The biophysical diversity that is intrinsic to spiral ganglion neurons emerges as spatial gradients during early post-natal development and endures through subsequent maturation to likely contribute to sound intensity coding.
Supporting cells in the cochlea change their shape in response to purinergic receptor activation, which influences hair cell excitability by altering potassium redistribution in the extracellular space.
Heterodyne low-coherence interferometry demonstrates that the latency of the sound-induced reticular lamina vibration is significantly greater than that of the basilar membrane vibration in living gerbil cochleae.
Principal neurons of the brainstem nucleus comparing sound level at the two ears do not have the slow response properties previously attributed to them, but are instead specialized for fast weighing of excitation and inhibition.
The development of the mammalian cochlea undergoes a period of embryonic refinement in which the outer hair cell region repels incoming type I spiral ganglion neurons, thus ensuring these neurons instead form connections with inner hair cells.