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Neural Plasticity
Volume 2012 (2012), Article ID 569149, 13 pages
Review Article

Maintenance of Synaptic Stability Requires Calcium-Independent Phospholipase A2 Activity

1Département de Chimie-Biologie, Université du Québec à Trois-Rivières, 3351 Boulevard des Forges, QC, Canada G9A 5H7
2Graduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, CA 91766-1854, USA

Received 7 October 2011; Revised 3 February 2012; Accepted 7 February 2012

Academic Editor: Lucas Pozzo-Miller

Copyright © 2012 Julie Allyson et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Phospholipases A2 (PLA2s) represent one of the largest groups of lipid-modifying enzymes. Over the years, significant advances have been made in understanding their potential physiological and pathological functions. Depending on their calcium requirement for activation, PLA2s are classified into calcium dependent and independent. This paper mainly focuses on brain calcium-independent PLA2 (iPLA2) and on the mechanisms by which they influence neuronal function and regulate synaptic plasticity. Particular attention will be given to the iPLA2γ isoform and its role in the regulation of synaptic glutamate receptors. In particular, the paper discusses the possibility that brain iPLA2γ deficiencies could destabilise normal synaptic operation and might contribute to the aetiology of some brain disorders. In this line, the paper presents new data indicating that iPLA2γ deficiencies accentuate AMPA receptor destabilization and tau phosphorylation, which suggests that this iPLA2 isoform should be considered as a potential target for the treatment of Tau-related disorders.