Spare respiratory capacity, oxidative stress and excitotoxicity.
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.
Nicholls
David G
DG
Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA. dnicholls@buckinstitute.org
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
D009498:Neurotoxins; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D000255:Adenosine Triphosphate