MF1 Multi-Field Magnetic Speakers

Cochlear and auditory brainstem implants are the primary treatments for profound deafness. However, the inherently low resolution of electrical stimulation used by these devices limits information transfer to a small number of independent stimulation channels and results in perceptual difficulties. An alternative approach is to target the auditory cortex, a brain region large enough to accommodate hundreds of stimulation channels and whose stimulation evokes sound percepts. Although modern brain interfaces offer large channel counts and spatial resolution, developing encoding algorithms capable of accurately transmitting interpretable sound information remains challenging. Here we introduce Braincodec, a deep network that optimizes both sound information transmission and the alignment of stimulation patterns with the spatial, temporal, and high-level properties of the auditory cortex neural code. Braincodec operates online and requires only a few hundred channels to transmit sufficient information for the reconstruction of natural sounds with high fidelity, a performance inaccessible to cochlear implant encoders. Moreover, mice equipped with a Braincodec-driven auditory cortical prosthesis matched the accuracy of non-implanted mice in discriminating real sounds. Braincodec therefore enables the development of high-throughput cortical neuroprosthetics with the potential to overcome the limitations of current auditory implants and provides a generic framework applicable to other sensory modalities.

Neural presbycusis disrupts auditory timing and speech perception, yet its molecular basis remains poorly understood. This study identifies Cntn2 as the Ranvier's nodal molecule significantly downregulated in aged auditory nerves. Cntn2 heterozygous knockout (Cntn2 +/- ) mice showed elevated auditory brainstem response thresholds and prolonged wave latencies and interpeak intervals, whereas distortion product otoacoustic emission thresholds were largely preserved. Hair cell and ribbon synapses were preserved, with no obvious ultrastructural changes, suggesting that overt hair cell loss or synaptic structural loss is unlikely to be the main cause of the early phenotype. Instead, transmission…

Hearing relies on the lifelong stability of the actin core within hair cell stereocilia, yet the molecular mechanisms ensuring this stability are largely unknown. Here, we identify the transcription factor Sox3 as a key regulator of this core structure in mice. In the absence of Sox3, the stereocilia core progressively disassembles, leading to hearing loss and impaired mechanotransduction. Sox3-deficient stereocilia are also more susceptible to acoustic trauma and fail to repair structural gaps, whereas Sox3 overexpression confers resilience against noise-induced damage. Mechanistically, Sox3 deletion downregulates β-thymosin genes in hair cells, most prominently Tmsb10, an essential regulator of actin monomer availability. Depleting Tmsb10 recapitulates the core degeneration observed in Sox3-deficient hair cells, establishing the Sox3-Tmsb10 axis as a novel molecular mechanism governing the lifelong preservation of the stereocilia actin core. This regulatory pathway also represents a promising target for therapeutic intervention in noise-induced hearing loss.