Excitotoxicity

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WiseOne said:
Does excitotoxicity only occur in situations involving low [O2] or glucose? What other situations would result in excitotoxic damage?
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Another thing that comes to mind (possibly) is like withdrawal of EtOH in a chronic alcoholic since they have upregulated their NMDA receptors and now with no EtOH to stimulate the gabas the increased NMDAs could lead to excitotox...
 
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Another thing that comes to mind (possibly) is like withdrawal of EtOH in a chronic alcoholic since they have upregulated their NMDA receptors and now with no EtOH to stimulate the gabas the increased NMDAs could lead to excitotox...
Click to expand...

Good point, also along those lines from Neuro roadmap pg 42:

Ischemia in stroke patients: decreased O2= decreased ATP which means Glutamate cannot be taken back up by damaged neurons which in turn prolongs its effect.

Epilepsy causes Glut-induced damage to GABA neurons which means less inhibition, and consequently, future seizures.

Basically Glut works on NMDA receptors and increases intracellular Ca2+, which then wreaks havoc on organelles by activating a bunch of enzymes and screwing with the membrane permeability, and eventually causes apoptosis (goljan 6-7).
 
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AFAIK, excitotoxicity is always associated with stroke, seizures, or brain injury. Nothing else. Someone correct me if I'm wrong.

(Even in alcohol withdrawal, seizures trigger excessive glutamate release, or are caused by excess glutamate).
 
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