Human glioma cells induce hyperexcitability in cortical networks

摘要: SUMMARY Purpose: Patients with gliomas frequently present seizures, but the factors associated seizure development are still poorly understood. In this study, we assessed peritumoral synaptic network activity in a glioma animal model and tested contribution of aberrant glutamate release from on glioma-associated epileptic activity. Methods: vitro brain slices were made gliomaimplanted mice. Using extracellular field recordings, analyzed epileptiform induced by Mg 2+ -free medium tumor-bearing animals sham-operated controls. We effect sulfasalazine (SAS), blocker system x c release, spontaneous evoked tumorassociated slices. Key Findings: Tumor-associated cortical networks hyperexcitable. The onset latency -free‐induced was significantly shorter tumorbearing slices, incidence ictal-like events higher. Block decreased response area completely blocked ictallike, not interictal-like events. Significance: Control seizures patients is an essential component clinical management; therefore, understanding origin vital. This work provides evidence that disrupted tumor masses resulting excitability. show blocking via SAS, drug already approved U.S. Food Drug Administration (FDA), can inhibit similar to other chemicals used decrease We, suggest further studies should consider SAS promising agent aid treatment gliomas.