Alteration of GLUR2 expression in the rat brain following absence seizuresinduced by gamma-hydroxybutyric acid

We explored the involvement of the glutamate receptor subunit B (GluR2) in the mechanism of absence seizures induced by gamma -hydroxybutyric acid (GH B). The expression and distribution of GluR2 protein in rat brain were exam ined during and after GHB-induced absence seizures. The data indicate that GluR2 protein expression significantly decreases following the onset of abs ence seizures. The suppression of GluR2 expression was prolonged and it out lasted the duration of the continuous absence seizure activity. The alterat ion of GluR2 protein levels was accompanied by a re-distribution of GluR2 e xpression from laminae V to IV in cerebral cortex. We also analyzed the dur ation and latency of absence seizures induced by GHB 72 h following an init ial GHB-induced absence seizure, a time when suppression of GluR2 protein w as maximal. The second absence seizure was significantly more prolonged tha n the first. These data may indicate that the putative down-regulation of G luR2 following GHB-induced absence seizure could have contributed to the po tentiation of subsequent seizures in animals. A related hypothesis posed by the data is that down-regulation of GluR2 is involved in the mechanisms of the maintenance of recurrent absence seizure activity once it is initiated and therefore, may contribute to the chronicity of seizures in absence epi lepsy. (C) 2001 Elsevier Science B.V. All rights reserved.