigens were injected into experimental animals , finally obtaining the murine multi-antiserum.Eventually , the multi-antiserums were detected via indirect inhibition ELISA method to judge whether the antigens were effectively or not.Results:After oximation reaction ,the migration distance of oxime compounds in the thin layer plate was shorter.The maximum absorption peak of AFM1-BSA occurred in 274 nm,and was inconsistent with both UV absorption peaks of BSA and AFM 1.The electrophoretic velocity of AFM 1-BSA was less than that of BSA.All the titers of three immunized mice were 1×10-4 approximately;the multi-antiserum from No.3 sample had the best sensitivity ,its IC50 was 359.9 ng/ml.Conclusion:In this study,we obtained AFM1 artificial antigen and murine multi-antiserum of high sensitivity.

Objective:To explore the relationship between the Spike and the Gamma rhythm of the local field potential (LFP) in Alzheimer's disease (AD) transgenic mice during fear memory activity.Methods:Six-month-old APP/PS1/tau three transgenic (3xTg) mice and wild-type (WT) mice were divided into 3xTg group and WT group, with 10 mice in each group. The electrodes were embedded into the hippocampus of mice under sterile conditions, and the behavioral experiment of conditioned fear box test was carried out two weeks later. The changes of Gamma rhythm, Spike and Burst firing were recorded and analyzed by the wireless telemetry device which embedded in the mouse head. Finally, the correlation between Gamma rhythm and Spike was calculated by entropy value.Results:(1) In behavioral experiments, the freezing ratio caused by conditioned stimulation (CS) in 3xTg mice was ((54.07±2.32)%), which was significantly lower than that of WT mice ((76.21±2.88)%) ( t=4.796, P<0.01). (2) Simultaneously recorded the average power of the Gamma oscillation in the Pre-CS period of the WT mice was ((11.574±1.147) dB), which increased to ((18.108±1.177) dB) after CS ( t=3.386, P<0.01). After CS administration, the average power of Gamma in 3xTg group((12.346±1.345) dB) was significantly lower than that of WT group ( t=3.423, P<0.01). (3) The frequency of Spike release in WT mice during the Pre-CS period was ((5.667±1.475)times/s), significantly increased to ((11.008±1.335) times/s) after CS ( t=3.542, P<0.01). The frequency of Spike release of 3xTg mice after CS ((5.249±1.033) times/s) was significantly lower than that of WT group ( t=4.788, P<0.01). (4) The Burst duration of WT group in pre-CS and CS period were ((0.550±0.043)s) and ((1.075±0.034)s), respectively. It suggested that the Burst firing frequency of WT group increased significantly after conditional stimulation ( t=5.188, P<0.01). However, the release interval of 3xTg group after CS ((0.619±0.033)s) was significantly lower than that of WT group ( t=3.352, P<0.01). (5) After CS, the Spike-Gamma entropy curve of WT mice was always higher than that of 3xTg mice. The maximum correlation of WT group and 3xTG group were (0.403±0.031) and (0.314±0.028), respectively. The Spike-Gamma correlation of the 3xTg group was significantly lower than WT mice ( t=3.372, P<0.01). Conclusion:The defect of fear memory in Alzheimer's disease may be caused by the disharmony of Spike-LFP (Gamma) distribution.