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Due to this dysfunction, there is an increase in the levels of glutamate in the synaptic cleft that activates the glutamate receptors which are present in the post-synaptic neurons (N-Methyl-D-aspartic acid (NMDA), α-amino-3-hidroxi-5-methyl-4-isoxazolpropionic acid (AMPA), Kainate, and metabotropic glutamate (mGLUR) receptors), leading to excitotoxicity