GABA receptor proteins within lipid rafts in the AY-9944 model of atypical absence seizures.

Purpose: The inhibition of cholesterol synthesis with AY-9944 (AY) results in chronic recurrent atypical absence seizures in rodents. We hypothesized that cholesterol inhibition during the course of creating the AY model of atypical absence seizures results in an alteration of the entry of gamma-aminobutyric acid (GABA)(A) and GABA(B) receptors into lipid rafts that contributes to epileptogenesis in this model.

Methods: The cholesterol synthesis inhibitor AY (7.

Ischemia and status epilepitcus result in enhanced phosphorylation of calcium and calmodulin-stimulated protein kinase II on threonine 253.

Ca2+-stimulated protein kinase II (CaMKII) is critically involved in the regulation of synaptic function and is implicated in the neuropathology associated with ischemia and status epilepticus (SE). The activity and localization of CaMKII is regulated by multi-site phosphorylation. In the present study we investigated the effects of global ischemia followed by reperfusion and of SE on the phosphorylation of CaMKII on T253 in rat forebrains and compared this to the phosphorylation of T286.

Typical versus atypical absence seizures: network mechanisms of the spread of paroxysms.

Purpose: Typical absence seizures differ from atypical absence seizures in terms of semiology, EEG morphology, network circuitry, and cognitive outcome, yet have the same pharmacological profile. We have compared typical to atypical absence seizures, in terms of the recruitment of different brain areas. Our initial question was whether brain areas that do not display apparent paroxysmal discharges during typical absence seizures, are affected during the ictal event in terms of synchronized activity, by other, distant areas where seizure activity is evident.

Increase in tyrosine phosphorylation of the NMDA receptor following the induction of status epilepticus.

The administration of lithium followed by pilocarpine induces status epilepticus (SE) that produces neurodegeneration and the subsequent development of spontaneous recurrent seizures. We have reported that tyrosine phosphorylation of the NMDA receptor is elevated over controls for several hours following 60 min of SE. In the current study, we assessed the temporal relationship between tyrosine phosphorylation of the NMDA receptor and the onset of SE.