Neuroprotection in ischemia: blocking calcium-permeable acid-sensing ion channels.

By Z. Xiong, Xiao-man Zhu, X. Chu, M. Minami, Jessica Hey, Wenlin Wei, J. Macdonald, J. Wemmie, M. Price, M. Welsh and 1 more. Cell, 2004

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Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, background): “acidosis, which in turn increases Ca influx by activating acidsensing ion channels [113].”
Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications (2021, background): “Specific ASIC1a blockade by the tarantula toxin psalmotoxin (PcTX) reduced infarct volume following ischemic stroke in rodents.(371,372) Hi1a, a disulfide‐rich spider venom peptide and an ASIC1a inhibitor, has also shown similar neuroprotection in MCAO rats.”
NMDA Receptor Subunits Have Differential Roles in Mediating Excitotoxic Neuronal Death Both In Vitro and In Vivo (2007, background): “Whatever the precise mechanism, our study establishes that NR2A- and NR2B-containing subpopulations of NMDA receptors have differential roles in mediating neuronal survival and death and hence provides a molecular basis for the paradoxical actions of NMDA receptor antagonism in producing both…”
Necrotic death as a cell fate. (2006, background): “Extracellular Ca2+ can enter cells through three types of channels in the plasma membrane: voltage-gated channels controlled by the potential across the plasma membrane (Fatt and Ginsborg 1958), capacitive entry channels that are activated by the emptying of the ER Ca2+ store (Putney 1986; Berridge ”