Excitotoxicity pathways

Excitotoxicity pathways represent a set of molecular and cellular mechanisms initiated by excessive activation of excitatory amino acid receptors, notably glutamate receptors such as NMDA, AMPA, and kainate receptors, on neurons. This leads to pathological calcium influx, mitochondrial dysfunction, oxidative stress, activation of proteolytic enzymes, and downstream cell death cascades including apoptosis and necrosis[3][5][7]. Excitotoxicity is implicated in diverse neurological diseases, especially acute injury (stroke, trauma) and chronic neurodegenerative diseases. While not a drug target itself, many therapeutic strategies focus on modulating specific components of these pathways, such as receptor antagonists or glutamate transporter enhancers, aiming to prevent or lessen neuronal damage[3][4][5][7].

Other names

Excitotoxic signaling pathwayGlutamate excitotoxicity cascadeNeuronal excitotoxicity pathway

Inhibition of NMDA receptor channel opening; Modulation of synaptic glutamate levels (glutamate transporter enhancement); Antagonism of AMPA, kainate, or metabotropic glutamate receptors; Reduction in calcium influx