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Summary  Seizures are a common manifestation of acute neurologic insults in neonates and are often resistant to the standard antiepileptic drugs that are efficacious in children and adults. The paucity of evidence‐based treatment guidelines, coupled with a rudimentary understanding of disease pathogenesis, has made the current treatment of neonatal seizures empiric and often ineffective, highlighting the need for novel therapies. Key developmental differences in γ‐aminobutyric acid ( GABA) ergic neurotransmission between the immature and mature brain, and trauma‐induced alterations in the function of the cation‐chloride cotransporters ( CCC s)  NKCC 1 and  KCC 2, probably contribute to the poor efficacy of standard antiepileptic drugs used in the treatment of neonatal seizures. Although  CCC s are attractive drug targets, bumetanide and other existing  CCC  inhibitors are suboptimal because of pharmacokinetic constraints and lack of target specificity. Newer approaches including isoform‐specific  NKCC 1 inhibitors with increased central nervous system penetration, and direct and indirect strategies to enhance  KCC 2‐mediated neuronal chloride extrusion, might allow therapeutic modulation of the  GABA ergic system for neonatal seizure treatment.  A PowerPoint slide summarizing this article is available for download in the Supporting Information section  here .

Pharmacotherapeutic targeting of cation‐chloride cotransporters in neonatal seizures