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…
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The endocannabinoid N-arachidonoyldopamine (NADA) exerts neuroprotective effects after excitotoxic neuronal damage via cannabinoid receptor 1 (CB1)
Opposite Effects of Neuroprotective Cannabinoids, Palmitoylethanolamide, and 2-Arachidonoylglycerol on Function and Morphology of Microglia
TLDR
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
TLDR
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
TLDR
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
TLDR
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
TLDR
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
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
TLDR
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
TLDR
This study unmasked a yet unknown role for GPR55 in neuroprotection driven by LPI‐mediated modulation of microglia function.
Antiepileptic action of N-palmitoylethanolamine through CB1 and PPAR-α receptor activation in a genetic model of absence epilepsy
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TLDR
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