HIV-1 gp120对鼠海马长时程增强效应的影响  

Effect of Long-term Potentiation by HIV-1 gp120 in Rat Hippocampus in vitro

作　　者：董军[1] 陆大祥[1] 沈伟哉[2] 

机构地区：[1]暨南大学医学院病理生理教研室 [2]暨南大学医学院解剖教研室,广东广州510632

出　　处：《病毒学报》2004年第1期34-39,共6页Chinese Journal of Virology

摘　　要：为了探讨人类免疫缺陷病毒Ⅰ型 (HIV 1 )的包膜糖蛋白 gp1 2 0对鼠海马脑片CA1 区的突触传递及可塑性的影响 ,应用离体脑片记录技术 ,记录大鼠海马CA1 区的兴奋性突触后电位 (excitatorypostsynapticpotential,EPSP) ,研究了 gp1 2 0对高频电刺激Schaffer侧支引起的鼠长时程增强效应 (long term potentiation ,LTP)的影响。结果发现 :gp1 2 0对大鼠海马CA1 区LTP产生抑制作用 ,对其基础EPSP没有影响 ,而且这种抑制效应随着gp1 2 0浓度增大而增强 ,即具有剂量依赖性。PKA/PKC蛋白激酶抑制剂H7可以反转这种抑制效应。提示 :gp1 2 0可能是通过抑制海马CA1 区的LTP而参与艾滋病相关性痴呆 (HIV 1associateddementia ,HAD)To understand the effect of gp120 on synaptic transmission and plasticity in the CA 1 region of rat hippocampal slices,we recorded the excitatory postsynaptic potentials (EPSPs) and investigated effect of long term potentiation by gp120 in rat hippocampus in vitro.The results showed that HIV 1 gp120 could inhibit the LTP of CA 1,but it could not inhibit the EPSP of basal.The greater the gp120 concentration was, the stronger the inhibitory effect exerted.Protein kinase A and C inhibitors and the H7 could reverse the inhibition effect.Taken together,this inhibition of LTP by gp120 may contribute to the HAD pathogenesis.

关 键 词：艾滋病 HIV-1 海马脑片 LTP 蛋白激酶抑制剂 

分 类 号：R512.91[医药卫生—内科学]