ArticleFrontiers in cellular neuroscience2020
Activation of Melanocortin-4 Receptor Inhibits Both Neuroinflammation Induced by Early Exposure to Ethanol and Subsequent Voluntary Alcohol Intake in Adulthood in Animal Models: Is BDNF the Key Mediator?
Article in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Electroacupuncture alleviates blood-brain barrier disruption and neuroinflammation via astrocytic MC4R in a mouse model of multiple sclerosis.Journal of neuroinflammation · 2025Article
- Alcohol exposure significantly influences gene expression in the hypothalamus, highlighting complex links with gonadotropin-releasing hormone signaling and thyroid hormone production in adolescent mice.BMC medical genomics · 2025Article
- Probiotic Bactolac alleviates depression-like behaviors by modulating BDNF, NLRP3 and MC4R levels, reducing neuroinflammation and promoting neural repair in rat model.Pflugers Archiv : European journal of physiology · 2025Article
- Fenofibrate treatment during withdrawal reverses symptoms of ethanol-induced depression in male rats.Frontiers in pharmacology · 2025Article
- Effects of early maternal separation on the expression levels of hippocampal and prefrontal cortex genes and pathways in lactating piglets.Frontiers in molecular neuroscience · 2023Article
- Melanocortin-4 receptor signaling in the central amygdala mediates chronic inflammatory pain effects on nociception.Neuropharmacology · 2022Article
- Low-Molecular-Weight Mimetic of BDNF Loop 2 Reduces Ethanol Consumption in Female Rats.Bulletin of experimental biology and medicine · 2021Article
- Antifibrotic and Anti-Inflammatory Actions of α-Melanocytic Hormone: New Roles for an Old Player.Pharmaceuticals (Basel, Switzerland) · 2021Review
- The Role of Melanocortin Plasticity in Pain-Related Outcomes After Alcohol Exposure.Frontiers in psychiatry · 2021Review
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3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The concept that neuroinflammation induced by excessive alcohol intake in adolescence triggers brain mechanisms that perpetuate consumption has strengthened in recent years. The melanocortin system, composed of the melanocortin 4 receptor (MC4R) and its ligand α-melanocyte-stimulating hormone (α-MSH), has been implicated both in modulation of alcohol consumption and in ethanol-induced neuroinflammation decrease. Chronic alcohol consumption in adolescent rats causes a decrease in an α-MSH release by the hypothalamus, while the administration of synthetic agonists of MC4R causes a decrease in neuroinflammation and a decrease in voluntary alcohol consumption. However, the mechanism that connects the activation of MC4R with the decrease of both neuroinflammation and voluntary alcohol consumption has not been elucidated. Brain-derived neurotrophic factor (BDNF) has been implicated in alcohol drinking motivation, dependence and withdrawal, and its levels are reduced in alcoholics. Deficiencies in BDNF levels increased ethanol self-administration in rats. Further, BDNF triggers important anti-inflammatory effects in the brain, and this could be one of the mechanisms by which BDNF reduces chronic alcohol intake. Interestingly, MC4R signaling induces BDNF expression through the activation of the cAMP-responsive element-binding protein (CREB). We hypothesize that ethanol exposure during adolescence decreases the expression of α-MSH and hence MC4R signaling in the hippocampus, leading to a lower BDNF activity that causes dramatic changes in the brain (e.g., neuroinflammation and decreased neurogenesis) that predispose to maintain alcohol abuse until adulthood. The activation of MC4R either by α-MSH or by synthetic agonist peptides can induce the expression of BDNF, which would trigger several processes that lead to lower alcohol consumption.
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