AXON INITIAL SEGMENT PLASTICITY IN THE AUDITORY SYSTEM IN ADULT RATS FOLLOWING ACOUSTIC TRAUMA

Reduced afferent input from noise-induced hearing-loss (NIHL) is known to cause central plasticity, inducing an increase in neuronal spontaneous firing rates (hyperactivity), which may play a role in tinnitus development. A candidate mechanism for generation of hyperactivity is the axon initial segment (AIS), which is the site of action potential initiation and thus determines how efficiently synaptic input is converted into an output signal. Recent studies have shown AIS length is dynamically regulated by changes in neural activity. Indeed, in the developing avian auditory system, hearing loss resulted in AIS elongation and an increase in neuronal excitability. Therefore, AIS elongation may play a role in hyperactivity generation in the adult auditory system following NIHL. In this study, the effect of NIHL on AIS length in auditory system of adult Sprague Dawley (SD) rats was investigated. Rats (n=9) were unilaterally exposed to acoustic trauma (AT, 16 kHz, 1 hour, 120 dB SPL) (n = 5) or sham (n = 4). Two weeks later hearing thresholds were measured using auditory brainstem responses to confirm effects of AT and brains harvested. AIS length was quantified using immunostaining for Ankyrin-G. Preliminary analysis revealed the AIS was significantly longer in the ipsilateral dorsal and ventral cochlear nucleus as compared to shams. In addition, in ventral cochlear nucleus this was also observed on the contralateral side. No effect was observed in auditory thalamus and cortex. These preliminary data support a role of AIS in generation of hyperactivity following NIHL.