Abstract
N-acyl-ethanolamine phospholipids (NAPE) can be formed as a stress response during neuronal injury, and they are precursors for N-acyl-ethanolamines (NAE), some of which are endocannabinoids. The levels of NAPE accumulated during post-decapitative ischemia (6 h at 37°C) were studied in rat brains of various age (1, 6, 12, 19, 30, and ~70 days) by the use of 31P NMR spectroscopy of lipid extracts. This ability to accumulate NAPE was compared with the activity of N-acyltransferase and of NAPE-hydrolyzing phospholipase D (NAPE-PLD) in brain microsomes. These two enzymes are involved in the formation and degradation of NAPE, respectively.The results showed that 1) the ability to accumulate NAPE during post-decapitative ischemia is especially high in the youngest rats and is markedly reduced in older brains [in 1-day-old rat brains NAPE accumulated to 1.5% of total phospholipids, while in 30-day-old rat brains NAPE accumulation could not be detected (detection limit 0.09 %)]; and 2) this age pattern of accumulation can be explained by a combination of the decreased activity of N-acyltransferase and the increased activity of NAPE-PLD during development. These results point out that it would be advantageous to investigate a potential cytoprotective role of NAPE in the brains of very young rats.
Highlights
N-acyl-ethanolamine phospholipids (NAPE) can be formed as a stress response during neuronal injury, and they are precursors for N-acyl-ethanolamines (NAE), some of which are endocannabinoids
Studies of primary cultures of mouse cortical neurons showed a Glu-induced formation of NAPE and NAE mediated via activation of the NMDA-receptor, and that the ability to form these two lipids is dependent on the maturity of the cell cultures [5,6,7]
The formation of NAPE and NAE under pathophysiological conditions is suggested to serve a neuroprotective role [1], e.g., NAPE may be membrane stabilizing [23, 24] and the different NAE species may be cytoprotective via non-receptor-mediated actions, as well as via activation of cannabinoid receptors [8, 9, 25,26,27,28]
Summary
N-acyl-ethanolamine phospholipids (NAPE) can be formed as a stress response during neuronal injury, and they are precursors for N-acyl-ethanolamines (NAE), some of which are endocannabinoids. The levels of NAPE accumulated during post-decapitative ischemia (6 h at 37؇C) were studied in rat brains of various age (1, 6, 12, 19, 30, and ϳ70 days) by the use of 31P NMR spectroscopy of lipid extracts. This ability to accumulate NAPE was compared with the activity of N-acyltransferase and of NAPE-hydrolyzing phospholipase D (NAPE-PLD) in brain microsomes. Studies of primary cultures of mouse cortical neurons showed a Glu-induced formation of NAPE and NAE mediated via activation of the NMDA-receptor, and that the ability to form these two lipids is dependent on the maturity of the cell cultures [5,6,7].
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