Chrna9, encoding the nicotinic acetylcholine receptor (nAChR) subunit alpha-9, is a crucial gene. nAChR-mediated signaling pathways, in which Chrna9 is involved, affect the proliferation and differentiation of pluripotent stem cells. It is also associated with the JAK/STAT pathway in glioma [1,2].

Mouse models have been instrumental in understanding Chrna9. In α9-KO mice (lacking the Chrna9 gene), hearing thresholds are normal, but more complex auditory functions like frequency selectivity and sound localization are altered. They also show a reduced capacity to suppress auditory distractors during visual selective attention [4]. In α9α10KO mice (deficient in both alpha9 and alpha10 receptor subunits), there are abnormal auditory processing features despite grossly normal auditory function in quiet and noise, such as larger ABR amplitudes and hyperreactive startles [3].

In conclusion, Chrna9 is vital for the proper function of nAChR-mediated signaling, influencing processes like stem cell regulation and auditory function. Gene-knockout mouse models, especially those targeting Chrna9, have significantly contributed to understanding its role in auditory-related disorders, potentially guiding future research and therapeutic strategies in this area.