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dc.contributor.authorTorres A.K.
dc.contributor.authorTapia-Rojas C.
dc.contributor.authorCerpa W.
dc.contributor.authorQuintanilla R.A.
dc.date.accessioned2020-09-02T22:29:18Z
dc.date.available2020-09-02T22:29:18Z
dc.date.issued2020
dc.identifier10.1016/j.neuroscience.2020.05.005
dc.identifier.citation438, , 70-85
dc.identifier.issn03064522
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6408
dc.descriptionBinge drinking is a common pattern of adolescent alcohol consumption characterized by a high alcohol intake within a short period of time; which may seriously affect brain function, triggering in some cases an addictive behavior. Current evidence indicates that alcohol addictive conduct is related to the impairment of the Melanocortin System (MCS). This system participates in the regulation of food intake and promotes anti-inflammatory response in the brain. However, the cellular mechanisms involved in the protective effects induced by MCS against binge-alcohol intoxication are still unknown. Here, we studied the effects of MCS activation on mitochondrial and oxidative damage induced by a binge-like protocol in the hippocampus of adolescent rats. We used a pharmacological activator of MC4R (RO27-3225) and evaluated its effects against oxidative injury, mitochondrial failure, and bioenergetics impairment induced by binge ethanol protocol in the hippocampus of adolescent's rats. Our results indicate that MC4R agonist reduces hippocampal oxidative damage promoting antioxidant (Nrf-2) and mitochondrial biogenesis (PGC1-alpha) pathways in animals subjected to the binge-like protocol. Additionally, MC4R activation prevented mitochondrial potential loss and increased mitochondrial mass that were significantly reduced by binge ethanol protocol. Finally, RO27-3225 treatment increased ATP production and mitochondrial respiratory complex expression in adolescent rats exposed to ethanol. Altogether, these findings show that activation of the MCS pathway through MC4R prevents these negative effects of binge ethanol protocol, suggesting a possible role of the MCS in the reduction of the neurotoxic effects induced by alcohol intoxication in adolescents. © 2020 IBRO
dc.language.isoen
dc.publisherElsevier Ltd
dc.subjectadolescence
dc.subjectalcohol
dc.subjectbinge-drinking
dc.subjectmelanocortin
dc.subjectmitochondria
dc.subjectadenosine triphosphate
dc.subjectalcohol
dc.subjectmelanocortin 4 receptor
dc.subjectperoxisome proliferator activated receptor gamma coactivator 1alpha
dc.subjectprotein inhibitor
dc.subjectro 27 3225
dc.subjecttranscription factor Nrf2
dc.subjectunclassified drug
dc.subjectadolescent
dc.subjectalcohol intoxication
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectantiinflammatory activity
dc.subjectArticle
dc.subjectbinge drinking
dc.subjectbioenergy
dc.subjectcontrolled study
dc.subjectdisorders of mitochondrial functions
dc.subjectenzyme activation
dc.subjecthippocampus
dc.subjectmale
dc.subjectmitochondrial biogenesis
dc.subjectneurotoxicity
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectprotein depletion
dc.subjectprotein expression
dc.subjectrat
dc.titleStimulation of Melanocortin Receptor-4 (MC4R) Prevents Mitochondrial Damage Induced by Binge Ethanol Protocol in Adolescent Rat Hippocampus
dc.typeArticle


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