What neurotransmitter is primarily responsible for excitotoxicity following cerebral artery blockage?

Excitotoxicity is a process where nerve cells become damaged and die due to excessive stimulation by neurotransmitters. In the context of cerebral artery blockage, the primary neurotransmitter involved in the excitotoxic process is glutamate.

When cerebral ischemia occurs, there is an increase in extracellular glutamate levels due to the impairment of its uptake and the release from neurons that are depolarized. This elevated glutamate concentration leads to overstimulation of glutamate receptors, particularly the NMDA (N-methyl-D-aspartate) receptors, resulting in an influx of calcium ions into the cells. The excessive calcium influx triggers a cascade of pathological processes, including the activation of various enzymes that can damage cellular structures and ultimately lead to neuronal death.

Understanding this mechanism is crucial, especially in the context of stroke or other conditions causing reduced blood flow to the brain, as targeting glutamate signaling pathways is being explored for potential neuroprotective strategies.