Pharmacological inhibition of microglia (minocycline) or TrkB (K252a) effectively restored KCC2 expression, normalized E<sub>GABA</sub>, and reduced post-stroke seizure severity.<h4>Conclusion</h4>Our findings identify microglia-derived BDNF/TrkB signaling as a critical upstream pathway mediating KCC2 dysfunction in early post-stroke seizure. Here, SLC12A5 is linked to Stroke.