Long-term potentiation (LTP) of synaptic transmission is a well defined form of neuronal plasticity. The induction of LTP at perforant path-dentate granule cell and Schaffer collateral-CA1 pyramidal cell synapses of the hippocampus is known to require influx of Ca2+ through postsynaptic N-methy1-D-aspartate (NMDA) receptors, while the expression of LTP has been proposed to be mediated at least in part through presynaptic1) Epileptic seizures which are associated with massive increases of intracellular cation concentration may also account for the persistent increases in efficacy of excitatory synaptic transmission in the hippocampus2) This seizure-induced synaptic potentiation (SIP) and LTP have some features in common such as the requirement of NMDA receptor activation1,3) and the consequent increase in neurotransmitter release4,5). These findings led to the concept of a retrograde messenger by which the presynaptic terminals are informed that the postsynaptic sites have been activated. Arachidonic acid (AA) has been recognized as the potential candidate for a retrograde messenger1). Here, we have addressed the involvement of lipid peroxides, especially lipoxygenase metabolites, in neuronal plasticity.