At the initial stages in neuronal development, GABAergic and glycinergic neurotransmission exert depolarizing responses, assumed to be of importance for maturation, which in turn shift to hyperpolarizing in early postnatal life due to development of the chloride homeostasis system. Spherical bushy cells (SBC) of the mammalian cochlear nucleus integrate excitatory glutamatergic inputs with inhibitory (GABAergic and glycinergic) inputs in order to compute signals that contribute to sound localization based on interaural time differences. To provide a fundamental understanding of the properties of GABAergic neurotransmission in mammalian cochlear nucleus, we investigated the reversal potential of the GABA-evoked currents (E_GABA) by means of gramicidin-perforated patch recordings in developing SBC. The action of GABA switches from depolarizing to hyperpolarizing by the postnatal day 7 due to the negative shift in E_GABA. Furthermore, we studied the expression pattern of the K⁺-Cl^--extruding cotransporter KCC2, previously shown to induce a switch from neonatal Cl^- efflux to the mature Cl^- influx in various neuron types thereby causing a shift from depolarizing to hyperpolarizing GABA action. The KCC2 protein is expressed in SBC already at birth, yet its activity is attained towards the end of the first postnatal week, as indicated by pharmacological inhibition. Interruption of the Cl^- extrusion by DIOA or furosemide gradually shifted E_GABA in positive direction with increasing maturity, suggesting that KCC2 could be involved in maintaining low [Cl^-]_i after the postnatal day 7 thereby providing the hyperpolarizing Cl^--mediated inhibition in SBC.