Chapter 16: A tale of two contingent protein kinase C activators: Both neutral and acidic lipids regulate synaptic plasticity and information storage

Aryeh Routtenberg*

*Corresponding author for this work

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)249-261
Number of pages13
JournalProgress in brain research
Volume89
Issue numberC
DOIs
StatePublished - Jan 1 1991

ASJC Scopus subject areas

  • Neuroscience(all)

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