Platelet-activating factor (PAF; 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine), which is thought to be a retrograde messenger in long-term potentiation (LTP), enhances glutamate release and LTP through an action on presynaptic nerve endings. The PAF antagonist BN 52021 blocks CAI LTP in hippocampal slices, and, when infused into rat dorsal hippocampus pre-or posttraining, blocks retention of inhibitory avoidance. Here we report that memory is affected by pre-or posttraining infusion of the PAF analog 1-O-hexadecyl-2-N-methylcarbamoyl-sn-glycero-3-phosphocholine (mc-PAF) into either rat dorsal hippocampus, amygdala, or entorhinal cortex. Male Wistar rats were implanted bilaterally with cannulae in these brain regions. After recovery from surgery, the animals were trained in step-down inhibitory avoidance or in a spatial habituation task and tested for retention 24 h later. mc-PAF (1.0 ,ug per side) enhanced retention test performance of the two tasks when infused into the hippocampus before training without altering training session performance. In addition, mc-PAF enhanced retention test performance of the avoidance task when infused into (i) the hippocampus 0 but not 60 min after training; (ii) the amygdala immediately after training; and (iii) the entorhinal cortex 100 but not 0 or 300 min after training. In confirmation of previous findings, BN 52021 (0.5 ,lg per side) was found to be amnestic for the avoidance task when infused into the hippocampus or the amygdala immediately but not 30 or more minutes after training or into the entorhinal cortex 100 but not 0 or 300 min after training. These findings support the hypothesis that memory involves PAF-regulated events, possibly LTP, generated at the time of training in hippocampus and amygdala and 100 min later in the entorhinal cortex.Learning and memory probably involve activity-dependent modifications of synaptic efficiency (1, 2). Although this concept of synaptic plasticity in information storage originated from the century-old work of Santiago Ramon y Cajal, the cellular and molecular events underlying memory and learning are not clearly understood.LTP (long-term potentiation) is a model of activitydependent synaptic plasticity (1) and is a candidate mechanism for certain forms of memory in the mammalian brain (3). LTP is a persistent enhancement of excitatory neurotransmission that results from high-frequency activation of hippocampal synapses as well as of other brain regions (1,4). Activitydependent potentiation involves the N-methyl-D-aspartate

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