Palmitoylethanolamide Protects Dentate Gyrus Granule Cells via Peroxisome Proliferator-Activated Receptor-Alpha
@article{Koch2010PalmitoylethanolamidePD, title={Palmitoylethanolamide Protects Dentate Gyrus Granule Cells via Peroxisome Proliferator-Activated Receptor-Alpha}, author={Marco Koch and Susanne Kreutz and Charlotte B{\"o}ttger and Alexander H Benz and Erik Maronde and Chalid Ghadban and Horst-Werner Korf and Faramarz Dehghani}, journal={Neurotoxicity Research}, year={2010}, volume={19}, pages={330-340} }
Endocannabinoids like 2-arachidonoylglycerol strongly modulate the complex machinery of secondary neuronal damage and are shown to improve neuronal survival after excitotoxic lesion. [] Key Result Here we show that PEA (0.001–1 μM) and the synthetic peroxisome proliferator-activated receptor (PPAR)-alpha agonist 4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio acetic acid (Wy-14,643; 0.1–1 μM) reduced the number of microglial cells and protected dentate gyrus granule cells in excitotoxically lesioned organotypic…
39 Citations
The endocannabinoid N-arachidonoyldopamine (NADA) exerts neuroprotective effects after excitotoxic neuronal damage via cannabinoid receptor 1 (CB1)
- BiologyNeuropharmacology
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Opposite Effects of Neuroprotective Cannabinoids, Palmitoylethanolamide, and 2-Arachidonoylglycerol on Function and Morphology of Microglia
- BiologyFront. Neurosci.
- 2019
While PEA or 2-AG alone were neuroprotective, their co-application vanished the protective effect, and the role of microglial cells in PEA and 2- AG mediated protection was investigated.
Physiological Role of Peroxisome Proliferator-Activated Receptors Type Alpha on Dopamine Systems
- Biology, Chemistry
- 2013
Using pharmacological and/or nutritional strategies which target PPARα might represent a promising therapeutic approach to prevent disorders often related to neuro-inflammation, stress and abnormal β2*-nAChR function.
Protective Effect of N-Arachidonoyl Glycine-GPR18 Signaling after Excitotoxical Lesion in Murine Organotypic Hippocampal Slice Cultures
- Biology, ChemistryInternational journal of molecular sciences
- 2019
Treatment with NAGly reduced neuronal damage and this effect was abolished by GPR18 and cannabinoid receptor (CB)2 receptor antagonists and it is speculated that GPR 18 and its ligand N AGly are modulators of glial and neuronal cells during neuronal damage.
Localization of peroxisome proliferator-activated receptor alpha (PPARα) and N-acyl phosphatidylethanolamine phospholipase D (NAPE-PLD) in cells expressing the Ca2+-binding proteins calbindin, calretinin, and parvalbumin in the adult rat hippocampus
- BiologyFront. Neuroanat.
- 2014
The hippocampal subpopulations of NAPE-PLD/PPARα-containing neurons that express selective Ca2+-binding proteins (CaBPs) should be considered when analyzing the role of NAEs/PParα-signaling system in the regulation of hippocampal functions.
Intrinsic Up-Regulation of 2-AG Favors an Area Specific Neuronal Survival in Different In Vitro Models of Neuronal Damage
- BiologyPloS one
- 2012
Increase in 2-AG levels during secondary neuronal damage reflects a general neuroprotective mechanism since it occurred independently in both different lesion models and represents a protective system for neurons that is involved in dendritic reorganisation.
Palmitoylethanolamide induces microglia changes associated with increased migration and phagocytic activity: involvement of the CB2 receptor
- BiologyScientific Reports
- 2017
The endogenous fatty acid amide palmitoylethanolamide (PEA) has been shown to exert anti-inflammatory actions mainly through inhibition of the release of pro-inflammatory molecules from mast cells,…
Palmitoylethanolamide Inhibits Glutamate Release in Rat Cerebrocortical Nerve Terminals
- Biology, ChemistryInternational journal of molecular sciences
- 2015
It is suggested that PEA exerts its presynaptic inhibition, likely through a reduction in the Ca2+ influx mediated by Cav2.1 (P/Q-type) channels, thereby inhibiting the release of glutamate from rat cortical nerve terminals.
The G Protein‐Coupled Receptor 55 Ligand l‐α‐Lysophosphatidylinositol Exerts Microglia‐Dependent Neuroprotection After Excitotoxic Lesion
- Biology, ChemistryGlia
- 2013
This study unmasked a yet unknown role for GPR55 in neuroprotection driven by LPI‐mediated modulation of microglia function.
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