Anandamide, but not 2‐arachidonoylglycerol, accumulates during in vivo neurodegeneration

@article{Hansen2001AnandamideBN,
  title={Anandamide, but not 2‐arachidonoylglycerol, accumulates during in vivo neurodegeneration},
  author={Henrik H. Hansen and Patricia C. Schmid and Petra Bittigau and Isabel Lastres-Becker and Fernando Berrendero and Jorge Manzanares and Chrysanthy Ikonomidou and Harald H. O. Schmid and Javier Fern{\'a}ndez-Ruiz and Harald S Hansen},
  journal={Journal of Neurochemistry},
  year={2001},
  volume={78}
}
Endogenous cannabinoid receptor ligands (endocannabinoids) may rescue neurons from glutamate excitotoxicity. As these substances also accumulate in cultured immature neurons following neuronal damage, elevated endocannabinoid concentrations may be interpreted as a putative neuroprotective response. However, it is not known how glutamatergic insults affect in vivo endocannabinoid homeostasis, i.e. N‐arachidonoylethanolamine (anandamide) and 2‐arachidonoylglycerol (2‐AG), as well as other… 
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Palmitoylethanolamide and other anandamide congeners. Proposed role in the diseased brain
  • H. Hansen
  • Medicine, Biology
    Experimental Neurology
  • 2010
TLDR
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 acyle Thanolamide species are starting to emerge.
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Data indicate that AM374 crosses the blood-brain barrier, enhances endocannabinoid responses in key neuronal circuitries, and protects the brain against excitotoxic damage.
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References

SHOWING 1-10 OF 62 REFERENCES
Accumulation of the anandamide precursor and other N‐acylethanolamine phospholipids in infant rat models of in vivo necrotic and apoptotic neuronal death
TLDR
The data suggest that excitotoxic necrotic mechanisms of neurodegeneration, as opposed to apoptotic neurodegenersation, have a profound effect on in vivo NAE precursor homeostasis.
The ALIAmide palmitoylethanolamide and cannabinoids, but not anandamide, are protective in a delayed postglutamate paradigm of excitotoxic death in cerebellar granule neurons.
  • S. Skaper, A. Buriani, +4 authors A. Leon
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 1996
TLDR
The results suggest that non-CB1 cannabinoid receptors control, upon agonist binding, the downstream consequences of an excitotoxic stimulus and activation of such receptors may serve to downmodulate deleterious cellular processes following pathological events or noxious stimuli in both the nervous and immune systems.
Biosynthesis of an Endogenous Cannabinoid Precursor in Neurons and its Control by Calcium and cAMP
TLDR
The results thus indicate that NAPE levels in cortical neurons are controlled by Ca2+ ions and cAMP, and regulatory effect may participate in maintaining a supply of cannabimimetic N-acylethanolamines during synaptic activity, and prime target neurons for release of these bioactive lipids.
Biosynthesis, release and degradation of the novel endogenous cannabimimetic metabolite 2-arachidonoylglycerol in mouse neuroblastoma cells.
TLDR
The results suggest that the Ca2+-induced formation of 2-AG proceeds through the intermediacy of AcAGs but not necessarily through phospholipase C activation, and supports the hypothesis that this cannabimimetic monoacylglycerol might be a physiological neuromodulator.
The palmitoylethanolamide and oleamide enigmas : are these two fatty acid amides cannabimimetic?
TLDR
PEA is a sleep inducing lipid whose mechanism of action is far from being understood and although it does not bind with high affinity to CB1 or CB2 receptors, it exhibits some cannabimimetic actions which could be explained at least in part by entourage effects.
Characterization of Glutamate‐Induced Formation of N‐Acylphosphatidylethanolamine and N‐Acylethanolamine in Cultured Neocortical Neurons
TLDR
The results suggest that the glutamate‐induced formation of NAPE and NAE was mediated by the NMDA receptor and the formation of these lipids may be associated with neuronal death.
Evidence That the Cannabinoid CB1 Receptor Is a 2-Arachidonoylglycerol Receptor
TLDR
The results strongly suggested that the cannabinoid CB1 receptor is originally a 2-arachidonoylglycerol receptor, and 2-Arachidonoyslglycersol is the intrinsic physiological ligand for the cannabinoidCB1 receptor.
Occurrence and Biosynthesis of Endogenous Cannabinoid Precursor,N-Arachidonoyl Phosphatidylethanolamine, in Rat Brain
TLDR
The results demonstrate, therefore, that rat brain tissue contains the complement of enzymatic activity and lipid substrates necessary for the biosynthesis of the anandamide precursor N-arachidonoyl PE, and suggest that biosynthesis and formation of an andamide are tightly coupled processes, which may be stimulated by elevations in intracellular Ca2+ occurring during neural activity.
Transacylase-mediated and phosphodiesterase-mediated synthesis of N-arachidonoylethanolamine, an endogenous cannabinoid-receptor ligand, in rat brain microsomes. Comparison with synthesis from free arachidonic acid and ethanolamine.
TLDR
Several lines of evidence strongly suggest that the second pathway, rather than the first one, meets the requirements and conditions for the synthesis of various species of N-acylethanolamine including anandamide in the brain.
N-Acylethanolamines and precursor phospholipids - relation to cell injury.
TLDR
A number of mechanisms are proposed by which these two groups of lipids may have cytoprotective properties and involve activation of cannabinoid receptors, as well as non-receptor-mediated effects such as stabilization of membrane bilayers, antioxidant mechanisms, inhibition of calcium leakage from mitochondria, and direct inhibition of ceramidase.
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