Hippocalcin protects hippocampal neurons against excitotoxin damage by enhancing calcium extrusion.

摘要: Hippocalcin, which is a member of the neuronal calcium-sensor protein family, highly expressed in hippocampal pyramidal cells. Recently, it was demonstrated that hippocalcin deficit caused an increase cell death field CA3 Ammon's horn (CA3) region hippocampus following systemic injection kainic acid. Treatment with acid results seizure-induced CA3. In present study, we injected quinolinic acid, N-methyl-d-aspartate receptor agonist, into CA1 (CA1) hippocalcin-knockout (-/-) mice, procedure mimics transient ischemia. Although significant pyknotic changes were observed at site wild-type (+/+) mice 24 h after injection, area cells extended throughout -/- mice. The quantification numbers Nissl-stained sections indicated damage more severe than +/+ density terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling-positive roughly paralleled Primary cultures neurons showed number surviving from 7 days culture smaller measurement intracellular calcium concentrations single revealed extrusion slower neurons. involvement upkeep confirmed using hippocalcin-expressing COS7 These suggest plays important role and, turn, helps to protect them against calcium-dependent excitotoxin hippocampus.