In terms of KCC2 functionality, the results showed changes that were more robust; the EtOH diet post-ischemia completely rescued the positive shift in ΔEGABA caused by the decrease in Cl ̄ extrusion capability due to KCC2 removal (Fig. 3c; sham = − 0.14 ± 0.008 mV/μm; sucrose post-ischemia = − 0.07 ± 0.017 mV/μm; EtOH pI = − 0.15 ± 0.009 mV/μm). This evidence concerns the gene SLC12A5 and ischemia.