In vivo recordings show that cochlear afferent neurons fire bursts of action potentials from P0 on (1), about two weeks before hearing onset in rats. This ‘spontaneous’ activity of the auditory nerve fibers is driven by glutamate release from inner hair cells (IHCs), that themselves can fire spontaneous calcium action potentials. By analogy to retinal development, it has been suggested that such a spontaneous activity may promote the survival and functional maturation of auditory neurons and guide the refinement of synaptic connections in the auditory brainstem (for review see (2)). Different mechanisms have been shown to contribute to IHCs depolarization. Those include the release of ATP from supporting cells, which drive bursts of action potentials in auditory nerve fibers for most of the postnatal, pre-hearing period (3). Resting level of activation of the mechanotransduction channels, present in the sensory cells from post natal day 1 to post natal day 3 (P1/P3) on, may also contribute to the IHCs depolarization. Interestingly, P0 is also the age at which the cholinergic efferent axons originating in the superior olive complex, are first observed in close vicinity to the IHCs and seem to make initial contact ((4), for review see (5)). Here, I will present recent results obtained using ex vivo whole cell recordings, immunohistochemistry and imaging, which demonstrate a ‘developmental switch’ whereby the hair cell’s cholinergic response changes from excitatory to inhibitory during synapse formation. Thus, as in vertebrate skeletal muscle, the nicotinic acetylcholine receptors (nAChRs), most likely formed by α9 and α10 nAChRs subunits (6), are functional and present in the sensory hair cell plasma membrane before synapses are formed. Then, in a second step, nAChRs clustering, coupling to calcium-dependent small conductance potassium channels (SK2) and synaptic currents appear, suggesting that efferent synaptic function is contemporaneous with, and may require, SK2 channel expression, a hypothesis consistent with the lack of functional efferent activity reported in SK2 knockout IHCs (7).