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Updated: May 15, 2026

Induction of Protein Deletion Through In Utero Electroporation to Define Deficits in Neuronal Migration in Transgenic Models
Published on: January 12, 2015
cPLA2α knockout mice exhibit abnormalities in the architecture and synapses of cortical neurons
Bao-Xi Qu1, Yunhua Gong, David Sinclair
1Department of Neurology, Center for Neuroscience and Regenerative Medicine, Uniformed Services University of Health Sciences, Rockville, MD 20852, USA. bao-xi.qu.ctr@usuhs.edu
Abstract:
Cytosolic phospholipase A2α (cPLA2α) affects membrane fluidity and permeability by catalyzing the hydrolysis of membrane phospholipids. We hypothesize that cPLA2α deficiency induces rigidity and architectural changes in cell membranes, especially in large cortical neurons. These membrane changes are discernible using light and electron microscopy. Through careful comparison with wild-type counterparts, we observed significant morphological changes in cortical neurons of cPLA2α knockout mice. These changes included the following: (1) increased numbers of nucleoli and enlarged nuclei, (2) narrower spaces between the inner and outer nuclear membranes, (3) reduced numbers of nuclear pores and altered nuclear pore structure, and (4) morphological changes in synaptic clefts. These results further suggest that cPLA2α and its cleaved arachidonic acids play important roles in cortical neuronal maturation and in normal neurochemical processes.

