B. Moesgaard et al., Age dependent accumulation of N-acyl-ethanolamine phospholipids in ischemic rat brain: a P-31 NMR and enzyme activity study, J LIPID RES, 41(6), 2000, pp. 985-990
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 du
ring post-decapitative ischemia (6 h at 37 degrees C) were studied in rat b
rains of various age (1, 6, 12, 19, 30, and similar to 70 days) by the use
of P-31 NMR spectroscopy of lipid extracts. This ability to accumulate NAPE
was compared with the activity of N-acyltransferase and of NAPE-hydrolyzin
g phospholipase D (NAPE-PLD) in brain microsomes. These two enzymes are inv
olved in the formation and degradation of NAPE, respectively. The results s
helved that 1) the ability to accumulate NAPE during post-decapitative isch
emia is especially high in the youngest rats and is markedly reduced in old
er brains [in 1-day-old rat brains NAPE accumulated to 1.5% of total phosph
olipids, while in 30-day-old rat brains NAPE accumulation could not be dete
cted (detection limit 0.09 %)]; and 2) this age pattern of accumulation can
be explained by a combination of the decreased activity of N-acyltransfera
se and the increased activity of NAPE-PLD during development. These results
point out that it would be advantageous to investigate a potential cytopro
tective role of NAPE in the brains of very young rats.