Spatial Distribution and Temporal Dynamics of Neomycin-Induced Neuromast Cell Damage and Regeneration in the Mexican tetra (Astyanax mexicanus)

Neuromast cells are specialized mechanosensory receptor cells embedded within the lateral line system of aquatic vertebrates, enabling the detection of water movement and vibration that are essential for navigation, prey capture, and predator avoidance. These cells share common evolutionary and functional homology with mammalian inner ear hair cells, both of which rely on stereocilia-mediated mechano-transduction and ion channel activation to convert mechanical stimuli into neural signals. Unlike their mammalian counterparts, neuromast hair cells possess a regenerative capacity following damage, making the lateral line system a unique model for studying hair cell regeneration and sensory restoration. This study examines the potential of the Mexican tetra (<i>Astyanax mexicanus</i>) as a novel model organism for investigating ototoxicity and regeneration of neurosensory hair cells. Here, we explore the cranial and trunk lateral line neuromasts, including deep canal neuromast cells located in facial bones, such as the mandible and circumorbital bones. In the present study, juvenile surface-dwelling Mexican tetra were exposed to a 500 µM neomycin for 4 h to induce targeted hair cell damage. The samples were collected at 4-, 12-, 24-, and 72 h post-exposure. Furthermore, neuromast cell viability was assessed using [2-(4-(Dimethylamino) styryl)-N-ethylpyridinium iodide] (DASPEI). Gene expression analysis revealed a modest increase in Fibroblast Growth Factor 1 (<i>fgf1</i>) and Axis Inhibition Protein 2 (<i>axin2</i>) expression following treatment; however, these changes were not statistically significant. The SRY-box transcription factor 2 (<i>sox2</i>) remains constant throughout the exposure and recovery period. These findings highlighted the regenerative dynamics of neuromast cells in Mexican tetra. This work lays the foundation for future therapeutic strategies targeting human sensory deficits, particularly those involving inner ear hair cell degeneration.