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Symposium S04: Dynamic Phospholipid Signaling in Life and Death

Synaptic activation promotes the synthesis of potent lipid messengers. Initially free arachidonic and docosahexaenoic acids and platelet-activating factor (PAF, 1-alkyl-2-acetyl-glycero-phosphocholine) are generated, and depending on the context, accumulate and/or are further metabolized into cascades of messengers, thus prostaglandins and leukotrienes are further synthesized. Lipid messengers are actively involved in modulating neuronal and glial cell function. However in some contexts (e.g. ischemia-reperfusion damage) overaccumulation of certain lipid messengers participates in neural damage. The bioactive phospholipid PAF is a retrograde messenger that regulates glutamate release, LTP, and memory formation. Two experimental models of synaptic activation and plasticity will be discussed. In the kindling model of epileptogenesis, there is enhanced selective neuronal induction of COX-2 and phospholipase A2 as aberrant synaptic plasticity evolves. Rapid initial activation of hippocampal COX-2 occurs, but later there is evolving induction of COX-2 in cortical areas. This suggests that either pre-existing circuits are activated or that new connections have been established. The second model is the middle-cerebral artery occlusion model of ischemiareperfusion damage in mice. AA, PAF, and other lipid messengers play a prominent role in modulating signaling critical for neuronal survival. Some of the specific targets include pro-inflammatory gene induction (e.g. COXs). The delineation of synaptic lipid messenger cascades will allow to identify novel targets for neuroprotection and to define signaling pathways critical to understanding neuronal survival in epilepsy, stroke, neurodegeneration, and other diseases. Acknowledgements: Supported by NIH R01NS23002, P20RR016816; NSF/LEQSF(2001-04)-RII-01.