ArticleGenes, brain, and behavior2017
Midkine in the mouse ventral tegmental area limits ethanol intake and Ccl2 gene expression.
Article in Genes, brain, and behavior, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Alcohol and the brain: from genes to circuits.Trends in neurosciences · 2021Review
- Binge-Like Ethanol Drinking IncreasesNeuroscience insights · 2021Article
- Growth Factors and Alcohol Use Disorder.Cold Spring Harbor perspectives in medicine · 2020Review
- Receptor Tyrosine Kinases as Therapeutic Targets for Alcohol Use Disorder.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Neuroimmune signaling in alcohol use disorder.Pharmacology, biochemistry, and behavior · 2019Review
- Molecular tools to elucidate factors regulating alcohol use.Alcohol (Fayetteville, N.Y.) · 2019Review
- Pharmacological inhibition of Receptor Protein Tyrosine Phosphatase β/ζ (PTPRZ1) modulates behavioral responses to ethanol.Neuropharmacology · 2018Article
- Altered hippocampal synaptic function in transgenic mice with increased astrocyte expression of CCL2 after withdrawal from chronic alcohol.Neuropharmacology · 2018Article
- Genetic variationsOncotarget · 2018Article
- Development of inhibitors of receptor protein tyrosine phosphatase β/ζ (PTPRZ1) as candidates for CNS disorders.European journal of medicinal chemistry · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Midkine (MDK) is a cytokine and neurotrophic factor that is more highly expressed in the brains of alcoholics and in mice predisposed to drink large amounts of ethanol, suggesting that MDK may regulate ethanol consumption. Here we measured ethanol consumption in male and female Mdk knockout (-/-) mice using the two-bottle choice and the drinking in the dark (DID) tests. We found that Mdk -/- mice consumed significantly more ethanol than wild-type controls in both tests. To determine if MDK acts in the ventral tegmental area (VTA) to regulate ethanol consumption, we delivered lentivirus expressing a Mdk shRNA into the VTA of male C57BL/6J mice to locally knockdown Mdk and performed the DID test. Mice expressing a Mdk shRNA in the VTA consumed more ethanol than mice expressing a control non-targeting shRNA, demonstrating that the VTA is one site in the brain through which MDK acts to regulate ethanol consumption. Since MDK also controls the expression of inflammatory cytokines in other organs, we examined gene expression of interleukin-1 beta (Il1b), tumor necrosis factor alpha (Tnfα) and the chemokine (C-C motif) ligand 2 (Ccl2) in the VTA of Mdk -/- mice and in mice expressing Mdk shRNA in the VTA. Expression of Ccl2 was elevated in the VTA of Mdk -/- mice and in mice expressing Mdk shRNA in the VTA. These results demonstrate that MDK functions in the VTA to limit ethanol consumption and levels of CCL2, a chemokine known to increase ethanol consumption.
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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.