Mostrar el registro sencillo del ítem
Alcohol impairs hippocampal function: From NMDA receptor synaptic transmission to mitochondrial function
dc.contributor.author | Mira R.G. | |
dc.contributor.author | Tapia-Rojas C. | |
dc.contributor.author | Pérez M.J. | |
dc.contributor.author | Jara C. | |
dc.contributor.author | Vergara E.H. | |
dc.contributor.author | Quintanilla R.A. | |
dc.contributor.author | Cerpa W. | |
dc.date.accessioned | 2020-09-02T22:23:01Z | |
dc.date.available | 2020-09-02T22:23:01Z | |
dc.date.issued | 2019 | |
dc.identifier | 10.1016/j.drugalcdep.2019.107628 | |
dc.identifier.citation | 205, , - | |
dc.identifier.issn | 03768716 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/5338 | |
dc.description | Many 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.iso | en | |
dc.publisher | Elsevier Ireland Ltd | |
dc.subject | Alcohol | |
dc.subject | Glutamate | |
dc.subject | Mitochondria | |
dc.subject | Neurotoxicity | |
dc.subject | Oxidative stress | |
dc.subject | Synapses | |
dc.subject | alcohol | |
dc.subject | immunoglobulin enhancer binding protein | |
dc.subject | n methyl dextro aspartic acid receptor | |
dc.subject | alcohol | |
dc.subject | n methyl dextro aspartic acid receptor | |
dc.subject | bioenergy | |
dc.subject | brain function | |
dc.subject | cell communication | |
dc.subject | cell function | |
dc.subject | cognitive defect | |
dc.subject | cytokine production | |
dc.subject | disorders of mitochondrial functions | |
dc.subject | excitotoxicity | |
dc.subject | exposure | |
dc.subject | human | |
dc.subject | mental deterioration | |
dc.subject | microglia | |
dc.subject | nerve cell | |
dc.subject | nerve degeneration | |
dc.subject | nervous system inflammation | |
dc.subject | nonhuman | |
dc.subject | oxidative stress | |
dc.subject | priority journal | |
dc.subject | protein localization | |
dc.subject | Review | |
dc.subject | signal transduction | |
dc.subject | synaptic transmission | |
dc.subject | animal | |
dc.subject | drug effect | |
dc.subject | hippocampus | |
dc.subject | metabolism | |
dc.subject | mitochondrion | |
dc.subject | synaptic transmission | |
dc.subject | Animals | |
dc.subject | Ethanol | |
dc.subject | Hippocampus | |
dc.subject | Humans | |
dc.subject | Mitochondria | |
dc.subject | Receptors, N-Methyl-D-Aspartate | |
dc.subject | Synaptic Transmission | |
dc.title | Alcohol impairs hippocampal function: From NMDA receptor synaptic transmission to mitochondrial function | |
dc.type | Review |