Induction but not maintenance of calcium-induced long-term potentiation in dentate gyrus and area CA1 of the hippocampal slice is blocked by nordihydroguaiaretic acid.

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.