Excitotoxicity

Excitotoxicity is a pathological process by which nerve cells are damaged and killed by excessive stimulation by neurotransmitters such as glutamate and similar substances. This process can occur in various neurological disorders including stroke and Alzheimer's disease.

Overview

Excitotoxicity can be caused by overactivation of NMDA receptors, which leads to an influx of calcium ions into the cell. This influx of calcium can activate enzymes that damage cell structures such as components of the cytoskeleton, membrane, and DNA.

Mechanism

The process of excitotoxicity is initiated by the binding of glutamate to the NMDA receptor, which allows calcium ions to enter the neuron. This influx of calcium activates a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain. These enzymes go on to damage cell structures such as components of the cytoskeleton, membrane, and DNA.

Role in disease

Excitotoxicity is implicated in various neurological diseases. For example, it is a major cause of damage in hypoxic-ischemic brain injury (stroke). In addition, excitotoxicity is thought to be the process by which overactive glutamate receptors contribute to the neuronal death observed in Alzheimer's disease.

Treatment

There are currently no effective treatments for excitotoxicity. However, research is ongoing to find ways to modulate glutamate receptors and prevent excitotoxicity.

See also

• Glutamate receptor
• NMDA receptor
• Stroke
• Alzheimer's disease

References

• Low Ca2+ buffering and excitotoxicity under physiological stress and pathophysiological conditions in motor neuron (MNs)
  Low Ca2+ buffering and excitotoxicity under physiological stress and pathophysiological conditions in motor neuron (MNs)