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Oleoylethanolamide restores alcohol-induced inhibition of neuronal proliferation and microglial activity in striatum.
- Source :
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Neuropharmacology [Neuropharmacology] 2019 Mar 01; Vol. 146, pp. 184-197. Date of Electronic Publication: 2018 Nov 26. - Publication Year :
- 2019
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Abstract
- Previous findings demonstrate a homeostatic role for oleoylethanolamide (OEA) signaling in the ethanol-related neuroinflammation and behavior. However, extensive research is still required in order to unveil the effects of OEA on a number of neurobiological functions such as adult neurogenesis, cell survival and resident neuroimmunity that become notably altered by alcohol. Daily consumption of ethanol (10%) for 2 weeks (6.3&#x202F;±&#x202F;1.1&#x202F;g/kg/day during last 5 days) caused hypolocomotor activity in rats. This effect appears to rely on central signaling mechanisms given that alcohol increased the OEA levels, the gene expression of OEA-synthesizing enzyme Nape-pld and the number of PPARα-immunoreactive neurons in the striatum. Ethanol-related neurobiological alterations such as a reduction in the number of microglial cells expressing iNOS (a cytokine-inducible immune defense) and in adult neural stem/progenitor cell (NSPC) proliferation (phospho-H3 and BrdU) and maturation (BrdU/β3-tubulin), as well as an increase in damage cell activity (FosB) and apoptosis (cleaved caspase 3) were also observed in the rat striatum. Pharmacological administration of OEA (10 mg/kg) for 5 days during ethanol exposure exacerbated ethanol-induced hypolocomotion and cell apoptosis in the striatum. Interestingly, OEA abrogated the impaired effects of ethanol on PPARα-positive cell population and NSPC proliferation and maturation. OEA also decreased astrocyte-related vimentin immunoreactivity and increased microglial cell population (Iba-1, iNOS) in the striatum. These results suggest that OEA-PPARα signaling modulates glial activation, cell apoptosis and NSPC proliferation and maturation in response to striatal-specific neurobiological alterations induced by prolonged ethanol intake in rats.<br /> (Copyright © 2018 Elsevier Ltd. All rights reserved.)
- Subjects :
- Alanine Transaminase blood
Alcohol Drinking drug therapy
Amidohydrolases blood
Animals
Apoptosis drug effects
Arachidonic Acids pharmacology
Aspartate Aminotransferases blood
Calcium-Binding Proteins metabolism
Caspase 3 metabolism
Cell Survival drug effects
Ethanolamines analysis
Ethanolamines blood
Glial Fibrillary Acidic Protein metabolism
Hepatobiliary Elimination
Locomotion drug effects
Male
Microfilament Proteins metabolism
Neurons drug effects
PPAR alpha metabolism
Phospholipase D blood
Polyunsaturated Alkamides pharmacology
Proto-Oncogene Proteins c-fos metabolism
Rats
Rats, Wistar
Signal Transduction drug effects
gamma-Glutamyltransferase blood
Cell Proliferation drug effects
Endocannabinoids pharmacology
Ethanol pharmacology
Microglia drug effects
Microglia metabolism
Neostriatum drug effects
Neostriatum metabolism
Oleic Acids pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 1873-7064
- Volume :
- 146
- Database :
- MEDLINE
- Journal :
- Neuropharmacology
- Publication Type :
- Academic Journal
- Accession number :
- 30496754
- Full Text :
- https://doi.org/10.1016/j.neuropharm.2018.11.037