Building a Bridge Between NMDAR‑Mediated Excitotoxicity and Mitochondrial Dysfunction in Chronic and Acute Diseases

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dc.catalogadorjlo
dc.contributor.authorMira, Rodrigo G.
dc.contributor.authorCerpa Nebott, Waldo Francisco
dc.date.accessioned2024-01-29T17:48:29Z
dc.date.available2024-01-29T17:48:29Z
dc.date.issued2021
dc.description.abstractGlutamate is the major excitatory neurotransmitter in the brain, and it is widely accepted to play a role in synaptic plasticity and excitotoxic cell death. Glutamate binds to several receptors, including ionotropic N-methyl-D-Aspartate receptor (NMDAR), which is essential in synaptic plasticity and excitotoxicity. This receptor is a calcium channel that is located in synaptic and extrasynaptic sites, triggering different signalling cascades in each case. The calcium entry through extrasynaptic NMDARs is linked to calcium overload in the mitochondria in neurons in vitro. The mitochondria, besides their role in ATP production in the cell, participate in calcium homeostasis, acting as a buffering organelle. Disruption of mitochondrial calcium homeostasis has been linked to neuronal death either by triggering apoptosis or driven by the opening of the mitochondrial transition pore. These cell-death mechanisms contribute to the pathophysiology of diverse diseases such as neurodegenerative Alzheimer’s disease or Parkinson’s disease, and acute neuropathological conditions such as stroke or traumatic brain injury. In this review, we will address the available evidence that positions the mitochondria as an essential organelle in the control of calcium-mediated toxicity, highlighting its role from the perspective of specific NMDAR signalling microdomains at the level of the central synapse.
dc.fuente.origenORCID-ene24
dc.identifier.doi10.1007/s10571-020-00924-0
dc.identifier.issn0272-4340
dc.identifier.urihttps://doi.org/10.1007/s10571-020-00924-0
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/81016
dc.information.autorucFacultad de Ciencias Biológicas; Mira Guzmán, Rodrigo Andrés; S/I; 215451
dc.information.autorucFacultad de Ciencias Biológicas; Cerpa Nebott, Waldo Francisco; 0000-0001-7344-0144; 16584
dc.language.isoen
dc.nota.accesoContenido completo
dc.pagina.final1430
dc.pagina.inicio1413
dc.revistaCellular and Molecular Neurobiology
dc.rightsacceso abierto
dc.subjectNMDAR
dc.subjectCalcium 
dc.subjectMitochondria
dc.subjectExcitotoxicity
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.titleBuilding a Bridge Between NMDAR‑Mediated Excitotoxicity and Mitochondrial Dysfunction in Chronic and Acute Diseases
dc.typeartículo
dc.volumen41
sipa.codpersvinculados215451|16584
sipa.trazabilidadORCID;2024-01-15
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