Williams J H, Bliss T V
Division of Neurophysiology and Neuropharmacology, National Institute for Medical Research, Mill Hill, London, U.K.
Neurosci Lett. 1988 May 16;88(1):81-5. doi: 10.1016/0304-3940(88)90319-9.
The effect of the lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA) on the long-term potentiation (LTP) of synaptic transmission produced in excitatory hippocampal pathways by brief exposure to high concentrations of calcium has been investigated in vitro. When high calcium was applied in the presence of 100 microM NDGA, induction of potentiation in the dentate gyrus was blocked, while in CA1 there was an initial potentiation which was not maintained on return to control medium. These effects were not seen with 50 microM NDGA. NDGA did not block the maintenance of calcium-induced LTP. Our results are consistent with the suggestion that arachidonic acid or its metabolites play a role in the genesis of LTP, perhaps by providing a retrograde message from a postsynaptic induction site to a presynaptic maintenance site.
在体外研究了脂氧合酶抑制剂去甲二氢愈创木酸（NDGA）对短暂暴露于高浓度钙所产生的兴奋性海马通路中突触传递长时程增强（LTP）的影响。当在100微摩尔NDGA存在的情况下施加高钙时，齿状回中增强的诱导被阻断，而在CA1区则有一个初始增强，但回到对照培养基后这种增强并未维持。50微摩尔NDGA未观察到这些效应。NDGA并未阻断钙诱导的LTP的维持。我们的结果与以下观点一致，即花生四烯酸或其代谢产物在LTP的发生中起作用，可能是通过从突触后诱导位点向突触前维持位点传递逆行信号来实现的。
