Protein kinase C (PKC) could be fully activated by cis unsaturated fatty acids (CUFAs) in the absence of calcium or phospholipid. It is suggested that calcium activated phospholipase A (PLA2) released CUFAs from the 2-acyl position of phospholipids, which in their monomeric form activated PKC. This chapter reviews the available information from different levels of analysis—molecular, biochemical, physiological, cellular, and behavioral—that converges in their support of the view that the CUFA/PKC mechanism has an important function in synaptic plasticity. Under physiological conditions the elevation of CUFAs and diacylglycerol along with calcium may be the required “contingency” for triggering synaptic plasticity. This might partially explain why CUFAs, which can fully activate purified PKC, have little influence by themselves, on long-term potentiation.
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