Outer hair cells (OHCs) function as electromotile amplifiers of basilar membrane motion, thereby increasing the mechanical sensory input to the inner hair cells (IHCs) that function as the primary auditory receptors in the cochlea. This action of OHCs is voltage-dependent, and is thought to be under efferent control via the olivocochlear pathway that in mammals targets the OHCs. The efferents exert inhibitory synaptic control via an acetylcholine receptor (AChR) in the OHCs that functions as a calcium influx pathway, leading to activation of calcium-activated potassium channels which increases cell conductance thereby reducing both the receptor potential and electromotility. During cochlear development in mice, which continues during the first two weeks after birth, the efferents transiently innervate the IHCs before reaching the OHCs. This might serve to modulate the firing properties of immature IHCs which are thought to help strengthen the formation of mature auditory neuronal connections. In this study we have investigated responses to ACh in mouse IHCs at 6-10 days after birth, when efferent-IHC synapses are present. The apical turn of the cochlea was isolated and the basal surfaces of the IHCs exposed by mechanically stripping away the outer rim of the organ of Corti, following removal of the tectorial membrane. Whole-cell voltage-clamp recordings were made in artificial perilymph and ACh (0.1 mM) was applied from a puffer pipette positioned nearby. The current-voltage (I-V) relation for the ACh-sensitive current showed inward and outward rectification with a reversal potential at 0 mV (cesium-based internal filling solution with 10 mM BAPTA). The current activated over about 0.5s. The current was cationic since in low (30 mM) external sodium (replaced by n-methyl-glucamine) the reversal potential was -19 mV and currents were much smaller, particularly at negative voltages. Preliminary data is suggestive of a block of the AChR by external divalent cations since the largest responses were observed in solutions lacking calcium or magnesium. The I-V data was fitted with a single energy barrier model, which assumes a single blocking site within the channel pore, usually assumed to be occupied by divalent cations. The fit indicated that the blocking site was 0.3-0.4 of the way through the channel from the outside. In comparison with data from adult outer hair cells the main difference is that AChRs in IHCs produce larger and more slowly activating cationic currents, although it is unclear whether this reflects differences in the respective AChRs. If so, this might indicate that the hair cell AChR itself undergoes maturation so that it is appropriately matched to modulate the function of IHCs and OHCs during development and in the mature cochlea respectively.