Uwe Heinemann

TL;DR: It is demonstrated that astrocytic gap junctions accelerate potassium clearance, limit potassium accumulation during synchronized neuronal firing, and aid in radial potassium relocation in the stratum lacunosum moleculare, and it is suggested that the perpendicular array of individualAstrocytes in thestratum radiatum makes these cells ideally suited for spatial buffering of potassium released by pyramidal cells, independent of gap junctional coupling.

TL;DR: It is proposed that the above-described cascade of events following common brain insults leads to brain dysfunction and eventually epilepsy and suggest TGF-betaRs as a possible therapeutic target.

TL;DR: This study established a model for focal disruption of the blood-brain barrier in the rat cortex by direct application of bile salts and found that a focus of epileptiform discharges developed within 4-7 d after treatment and could be recorded up to 49 d postoperatively in >60% of slices from treated animals but only rarely in sham-operated controls.

TL;DR: The present data identifies the TGF-β pathway as a novel putative epileptogenic signaling cascade and therapeutic target for the prevention of injury-induced epilepsy.

TL;DR: The data indicate a transcription-mediated astrocytic transformation early during epileptogenesis, which suggests that the resulting reduction in the clearance of extracellular potassium underlies frequency-dependent neuronal hyperexcitability and network synchronization.