Evidence supporting P2X7R contributing to brain hyperexcitability via driving inflammation include that (i) P2X7Rs are highly expressed on microglia, which increases following status epilepticus and increases during epilepsy [87,100], (ii) blocking of P2X7Rs during status epilepticus reduced hippocampal IL-1β levels [83] (iii) and the fact that while microglia from P2X7R-overexpressing mice showed a pro-inflammatory phenotype during status epilepticus [100], microglia from P2X7R KO mice presented an anti-inflammatory phenotype following hypoxia-induced seizures in neonatal mouse pups [98]. Here, IL1B is linked to status epilepticus.