Evidence for a Neural Stem Cell Niche in the Postnatal Rat Vestibular Ganglion: An In Vitro Study.

Vestibular dysfunction significantly contributes to dizziness, balance issues, and falls, yet causal treatments are still unavailable. The vestibular ganglion (VG), the primary sensory ganglion of the vestibular nerve, is increasingly seen as a key site of vestibular degeneration. Neural stem cells (NSCs) have been identified in several areas of the auditory and vestibular pathways. Endogenous activation of NSCs represents a promising regenerative strategy. However, the presence of NSCs within the VG remains uncertain. In this study, VG tissue from postnatal day (PND) 8 Sprague-Dawley rats was isolated, enzymatically dissociated, and cultured in serum-free neurosphere conditions. The dissociated VG cells reliably formed free-floating neurospheres that grew over multiple passages. Immunocytochemistry showed expression of NSC and progenitor markers, including Sox-2, Nestin, Musashi-1, Atoh-1, and doublecortin, in both neurospheres and VG tissue sections. Additional analyses demonstrated persistence of Sox-2-, Atoh-1-, and Nestin-positive populations in the adult VG. After differentiation, individual cells from neurospheres developed into β-III-tubulin-positive neurons, glial fibrillary acidic protein (GFAP)-positive astrocytes, and myelin basic protein (MBP)-positive myelinating glial cells, while a significant portion retained Nestin expression, indicating a progenitor-like state. These findings demonstrate that VG-derived cells meet the main criteria of NSCs: self-renewal, progenitor formation, and multipotent differentiation into neuronal and glial lineages. Our results provide the first evidence of a neurogenically capable cell population in the postnatal rat VG and support the persistence of progenitor-associated cell populations into adulthood. This identifies the VG as a novel endogenous regenerative reservoir, positioning it as a promising target for strategies that activate resident cells to restore vestibular function.