The actin binding protein ?-actinin-2 expression is associated with dendritic spine plasticity and migrating granule cells in the rat dentate gyrus following pilocarpine-induced seizures

?-actinin-2 (?-actn-2) is an F-actin-crosslinking protein, localized in dendritic spines. In vitro studies suggested that it involved spinogenesis, morphogenesis, actin organization, cell migration and anchoring of the NR1 subunit N-methyl-D-aspartate (NMDA) receptors However, little known regarding its function vivo. We examined levels ?-actn-2 expression within dentate gyrus (DG) during development chronic limbic seizures (epileptogenesis) induced by pilocarpine rats. this model, plasticity DG glutamatergic granule cells including spine loss, neo-synaptogenesis, aberrant migration, alterations NMDA have been well characterized. showed immunolabeling was reduced inner molecular layer at 1-2 weeks post-status epilepticus (SE), when spinogenesis morphogenesis occur. This low level persisted stage new functional synapses are established. decreased protein concomitant with recovery drebrin A (DA), another actin-binding stage. Indeed, we demonstrated cultured contrast to DA, did not protect F-actin destabilization DA inhibited binding F-actin. Such alteration could affect Furthermore, co-down-regulated membrane fractions animals Last, expressed migrating newly born observed hilus pilocarpine-treated Altogether, our results suggest critical for structural integrity stabilization Instead, regulated occur cells. Our data also balance between may modulate