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Logo of jbcThe Journal of Biological Chemistry
J Biol Chem. 2014 February 21; 289(8): 4652.
PMCID: PMC3931027

Different Cellular Responses Lead to Varying Vulnerabilities of Neurons to Oxygen and Glucose Deprivation♦

Distinct Subunit-specific α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid (AMPA) Receptor Trafficking Mechanisms in Cultured Cortical and Hippocampal Neurons in Response to Oxygen and Glucose Deprivation

♦ See referenced article, J. Biol. Chem. 2014, 289, 4644–4651

When the blood supply to the brain is choked off, brain ischemia sets in, along with oxygen and glucose deprivation (OGD). The deprivation causes an accumulation of glutamate at the synapses and an overactivation of glutamate receptors. For reasons that are not clear, some neurons, such as hippocampal CA1 neurons, are more sensitive than others, such as those found in the cortex, to ischemia. In this Paper of the Week, Elena Blanco-Suarez and Jonathan G. Hanley at the University of Bristol in the United Kingdom describe one reason. By analyzing cultured cells, the investigators showed that, in cortical neurons, OGD does not cause the internalization of a type of glutamate receptor called AMPAR. In contrast, the more vulnerable hippocampal CA1 pyramidal neurons endocytose the GluA2 subunit of AMPARs, which leads to cell death. “These data demonstrate that populations of neurons with different vulnerabilities to OGD recruit distinct cell biological mechanisms in response to insult,” say the authors. “A crucial aspect of the mechanism leading to OGD-induced cell death is absent in cortical neurons.”

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Hippocampal neurons in culture are more vulnerable to OGD than cortical neurons.

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