The primary sensory receptors of our auditory system, the inner hair cells (IHCs), are highly specialised to convert the mechanical energy of sound into receptor potentials which can then propagate along the auditory pathway, enabling us to perceive sound. For IHCs to perform this function they require a specific set of ion channels. The most important of these is the mechanoelectrical transducer (MET) channel, which initiates the depolarisation of hair cells when it is opened in response to mechanical stimulation: without this channel IHCs cannot transduce sound. The IHCs also require two types of basolateral ion channels to function correctly in the mature cochlea, these channels carry the large, fast-activating Ca2+-activated K+ current, IK,f, and the hyperpolarisation-activated K+ current, IK,n (Marcotti 2003). These basolateral currents start to appear from the onset of hearing, which is around postnatal day 12 in mice, indicating that IHCs undergo a coordinated change in ion channel expression at this time. Around the same time, there is a rearrangement of the neuronal circuitry within the cochlea, with the efferent fibres no longer contacting the IHCs. The mechanism that triggers these changes is currently unknown. Numerous models of deafness, including those caused by faulty stereociliary hair bundle proteins, fail to undergo this maturational change. We hypothesise that the presence of the MET current in IHCs is necessary for the expression of the mature configuration of ion channels. We investigated how the removal of myosin VIIa, an important stereociliary protein, affected the presence of IK,f and IK,n. We used Myo7a6J/6J mice which have greatly reduced levels of myosin VIIa throughout life and have no measurable MET currents (Kros et al. 2002). Myo7afl/fl X Myo15-cre+/- mice were also investigated; these have a delayed, specific knockdown of Myo7a in hair cells. We performed whole cell patch clamp recordings from IHCs in acutely dissected organ of Corti of these mice. MET function was assessed by applying sinusoidal stimuli via a fluid jet, whilst recording in voltage clamp. Basolateral function was assessed in both current and voltage clamp. Data are expressed as mean ± standard error. As expected, we could not identify any sign of IK,f and IK,n in IHCs of Myo7a6J/6J mice at P20, indicating that the IHCs had not matured correctly without the MET current. The MET current in Myo7afl/flMyo15-cre+/- mice was normal compared to wild-type mice at P9-P10 but started to deteriorate by P14 (P15 WT: -974 ± 63 pA, n = 6, vs P14 mutant: -669 ± 96 pA, n = 4, P<0.05). From this point onwards, the size of the MET progressively declined in Myo7afl/flMyo15-cre+/- mice (P16: -377 ± 64 pA, n = 6). Interestingly, IHCs from the Myo7afl/flMyo15-cre+/- mice had a normal IK,f and IK,n at P14-P15. However, these currents started to deteriorate in Myo7afl/flMyo15-cre+/- mice compared to their wild-type littermates by P19-P21 (IK,f: 1.3 ± 0.1, n = 13, vs 1.9 ± 0.2, n = 11; IK,n: 200 ± 16, n = 11, vs 275 ± 21, n = 11, both P<0.05) and were completely missing by P59. Further to this, at P22 the IHCs of Myo7afl/flMyo15-cre+/- mice were not responsive to efferent neuron stimulation, as would be expected for the mature configuration. By P33, however, these IHCs responded robustly to efferent neuronal stimulation, showing that efferent neurons were also returning to an immature configuration. Our results show that when the MET current is present prior to the onset of hearing, IHCs are capable of changing into their mature configuration, however, if the MET current is not present, IHCs remain in an immature state. Moreover, we show that even if IHCs make this transition into the mature configuration, they require functioning MET apparatus to maintain this mature status. Further investigation of this model and an understanding of the mechanism by which MET controls basolateral ion channel expression and efferent innervation, would help us to understand how IHC function deteriorates following damage to the MET apparatus in various forms of deafness, for example, in age-related hearing loss.