Palmitoylethanolamide and other anandamide congeners. Proposed role in the diseased brain

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Palmitoylethanolamide and other anandamide congeners. Proposed role in the diseased brain. / Hansen, Harald S.

In: Experimental Neurology, Vol. 224, No. 1, 01.07.2010, p. 48-55.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Hansen, HS 2010, 'Palmitoylethanolamide and other anandamide congeners. Proposed role in the diseased brain', Experimental Neurology, vol. 224, no. 1, pp. 48-55. https://doi.org/10.1016/j.expneurol.2010.03.022

APA

Hansen, H. S. (2010). Palmitoylethanolamide and other anandamide congeners. Proposed role in the diseased brain. Experimental Neurology, 224(1), 48-55. https://doi.org/10.1016/j.expneurol.2010.03.022

Vancouver

Hansen HS. Palmitoylethanolamide and other anandamide congeners. Proposed role in the diseased brain. Experimental Neurology. 2010 Jul 1;224(1):48-55. https://doi.org/10.1016/j.expneurol.2010.03.022

Author

Hansen, Harald S. / Palmitoylethanolamide and other anandamide congeners. Proposed role in the diseased brain. In: Experimental Neurology. 2010 ; Vol. 224, No. 1. pp. 48-55.

Bibtex

@article{1b597327c290420289960dd3bbc640ce,
title = "Palmitoylethanolamide and other anandamide congeners. Proposed role in the diseased brain",
abstract = "Acylethanolamides are formed in the brain {"}on demand{"} from membrane phospholipids called N-acylated phosphatidylethanolamines. The acylethanolamides are signaling molecules of lipid nature, and this lipofilicity suggests an autocrine function. The acylethanolamides include palmitoylethanolamide (PEA), oleoylethanolamide (OEA), stearoylethanolamide (SEA), and several other quantitative minor species including anandamide (= arachidonoylethanolamide). PEA and OEA can activate several different receptors and inhibit some ion channels, e.g., PPARalpha, vanilloid receptor, K(+) channels (Kv4.3, Kv1.5), and OEA can activate GPR119 and inhibit ceramidases. Targets for SEA are less clear, but it has some cannabimimetic actions in rats in vivo. All acylethanolamides accumulate during neuronal injury, and injected OEA has neuroprotective effects, and PEA has anti-inflammatory effects as studied in the peripheral system. Several of the pharmacological effects seem to be mediated via activation of PPARalpha. Recently, injected OEA has been found to consolidate memories in rats. Inhibitors of the acylethanolamide-degrading enzyme FAAH can increase levels of all acylethanolamides including annandamide, and some of the pharmacological effects caused by these inhibitors may be explained by increased cerebral levels of OEA and PEA, e.g., suppression of nicotine-induced activation of dopamine neurons. Furthermore, through activation of PPARalpha, OEA and PEA may stimulate neurosteroid synthesis, thereby modulating several biological functions mediated by GABA(A) receptors. The existence of acylethanolamides in the mammalian brain has been known for decades, but it is first within the last few years that the putative biological functions of the three most abundant acylethanolamides species are starting to emerge.",
keywords = "Animals, Arachidonic Acids, Brain, Cytoprotection, Humans, Nerve Degeneration, Neurons, Oleic Acids, Palmitic Acids, Polyunsaturated Alkamides, Receptors, Cannabinoid",
author = "Hansen, {Harald S.}",
note = "Copyright 2010 Elsevier Inc. All rights reserved.",
year = "2010",
month = jul,
day = "1",
doi = "10.1016/j.expneurol.2010.03.022",
language = "English",
volume = "224",
pages = "48--55",
journal = "Experimental Neurology",
issn = "0014-4886",
publisher = "Academic Press",
number = "1",

}

RIS

TY - JOUR

T1 - Palmitoylethanolamide and other anandamide congeners. Proposed role in the diseased brain

AU - Hansen, Harald S.

N1 - Copyright 2010 Elsevier Inc. All rights reserved.

PY - 2010/7/1

Y1 - 2010/7/1

N2 - Acylethanolamides are formed in the brain "on demand" from membrane phospholipids called N-acylated phosphatidylethanolamines. The acylethanolamides are signaling molecules of lipid nature, and this lipofilicity suggests an autocrine function. The acylethanolamides include palmitoylethanolamide (PEA), oleoylethanolamide (OEA), stearoylethanolamide (SEA), and several other quantitative minor species including anandamide (= arachidonoylethanolamide). PEA and OEA can activate several different receptors and inhibit some ion channels, e.g., PPARalpha, vanilloid receptor, K(+) channels (Kv4.3, Kv1.5), and OEA can activate GPR119 and inhibit ceramidases. Targets for SEA are less clear, but it has some cannabimimetic actions in rats in vivo. All acylethanolamides accumulate during neuronal injury, and injected OEA has neuroprotective effects, and PEA has anti-inflammatory effects as studied in the peripheral system. Several of the pharmacological effects seem to be mediated via activation of PPARalpha. Recently, injected OEA has been found to consolidate memories in rats. Inhibitors of the acylethanolamide-degrading enzyme FAAH can increase levels of all acylethanolamides including annandamide, and some of the pharmacological effects caused by these inhibitors may be explained by increased cerebral levels of OEA and PEA, e.g., suppression of nicotine-induced activation of dopamine neurons. Furthermore, through activation of PPARalpha, OEA and PEA may stimulate neurosteroid synthesis, thereby modulating several biological functions mediated by GABA(A) receptors. The existence of acylethanolamides in the mammalian brain has been known for decades, but it is first within the last few years that the putative biological functions of the three most abundant acylethanolamides species are starting to emerge.

AB - Acylethanolamides are formed in the brain "on demand" from membrane phospholipids called N-acylated phosphatidylethanolamines. The acylethanolamides are signaling molecules of lipid nature, and this lipofilicity suggests an autocrine function. The acylethanolamides include palmitoylethanolamide (PEA), oleoylethanolamide (OEA), stearoylethanolamide (SEA), and several other quantitative minor species including anandamide (= arachidonoylethanolamide). PEA and OEA can activate several different receptors and inhibit some ion channels, e.g., PPARalpha, vanilloid receptor, K(+) channels (Kv4.3, Kv1.5), and OEA can activate GPR119 and inhibit ceramidases. Targets for SEA are less clear, but it has some cannabimimetic actions in rats in vivo. All acylethanolamides accumulate during neuronal injury, and injected OEA has neuroprotective effects, and PEA has anti-inflammatory effects as studied in the peripheral system. Several of the pharmacological effects seem to be mediated via activation of PPARalpha. Recently, injected OEA has been found to consolidate memories in rats. Inhibitors of the acylethanolamide-degrading enzyme FAAH can increase levels of all acylethanolamides including annandamide, and some of the pharmacological effects caused by these inhibitors may be explained by increased cerebral levels of OEA and PEA, e.g., suppression of nicotine-induced activation of dopamine neurons. Furthermore, through activation of PPARalpha, OEA and PEA may stimulate neurosteroid synthesis, thereby modulating several biological functions mediated by GABA(A) receptors. The existence of acylethanolamides in the mammalian brain has been known for decades, but it is first within the last few years that the putative biological functions of the three most abundant acylethanolamides species are starting to emerge.

KW - Animals

KW - Arachidonic Acids

KW - Brain

KW - Cytoprotection

KW - Humans

KW - Nerve Degeneration

KW - Neurons

KW - Oleic Acids

KW - Palmitic Acids

KW - Polyunsaturated Alkamides

KW - Receptors, Cannabinoid

U2 - 10.1016/j.expneurol.2010.03.022

DO - 10.1016/j.expneurol.2010.03.022

M3 - Journal article

C2 - 20353771

VL - 224

SP - 48

EP - 55

JO - Experimental Neurology

JF - Experimental Neurology

SN - 0014-4886

IS - 1

ER -

ID: 33221301