FIG. 3.

A working model of NMDA antagonist-induced neuronal cell death. Excessive activation of upregulated NMDA receptors results in a calcium overload that exceeds the buffering capacity of the mitochondria and interferes with electron transport yielding ROS. This in turn causes dissociation and nuclear translocation of transcription proteins such as NF-κB that bind to genes such as P53 and Bcl-XL. The downregulation of Bcl-XL combined with an increase in Bax, diminishes the formation of antiapoptotic Bax/Bcl-XL heterodimers in favor of proapoptotic Bax/Bax homodimers.