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机构地区:[1]暨南大学医学院病理生理教研室,广东广州510632
出 处:《中国应用生理学杂志》2005年第2期133-136,共4页Chinese Journal of Applied Physiology
基 金:广东省医学科研基金项目(A2004327);广东省自然科学基金团队项目(039213);广东省中医药管理局项目(400017);国家中管局择优项目(国中医药科2003LHR13号)
摘 要:目的:为了探讨血小板激活因子(platelet activatingfactor,PAF)对大鼠海马脑片CA1区的长时程增强效应(long termpotentiation,LTP)的影响。方法:应用离体脑片电生理记录技术,记录大鼠海马CA1区的兴奋性突触后电位EPSP,研究了PAF对大鼠海马脑片CA1区的突触传递和可塑性的影响。结果:小剂量(1μmol/L)PAF可诱发大鼠海马CA1区LTP的产生;大剂量(10~50μmol/L)PAF不能诱发大鼠海马CA1区LTP的产生,且不能阻止高频电刺激(HFS,100Hz,1000ms×2,每隔20s给予)Schaffer侧支引起的大鼠海马脑片CA1区LTP的形成和维持。大剂量PAF对海马CA1区基础EPSP没有影响。PAF受体拮抗剂银杏苦内酯(ginkgolideB,GB)可拮抗小剂量PAF诱发大鼠海马CA1区LTP的产生。结论:大剂量PAF具有神经毒性,可能是通过抑制海马CA1区的LTP的形成而参与艾滋病痴呆(HIV1associateddementia,HAD)的形成机制。Aim: To explore the effect of platelet-activating factor on long-term potentiation in the CA1 region of rat hippocampal slices. Methods: We recorded the excitatory postsynaptic potentials (EPSPs) and investigated effect of long-term potentiation by PAF in rat hippocampus in vitro. Results: Low doses (1 μmol/L ) of PAF could induce LTP, while higher doses(10~50 μmol/L) of PAF could inhibit induction of LTP.But it could't inhibit the LTP induced by subsequent high frequency stimulation and the EPSP of basal.GB of PAF receptor antagonists could prevent the LTP induced by low doses of PAF,and could't inhibit the LTP induced by HFS. Conclusion: Higher doses of PAF is an HIV-1-induced neurotoxin,it may contribute to the HAD pathogenesis by inhibition of LTP.
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