Abstract
The etiology of temporal lobe epilepsy is unclear, but proinflammatory molecules and disturbed neuron-glia communications are emerging as potential causers. A recent study (Nikolic et al. Glia 2018; https://doi.org/10.1002/glia.23519) revealed that pathologically elevated tumor necrosis factor α contributes to epileptogenesis, by boosting hyperexcitation through an autocrine mechanism involving purinergic signaling, astrocyte glutamate release, and modulation of neuronal transmitter release.
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