Our results also indicate that neonatal stroke/seizures left undetected or untreated for extended periods of time alter the acute and sub-acute developmental profiles of the adult-form chloride co-transporter KCC2 such that the later seizures may become resistant to treatment with the conventional anticonvulsants that act as GABAA agonists (Puskarjov et al., 2014b, 2015). This evidence concerns the gene SLC12A5 and stroke disorder.