Pericytes in the adult ear are critical for vascular stability and spiral ganglion neuron health.

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.

RNA-Seq analysis and in vivo validation via genetic approach uncover that Scrt2 and Celf4 are expressed in inner ear auditory neurons throughout development.

Genetic studies in mice identify the transcription factor MafB as a potent regulator of specific features of the synapses underlying hearing.

The neural population of the Aplysia's pedal ganglion are a low-dimensional spiral attractor, and the parameters of the attractor directly define the properties of the Aplysia's escape locomotion behaviour.

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.

Synaptic diversity in the ear's inner hair cells significantly empowers sound encoding to enable our processing of sounds across a broad range of intensities.

In vitro and in vivo physiological analyses reveal that mammalian auditory neuron intrinsic mechanical sensitivity contributes to sound-evoked activity and explains other previously unexplained auditory neuron features.

The synaptic ribbon regulates calcium channel clustering and proper vesicle dynamics at cochlear inner hair cells to ensure precise sound encoding.

Mouse brain neurons response to transcranial ultrasound at the energy level of 5 mW/cm² and repeated stimulations lead to neurogenesis while ASIC1a is required both in vitro and in vivo as one of the mechanoreceptors.