Sensorineural hearing-loss (SNHL) is known to increase neuronal spontaneous firing rates (hyperactivity) in the ascending auditory system. Hyperactivity is proposed to be involved in the generation of tinnitus, a phantom auditory perception. However, the mechanisms underlying central hyperactivity remain unknown. A candidate mechanism is abnormal axon initial segment (AIS) structure and function. Action potentials are generated at the AIS which undergoes plasticity to maintain neuronal firing within physiological parameters. In the developing avian auditory system, SNHL results in AIS elongation and subsequent increase in neuronal excitability. Therefore, AIS elongation may be involved in the hyperactivity seen in the adult auditory system following SNHL. The present study investigated the effects of SNHL on AIS length in the auditory system of adult Sprague Dawley rats. Rats (n=13) were exposed to an acoustic trauma (AT) (n = 7) or sham procedure (n = 6). AIS length was quantified in several auditory nuclei using immunostaining for the AIS scaffolding protein Ankyrin-G. Preliminary analysis of 9 of 13 animals (5 = AT, 4 = sham) suggests AIS elongation in ipsilateral and contralateral dorsal (DCN) and ventral cochlear nucleus (VCN) 2-weeks after AT (Ipsilateral-DCN: AT = 12.0 ± 2.7 µm > Sham = 9.8 ± 3.4 µm; Contralateral-DCN: AT= 11.5 ± 3.0µm > Sham = 9.8 ± 3.7 µm; Ipsilateral-VCN: AT = 12.4 ± 3.3µm > Sham = 9.7 ± 2.5µm; Contralateral-VCN: AT= 11.2 ± 3.1µm > Sham = 9.8 ± 2.6µm). This suggests SNHL induces maladaptive AIS plasticity which could underlie neuronal hyperactivity.