Abstract
Excitotoxicity is the neuronal death produced by the aberrant and sustained activation of N-methyl-D-aspartate receptors (NMDARs) and the neurotransmitter glutamate. NADPH-diaphorase neurons [also known as nNOS (+) neurons] are a subpopulation of aspiny interneurons, largely spared in excitotoxic conditions. Previous findings from our group have indicated that, unlike nNOS (-) cells, nNOS (+) neurons lack the production of reactive oxygen species (ROS) in response to NMDAR activation. This is a critical divergent step in the excitotoxic cascade; however, additional mechanisms underlying the reduced vulnerability of nNOS (+) neurons to NMDAR-driven neuronal death have not been explored.
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