Research Article
Docosahexaenoic acid decreases phospholipase A2 activity in the neurites/nerve growth cones of PC12 cells
Article first published online: 12 DEC 1998
DOI: 10.1002/(SICI)1097-4547(19981215)54:6<805::AID-JNR8>3.0.CO;2-4
Copyright © 1998 Wiley-Liss, Inc.
Additional Information
How to Cite
Martin, R. E. (1998), Docosahexaenoic acid decreases phospholipase A2 activity in the neurites/nerve growth cones of PC12 cells. Journal of Neuroscience Research, 54: 805–813. doi: 10.1002/(SICI)1097-4547(19981215)54:6<805::AID-JNR8>3.0.CO;2-4
Publication History
- Issue published online: 12 DEC 1998
- Article first published online: 12 DEC 1998
- Manuscript Accepted: 31 AUG 1998
- Manuscript Revised: 28 AUG 1998
- Manuscript Received: 15 JUN 1998
Funded by
- OCAST
- The OU College of Medicine Alumni Foundation
- The Presbyterian Health Foundation
- Abstract
- References
- Cited By
Keywords:
- docosahexaenoic acid;
- neuronal development/differentiation;
- nutrition;
- omega-3 (n-3);
- fatty acid;
- phospholipase A
Abstract
Docosahexaenoic acid (DHA) accumulates in nerve growth cones (NGC) during perinatal development and it is neuroprotective in ischemia. Because the phospholipases A2 (PLA2) are present in NGC and these enzymes function in both ischemia and long-term potentiation, the relationship between DHA and PLA2 was investigated in the NGC of nerve growth factor-differentiated PC12 cells. When PC12 cells were incubated with [3H]DHA, it primarily esterified in ethanolamine glycerolipids and concentrated initially in cell bodies with similar levels present in the neurite/nerve growth cone (N/NGC) fraction after 4 days. PLA2 activity in the N/NGC fraction was investigated using [14C]arachidonic acid-labeled phosphatidylinositol ([14C-AA]PI) as substrate. Heat denaturation and pharmacological inhibition showed that much of the PLA2 activity was calcium-independent and secretory rather than cytosolic. Supplementing the media with as little as 33 nM DHA significantly reduced PLA2 activity in the N/NGC fraction. J. Neurosci. Res. 54:805–813, 1998. © 1998 Wiley-Liss, Inc.

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