GABAergic interneurons (INs) and their maturation play a pivotal role in various brain functions, with implications for a wide spectrum of neurological and psychiatric disorders. Among the key regulators of GABAergic inhibition, the cation chloride co-transporter KCC2 is central; influencing interneuronal function, CNS development, plasticity, and disease pathology. While KCC2's role in principal neurons’ transition of GABAergic signaling from depolarizing to hyperpolarizing is well-documented, its expression patterns and functional significance in interneurons, particularly during early neonatal stages, remain largely unexplored.This study employs advanced methodologies including patch-sequencing, gramicidin perforated patch, neurotransmitter uncaging, and transmission electron ultrastructure microscopy to unveil the early expression of KCC2 in neonatal INs. Additionally, it validates hyperpolarizing GABAergic function in these interneurons for the first time. Leveraging single-cell transcriptomics, the research further delineates distinct interneuronal populations expressing KCC2, characterized by precocious firing properties crucial for regulating cortical network activity and excitability.This pioneering investigation provides a comprehensive examination of somatosensory cortical interneurons during the neonatal stage, spanning morphology, electrophysiological properties, and transcriptomics. By shedding light on early developmental mechanisms and the unique chloride homeostatic profile of interneuronal populations, this study advances our understanding of fundamental processes underlying brain function and dysfunction.