dc.creatorMira, Rodrigo G.
dc.creatorTapia Rojas, Cheril
dc.creatorPérez, María José
dc.creatorJara, Claudia
dc.creatorVergara, Erick H.
dc.creatorQuintanilla, Rodrigo A.
dc.creatorCerpa Nebott, Waldo Francisco
dc.date.accessioned2024-01-29T17:48:28Z
dc.date.accessioned2024-05-02T19:54:18Z
dc.date.available2024-01-29T17:48:28Z
dc.date.available2024-05-02T19:54:18Z
dc.date.created2024-01-29T17:48:28Z
dc.date.issued2019
dc.identifier10.1016/j.drugalcdep.2019.107628
dc.identifier0376-8716
dc.identifierhttps://doi.org/10.1016/j.drugalcdep.2019.107628
dc.identifierhttps://repositorio.uc.cl/handle/11534/81013
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/9273148
dc.description.abstractMany 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.
dc.languageen
dc.rightsacceso restringido
dc.subjectAlcohol
dc.subjectSynapses
dc.subjectGlutamate
dc.subjectMitochondria
dc.subjectOxidative stress
dc.subjectNeurotoxicity
dc.titleAlcohol impairshippocampal function:FromNMDAreceptorsynaptic transmissiontomitochondrial function
dc.typeartículo de revisión


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