Yaron David

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.

TL;DR: It is found that functional Na+ channel density is approximately four times lower in the AP trigger zone than in the middle of the AIS, where it is highest, which suggests that cable properties play a central role in determining where the AP starts, such that small plastic changes in the local AIS Na- channel density could have a large influence on neuronal excitability as a whole.

TL;DR: The features of the blood-brain barrier and their significance for neuronal homeostasis are reviewed to discuss clinical implications for neurological complications following cerebral ischemia.

TL;DR: The data suggest that TGF-β signaling in the brain can cause astrocyte activation whereby IL-6 upregulation results in dysregulation of astroCyte–neuronal interactions and neuronal hyperexcitability, as well as in FVB/N mice characterized as a relatively more susceptible strain to seizure-induced cell death.