OBJECTIVE: To study the effect of the active fraction of Tiaoxin recipe (TXR-A), in inhibiting long-term potentiation (LTP) induced by beta amyloid protein (beta-AP) in CA1 area of rats' hippocampal slices. METHODS: The population spike (PS) in CA1 area of hippocampal slices incubated in different medium was recorded before and after LTP was evoked by a 100 Hz, 100 trains high frequency stimulation (HFS), using extracellular microelectrode recording techniques. RESULTS: The amplitude of PS significantly decreased after HFS in hippocampal slices incubated in medium containing 0.2 micromol/L beta-AP for more than 1.5 hour, as compared with that incubated in normal cerebrospinal fluid, the difference was significant, suggesting that beta-AP could inhibit LTP in hippocampal slices. The average amplitude of PS in slices incubated in beta-AP containing medium could be significantly enhanced by adding high-concentration TXR-A or TXR into the medium, and TXR-A showed a better effect of enhancing than that of TXR, indicating that TXR-A could increase the amplitude of LTP. CONCLUSION: TXR-A may be the chief ingredient extracted from TXR for improving beta-AP induced LTP in CA1 area of rats' hippocampus, to antagonise the inhibition of beta-AP on LTP is possibly one of the mechanisms for its intelligence benefiting action.
OBJECTIVE: To study the effect of the active fraction of Tiaoxin recipe (TXR-A), in inhibiting long-term potentiation (LTP) induced by beta amyloid protein (beta-AP) in CA1 area of rats' hippocampal slices. METHODS: The population spike (PS) in CA1 area of hippocampal slices incubated in different medium was recorded before and after LTP was evoked by a 100 Hz, 100 trains high frequency stimulation (HFS), using extracellular microelectrode recording techniques. RESULTS: The amplitude of PS significantly decreased after HFS in hippocampal slices incubated in medium containing 0.2 micromol/L beta-AP for more than 1.5 hour, as compared with that incubated in normal cerebrospinal fluid, the difference was significant, suggesting that beta-AP could inhibit LTP in hippocampal slices. The average amplitude of PS in slices incubated in beta-AP containing medium could be significantly enhanced by adding high-concentration TXR-A or TXR into the medium, and TXR-A showed a better effect of enhancing than that of TXR, indicating that TXR-A could increase the amplitude of LTP. CONCLUSION:TXR-A may be the chief ingredient extracted from TXR for improving beta-AP induced LTP in CA1 area of rats' hippocampus, to antagonise the inhibition of beta-AP on LTP is possibly one of the mechanisms for its intelligence benefiting action.