ArticleNeuropharmacology2016
N-Docosahexaenoylethanolamine ameliorates ethanol-induced impairment of neural stem cell neurogenic differentiation.
Article in Neuropharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Anti-Inflammatory Potential of Stearidonic Acid Ethanolamide in a Model of Mild Traumatic Brain Injury in Mice.Neuromolecular medicine · 2026Article
- Managing dry eye disease - a review of selected traditional Chinese medicine and some of their metabolites focusing on molecular mechanisms and signaling pathways.Frontiers in pharmacology · 2026Review
- Synergistic Antidepressant-like Effects of Biotics and n-3 Polyunsaturated Fatty Acids on Dopaminergic Pathway through the Brain-Gut Axis in Rats Exposed to Chronic Mild Stress.Probiotics and antimicrobial proteins · 2025Article
- Impact of Omega-3 on Endocannabinoid System Expression and Function, Enhancing Cognition and Behavior in Male Mice.Nutrients · 2024Article
- The Effect of Very-Long-ChainNutrients · 2023Review
- The effect of omega-3 fatty acids on alcohol-induced damage.Frontiers in nutrition · 2023Review
- Corticostriatal Circuit Models of Cognitive Impairments Induced by Fetal Exposure to Alcohol.Biological psychiatry · 2021Review
- Lower brain fatty acid amide hydrolase in treatment-seeking patients with alcohol use disorder: a positron emission tomography study with [C-11]CURB.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Murine Models for the Study of Fetal Alcohol Spectrum Disorders: An Overview.Frontiers in pediatrics · 2020Review
- The expanding functional roles and signaling mechanisms of adhesion G protein-coupled receptors.Annals of the New York Academy of Sciences · 2019Article
- Emerging class of omega-3 fatty acid endocannabinoids & their derivatives.Prostaglandins & other lipid mediators · 2019Review
- The phosphodiesterase-4 inhibitor roflumilast decreases ethanol consumption in C57BL/6J mice.Psychopharmacology · 2017Article
- Chronic Binge Alcohol Administration Dysregulates Hippocampal Genes Involved in Immunity and Neurogenesis in Simian Immunodeficiency Virus-Infected Macaques.Biomolecules · 2016Article
- N-Docosahexaenoylethanolamine ameliorates LPS-induced neuroinflammation via cAMP/PKA-dependent signaling.Journal of neuroinflammation · 2016Article
- Inflammatory responses to alcohol in the CNS: nuclear receptors as potential therapeutics for alcohol-induced neuropathologies.Journal of leukocyte biology · 2016Review
- Orphan GPR110 (ADGRF1) targeted by N-docosahexaenoylethanolamine in development of neurons and cognitive function.Nature communications · 2016Article
- Role of DHA in aging-related changes in mouse brain synaptic plasma membrane proteome.Neurobiology of aging · 2016Article
- Design, Synthesis, and Evaluation of Cytotoxic Effects of Functional Fatty Acid Derivatives as Potential Antineoplastic Agents for Breast Cancer.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies demonstrated that prenatal exposure to ethanol interferes with embryonic and fetal development, and causes abnormal neurodevelopment. Docosahexaenoic acid (DHA), an omega-3 polyunsaturated fatty acid highly enriched in the brain, was shown to be essential for proper brain development and function. Recently, we found that N-docosahexenoyethanolamine (synaptamide), an endogenous metabolite of DHA, is a potent PKA-dependent neurogenic factor for neural stem cell (NSC) differentiation. In this study, we demonstrate that ethanol at pharmacologically relevant concentrations downregulates cAMP signaling in NSC and impairs neurogenic differentiation. In contrast, synaptamide reverses ethanol-impaired NSC neurogenic differentiation through counter-acting on the cAMP production system. NSC exposure to ethanol (25-50 mM) for 4 days dose-dependently decreased the number of Tuj-1 positive neurons and PKA/CREB phosphorylation with a concomitant reduction of cellular cAMP. Ethanol-induced cAMP reduction was accompanied by the inhibition of G-protein activation and expression of adenylyl cyclase (AC) 7 and AC8, as well as PDE4 upregulation. In contrast to ethanol, synaptamide increased cAMP production, GTPγS binding, and expression of AC7 and AC8 isoforms in a cAMP-dependent manner, offsetting the ethanol-induced impairment in neurogenic differentiation. These results indicate that synaptamide can reduce ethanol-induced impairment of neuronal differentiation by counter-affecting shared targets in G-protein coupled receptor (GPCR)/cAMP signaling. The synaptamide-mediated mechanism observed in this study may offer a possible avenue for ameliorating the adverse impact of fetal alcohol exposure on neurodevelopment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.