Platelet-activating factor (PAF) is an ether phospholipid that serves as an autacoid in a wide range of biological processes. We found that when PAF was added to hippocampal slices, it induced a stable and concentrationdependent increase in excitatory postsynaptic potential and population spike recordings (long-term potentiation [LTP]). The PAF effect was blocked by the PAF receptor antagonists BN 52021 and WEB 2086 and the N-methylu-aspartate receptor antagonists MK 801 and 2-amino-S-phosphonovalerate. However, these PAF receptor antagonists did not block LTP induced by high frequency stimulation. The facilitation induced by PAF could not be reversed by PAF receptor antagonists. Induction of either PAF-or tetanus-triggered facilitation occluded the subsequent expression of the other, suggesting a common pathway. LTP is a type of synaptic plasticity associated with the formation of memory, and PAF may play an important modulatory role in this process. tntroduction

Platelet-activating factor (PAF, PAF-acether) is a naturally occurring alkyl ether phospholipid(I-0-alkyl, 2-acetyl-sn-glyceryl-3 phosphorylcholine) that acts as an extracellular mediator in a wide range of biological processes (Braquet et al., 1987; Barnes et al., 1989; Boumann, 1991). The finding that psychoactive drugs of the triazolobenzodiazepine class are potent antagonists of PAF action was the first suggestion of a role for PAF in the nervous system (Kornecki et al., 1984). Subsequently, biosynthesis of PAF was detected in neuronal cells (Bussolino et al., 1986) and brain tissue (Kumar et al., 1988); neuroregulatory and neuropathological actions of PAF were demonstrated in cultured neural cells (Kornecki and Ehrlich, 1988) and in brain synaptosomes(Kornecki and Ehrlich, 1991); and specific binding sites for PAF were found in brain membranes (Domingo et al., 1988; Marcheselli et al., 1990). PAF was shown to induce a transient increase in the intracellular Ca*+ concentration in several neuronal