title: Spare respiratory capacity, oxidative stress and excitotoxicity.
abstract: Chronic exposure to glutamate (glutamate excitotoxicity) exacerbates neuronal damage in the aftermath of stroke and is implicated in a variety of neurodegenerative disorders. Mitochondria play a central role in the survival or death of the exposed neuron. Calcium, oxidative stress and ATP insufficiency play closely interlocked roles that may be investigated with primary neuronal cultures.
authors.affiliation: Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA. dnicholls@buckinstitute.org
authors.forename: David G
authors.initials: DG
authors.lastname: Nicholls
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D019069:Cell Respiration / Q000502:physiology*; D018698:Glutamic Acid / Q000378:metabolism / Q000633:toxicity; D008928:Mitochondria / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000378:metabolism; D009498:Neurotoxins / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D017470:Receptors, Glutamate / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism
chemical_list: D009498:Neurotoxins; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D000255:Adenosine Triphosphate