Increased mitochondrial respiration maintains the mitochondrial membrane potential and promotes survival of cerebellar neurons in an endogenous model of glutamate receptor activation

Abstract

La activación de los receptores de glutamato, conseguida por inhibición de su transporte provocando incremento de las concentraciones extracelulares del aminoácido, causa un incremento de la velocidad del transporte electrónico a través de la cadena respiratoria mitocondrial en cultivos de neuronas de cerebelo. Esta activación tiene como fin mantener el potencial de membrana mitocrondrial en las neuronas, por lo que se trata de un mecanismo neuroprotector.

It is thought that the combination of extracellular glutamate accumulation and mitochondrial damage is involved in neuronal death associated with brain ischemia and hypoglycemia, and some neurodegenerative diseases such as Huntington s disease. However, the mechanism whereby those two factors interact together to trigger neurodegeneration in this and other neurodegenerative disorders is still elusive. Here, we have addressed this issue using a model of mild and sustained accumulation of extracellular glutamate in cerebellar cultured neurons, which are mostly glutamatergic and commonly used to study glutamate neurotoxicity.