Abstract
Importins, also called karyopherins, belong to a large family of proteins involved in cytoplasm‐to‐nucleus transport. Transport machinery generally involves a complex formed by two different importin subtypes (α and β). Both α and β importins are expressed in the brain, and their expression and localization is regulated by physiological neuronal activity. Little is known about regulation of importin expression in brain pathological conditions. Here we studied the expression of importin β1 (impβ1) in the rat hippocampus after acute and chronic seizures induced by the glutamate agonist kainic acid (KA). The overall content of impβ1 mRNA and protein did not change after acute KA seizures. However, acute KA seizures rapidly induced the translocation of impβ1 protein from the cytoplasm to the nucleus in pyramidal CA1 neurons. KA‐induced impβ1 translocation was prevented by the NMDA (N‐methyl‐D‐aspartic acid) receptor blocker MK‐801. After chronic seizures, the overall levels of impβ1 mRNA and protein did not change in the whole hippocampus. Immunohistochemistry revealed a massive loss of impβ1‐positive neurons in pyramidal layers (that degenerated after KA), whereas an increased number of impβ1‐positive cells was detected in the stratum radiatum of rats with chronic seizures compared with control animals. Double‐labeling experiments identified these cells as glial cells expressing the chondroitin sulfate proteoglycan NG2 (neuron/glial antigen 2), a glial subtype recently shown to regulate hippocampal neuron excitability. These data show a differential regulation of impβ1 expression after acute and chronic seizure activity in the rat hippocampus. © 2008 Wiley‐Liss, Inc.