HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Moesgaard, B. Articles by Hansen, H. S. Search for Related Content PubMed PubMed Citation Articles by Moesgaard, B. Articles by Hansen, H. S. Social Bookmarking                      What's this?

Journal of Lipid Research, Vol. 41, 985-990, June 2000
Copyright © 2000 by Lipid Research, Inc.

Original Article

Age dependent accumulation of N-acyl-ethanolamine phospholipids in ischemic rat brain: a ³¹P NMR and enzyme activity study

Correspondence to: Harald S. Hansen

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.—Moesgaard, B., G. Petersen, J. W. Jaroszewski, and H. S. Hansen. Age dependent accumulation of N-acyl-ethanolamine phospholipids in ischemic rat brain: a ³¹P NMR and enzyme activity study. J. Lipid Res. 41: 985;–990.

Supplementary key words: anandamide, ischemia, rat brain development, N-acyltransferase, N-acyl-ethanolamine phospholipid-hydrolyzing phospholipase D, ³¹P NMR

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				X.-H. Jin, Y. Okamoto, J. Morishita, K. Tsuboi, T. Tonai, and N. Ueda Discovery and Characterization of a Ca2+-independent Phosphatidylethanolamine N-Acyltransferase Generating the Anandamide Precursor and Its Congeners J. Biol. Chem., February 9, 2007; 282(6): 3614 - 3623. [Abstract] [Full Text] [PDF]

				M. Maccarrone, E. Fride, T. Bisogno, M. Bari, M.G. Cascio, N. Battista, A. Finazzi Agro, R. Suris, R. Mechoulam, and V. Di Marzo Up-regulation of the endocannabinoid system in the uterus of leptin knockout (ob/ob) mice and implications for fertility Mol. Hum. Reprod., January 1, 2005; 11(1): 21 - 28. [Abstract] [Full Text] [PDF]

				M. Maccarrone, M. DeFelici, F.G. Klinger, N. Battista, F. Fezza, E. Dainese, G. Siracusa, and A. Finazzi-Agro Mouse blastocysts release a lipid which activates anandamide hydrolase in intact uterus Mol. Hum. Reprod., April 1, 2004; 10(4): 215 - 221. [Abstract] [Full Text] [PDF]

				Y. Okamoto, J. Morishita, K. Tsuboi, T. Tonai, and N. Ueda Molecular Characterization of a Phospholipase D Generating Anandamide and Its Congeners J. Biol. Chem., February 13, 2004; 279(7): 5298 - 5305. [Abstract] [Full Text] [PDF]

				M. Maccarrone, M. Di Rienzo, N. Battista, V. Gasperi, P. Guerrieri, A. Rossi, and A. Finazzi-Agro The Endocannabinoid System in Human Keratinocytes: EVIDENCE THAT ANANDAMIDE INHIBITS EPIDERMAL DIFFERENTIATION THROUGH CB1 RECEPTOR-DEPENDENT INHIBITION OF PROTEIN KINASE C, ACTIVATING PROTEIN-1, AND TRANSGLUTAMINASE J. Biol. Chem., September 5, 2003; 278(36): 33896 - 33903. [Abstract] [Full Text] [PDF]

				M. Maccarrone, M. Bari, M. Di Rienzo, A. Finazzi-Agro, and A. Rossi Progesterone Activates Fatty Acid Amide Hydrolase (FAAH) Promoter in Human T Lymphocytes through the Transcription Factor Ikaros: EVIDENCE FOR A SYNERGISTIC EFFECT OF LEPTIN J. Biol. Chem., August 29, 2003; 278(35): 32726 - 32732. [Abstract] [Full Text] [PDF]

				L. Wang, J. Liu, J. Harvey-White, A. Zimmer, and G. Kunos Endocannabinoid signaling via cannabinoid receptor 1 is involved in ethanol preference and its age-dependent decline in mice PNAS, February 4, 2003; 100(3): 1393 - 1398. [Abstract] [Full Text] [PDF]

				M. Maccarrone, M. Bari, N. Battista, and A. Finazzi-Agro Estrogen stimulates arachidonoylethanolamide release from human endothelial cells and platelet activation Blood, December 1, 2002; 100(12): 4040 - 4048. [Abstract] [Full Text] [PDF]

				P. Gubellini, B. Picconi, M. Bari, N. Battista, P. Calabresi, D. Centonze, G. Bernardi, A. Finazzi-Agro, and M. Maccarrone Experimental Parkinsonism Alters Endocannabinoid Degradation: Implications for Striatal Glutamatergic Transmission J. Neurosci., August 15, 2002; 22(16): 6900 - 6907. [Abstract] [Full Text] [PDF]

				A. J. Rawyler and R. A. Braendle N-Acylphosphatidylethanolamine Accumulation in Potato Cells upon Energy Shortage Caused by Anoxia or Respiratory Inhibitors Plant Physiology, September 1, 2001; 127(1): 240 - 251. [Abstract] [Full Text] [PDF]