【摘 要】
：
Clinical studies have shown that about one third of patients with chronic pain suffer from shortterm memory deficit.Our recent work demonstrates that the up-regulation of TNF-α in hippocampus underlie
【机 构】
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Pain Research Center,Department of Physiology,Zhongshan School of Medicine,Sun Yat-sen University,Gu
【出 处】
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International Conference for Physiological Sciences 2012(201
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Clinical studies have shown that about one third of patients with chronic pain suffer from shortterm memory deficit.Our recent work demonstrates that the up-regulation of TNF-α in hippocampus underlies this form of memory impairment.In this study, we found that oral application of magnesiumL-threonate (MgT)could restore the short-term memory deficit and long-term potentiation (LTP) deficit at CA3-CA1 synapses in hippocampus induced by spare nerve injury (SNI).As NMDA receptor channels are critical for memory and LTP, we recorded the ratio of NMDA/AMPA current in hippocampal slices incubated at different concentrations of Mg2, from sham-operated and SNI rats.The results showed that with Mg2+ concentration at 0.8 mM/L, the ratio of NMDA/AMPA current was significantly lower in SNI rats than that in sham-operated rats.While after incubated in 1.2 mM Mg2+ for 5 h, the ratio in SNI rats was considerably higher than that in 0.8 mM Mg2+ in SNI rats, indicating that elevating Mg2 may improve NMDA channel function.Furthermore, we found that TNF-αcould decrease the ratio of NMDA/AMPA in a concentration-dependent manner in cultured hippocampal slices and the effect was inhibited when the slices were incubated in the culture medium with 1.2mM Mg2+.Also, western blot and immunohistochemical analysis showed that oral application of MgT inhibited the increase of TNF-α in hippocampus induced by SNI.Our findings suggested that MgT could restore the short term memory deficit induced by peripheral nerve injury via inhibition of TNF-α in rats.
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