Examples of excitotoxicity

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Neuronal injury in the cell cultures resulting from glutamate excitotoxicity is assessed by quantifying the release of lactate dehydrogenase into the culture medium.
Research into pathogenesis has shed light on the possible mechanisms of injury, which include mechanical, vascular, immunological and excitotoxicity.
These results show that l-glutamate can be used as an excitotoxic agent to eliminate cholinergic amacrine cells, but that this excitotoxicity is not selective.
One of the functions of membrane-associated glutamate transpor ters which has received considerable attention is that of preventing excitotoxicity.
Glutamate excitotoxicity contributes to oligodendrocytes death and myelin loss in multiple sclerosis and other neurodegenerative conditions.
Together these findings provide insights into how activation of microglia alters glutamate homeostasis, which results in oligodendrocyte excitotoxicity.
Excitotoxicity appears to play a role in both neurodegenerative and cerebrovascular diseases.
Therapies designed to directly abrogate neuronal excitotoxicity might also prove to be advantageous.
The molecular pathways that underlie these mechanisms might be important in protecting against excitotoxicity.
An experimental basis for implicating excitotoxicity in glaucomatous optic neuropathy.
Furthermore, the continual activation of high frequency cortical areas through the "edge effect" provides a framework for the development of excitotoxicity of cortical cells.
Furthermore, the continuous high frequency cortical activation due to the edge effect provides a framework for the development of excitotoxicity of cortical cells.
It is likely that inflammation and excitotoxicity together contribute to neuronal damage beyond the initial insult of acute trauma.
Several other trials of agents targeted against glutamate excitotoxicity have sadly been disappointing.
We believe that there is enough precedent to believe that these questions will lead to a uniquely useful view of the underlying mechanisms of excitotoxicity.
This increase was predominantly due to excitotoxicity as well as oxidative stress.
If initial responses of receptor desensitization and more inhibitory receptors are not sufficient to control overactivity, then excitotoxicity is likely.

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