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dc.contributor.authorMira R.G.
dc.contributor.authorTapia-Rojas C.
dc.contributor.authorPérez M.J.
dc.contributor.authorJara C.
dc.contributor.authorVergara E.H.
dc.contributor.authorQuintanilla R.A.
dc.contributor.authorCerpa W.
dc.date.accessioned2020-09-02T22:23:01Z
dc.date.available2020-09-02T22:23:01Z
dc.date.issued2019
dc.identifier10.1016/j.drugalcdep.2019.107628
dc.identifier.citation205, , -
dc.identifier.issn03768716
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5338
dc.descriptionMany studies have reported that alcohol produces harmful effects on several brain structures, including the hippocampus, in both rodents and humans. The hippocampus is one of the most studied areas of the brain due to its function in learning and memory, and a lot of evidence suggests that hippocampal failure is responsible for the cognitive loss present in individuals with recurrent alcohol consumption. Mitochondria are organelles that generate the energy needed for the brain to maintain neuronal communication, and their functional failure is considered a mediator of the synaptic dysfunction induced by alcohol. In this review, we discuss the mechanisms of how alcohol exposure affects neuronal communication through the impairment of glutamate receptor (NMDAR) activity, neuroinflammatory events and oxidative damage observed after alcohol exposure, all processes under the umbrella of mitochondrial function. Finally, we discuss the direct role of mitochondrial dysfunction mediating cognitive and memory decline produced by alcohol exposure and their consequences associated with neurodegeneration. © 2019 Elsevier B.V.
dc.language.isoen
dc.publisherElsevier Ireland Ltd
dc.subjectAlcohol
dc.subjectGlutamate
dc.subjectMitochondria
dc.subjectNeurotoxicity
dc.subjectOxidative stress
dc.subjectSynapses
dc.subjectalcohol
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectn methyl dextro aspartic acid receptor
dc.subjectalcohol
dc.subjectn methyl dextro aspartic acid receptor
dc.subjectbioenergy
dc.subjectbrain function
dc.subjectcell communication
dc.subjectcell function
dc.subjectcognitive defect
dc.subjectcytokine production
dc.subjectdisorders of mitochondrial functions
dc.subjectexcitotoxicity
dc.subjectexposure
dc.subjecthuman
dc.subjectmental deterioration
dc.subjectmicroglia
dc.subjectnerve cell
dc.subjectnerve degeneration
dc.subjectnervous system inflammation
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectprotein localization
dc.subjectReview
dc.subjectsignal transduction
dc.subjectsynaptic transmission
dc.subjectanimal
dc.subjectdrug effect
dc.subjecthippocampus
dc.subjectmetabolism
dc.subjectmitochondrion
dc.subjectsynaptic transmission
dc.subjectAnimals
dc.subjectEthanol
dc.subjectHippocampus
dc.subjectHumans
dc.subjectMitochondria
dc.subjectReceptors, N-Methyl-D-Aspartate
dc.subjectSynaptic Transmission
dc.titleAlcohol impairs hippocampal function: From NMDA receptor synaptic transmission to mitochondrial function
dc.typeReview


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