RESEARCH ARTICLE Death Associated Protein K neurodegenerative mecha To

Excitotoxicity is a neurodegenerative process believed to be the central mediator of brain damage in acute condi-excessive influx of ions (especially Ca) into the postsyn-aptic neurons leads to their cell death via a spectrum of Del Rosario et al. BMC Neuroscience (2015) 16:25 DOI 10.1186/s12868-015-0158-2specific signaling cascades in excitotoxicity downstream ofUSA Full list of author information is available at the end of the articletions such as brain ischemia and traumatic injury, and an important contributor to a range of chronic neurodegen-erative diseases [1-4]. In excitotoxicity, the malfunction of Glutamate (Glu) Transporters (GluTs) [5-7] causes accu-mulation of Glu in excitatory synapses and exaggerated mechanisms that range from necrosis (at the core of the ischemic damage) to apoptosis or even recovery (at the penumbra). Despite our familiarity with the first few steps in excitotoxicity, our understanding of the steps following Ca2+ influx is very limited. Clinical trials using GluRs an-tagonists ended with disappointment, and recent data sug-gests that using antagonists to block GluR functions might be counterproductive, because Glu signaling includes both neurotoxic and pro-survival cascades [9,10]. These com-plications emphasize the need to illuminate cell-death