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dc.contributor.authorOrellana J.A.
dc.contributor.authorCerpa W.
dc.contributor.authorCarvajal M.F.
dc.contributor.authorLerma-Cabrera J.M.
dc.contributor.authorKarahanian E.
dc.contributor.authorOsorio-Fuentealba C.
dc.contributor.authorQuintanilla R.A.
dc.date.accessioned2020-09-02T22:24:49Z
dc.date.available2020-09-02T22:24:49Z
dc.date.issued2017
dc.identifier10.3389/fncel.2017.00090
dc.identifier.citation11, , -
dc.identifier.issn16625102
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5657
dc.descriptionAlcohol dependence causes physical, social, and moral harms and currently represents an important public health concern. According to the World Health Organization (WHO), alcoholism is the third leading cause of death worldwide, after tobacco consumption and hypertension. Recent epidemiologic studies have shown a growing trend in alcohol abuse among adolescents, characterized by the consumption of large doses of alcohol over a short time period. Since brain development is an ongoing process during adolescence, short- and long-term brain damage associated with drinking behavior could lead to serious consequences for health and wellbeing. Accumulating evidence indicates that alcohol impairs the function of different components of the melanocortin system, a major player involved in the consolidation of addictive behaviors during adolescence and adulthood. Here, we hypothesize the possible implications of melanocortins and glial cells in the onset and progression of alcohol addiction. In particular, we propose that alcohol-induced decrease in α-MSH levels may trigger a cascade of glial inflammatory pathways that culminate in altered gliotransmission in the ventral tegmental area and nucleus accumbens (NAc). The latter might potentiate dopaminergic drive in the NAc, contributing to increase the vulnerability to alcohol dependence and addiction in the adolescence and adulthood. © 2017 Orellana, Cerpa, Carvajal, Lerma-Cabrera, Karahanian, Osorio-Fuentealba and Quintanilla.
dc.language.isoen
dc.publisherFrontiers Media S.A.
dc.subjectAlcohol drinking
dc.subjectMelanocortins
dc.subjectMetabolism and bioenergetics
dc.subjectNeuroinflammation
dc.subjectSynaptic dysfunction
dc.subjectaquaporin
dc.subjectcorticotropin releasing factor
dc.subjectcyclooxygenase 2
dc.subjectcytochrome P450
dc.subjectdynorphin
dc.subjectglial fibrillary acidic protein
dc.subjectglutathione
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinducible nitric oxide synthase
dc.subjectinterleukin 1beta
dc.subjectintermedin
dc.subjectmelanocortin
dc.subjectproopiomelanocortin
dc.subjecttoll like receptor 4
dc.subjecttumor necrosis factor
dc.subjectadolescent
dc.subjectalcohol abuse
dc.subjectArticle
dc.subjectbinge drinking
dc.subjectbrain development
dc.subjectbrain dysfunction
dc.subjectdrinking behavior
dc.subjecthomeostasis
dc.subjecthuman
dc.subjectimmunohistochemistry
dc.subjectin situ hybridization
dc.subjectlearning
dc.subjectmembrane potential
dc.subjectmemory
dc.subjectnerve cell plasticity
dc.subjectnervous system inflammation
dc.subjectoxidative stress
dc.subjectsynaptic transmission
dc.titleNew implications for the melanocortin system in alcohol drinking behavior in adolescents: The glial dysfunction hypothesis
dc.typeArticle


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