cPLA2α knockout mice exhibit abnormalities in the architecture and synapses of cortical neurons

Brain Res. 2013 Feb 25:1497:101-5. doi: 10.1016/j.brainres.2012.12.018. Epub 2012 Dec 22.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Arachidonic Acids / metabolism
  • Cell Nucleolus / pathology
  • Cell Nucleolus / ultrastructure
  • Cerebral Cortex / abnormalities*
  • Cerebral Cortex / pathology
  • Group IV Phospholipases A2 / deficiency*
  • Group IV Phospholipases A2 / genetics
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Microscopy, Electron, Transmission
  • Neurons / pathology*
  • Neurons / ultrastructure*
  • Nuclear Pore / genetics
  • Nuclear Pore / pathology
  • Synapses / ultrastructure*

Substances

  • Arachidonic Acids
  • Group IV Phospholipases A2