Tracking the expression of GABAA receptor subunit α1 in rat auditory cortex, inferior colliculus and dorsal cochlear nucleus following noise-induced hearing loss

Damage to the cochlea, produced by exposure to a loud noise or a mechanical insult results in a range of changes in key auditory nuclei in the auditory pathway. Neuronal changes observed include plasticity of tonotopic representation, changes in the pattern of spontaneous activity and changes in the balance of excitatory and inhibitory transmitter systems. Moreover, damage to the cochlea frequently results in tinnitus. This suggests that one or more of these neuronal changes may be involved in tinnitus generation, although the mechanism remains to be elucidated. In an attempt to determine which area(s) may be involved in the generation of tinnitus, we are investigating neuronal changes at different levels of the auditory system (brainstem, midbrain and cortex). In this study we examine the timecourse of changes in the expression of the GABAA receptor in cochlear nucleus, inferior colliculus and auditory cortex up to 32 days following exposure to a 16 kHz bandpass (1/10th octave noise (115 dB SPL)). Male Long Evans rats (n = 10) were unilaterally exposed to the damaging noise for 1hour. At 0, 4, 8, 16 or 32 days rats were euthanased, their brains were removed and processed for immunohistochemistry to identify GABAARα1 subunit expression, which was subsequently quantified in the cochlear nucleus, inferior colliculus and auditory cortex. Over the course of the study period we saw significant changes in GABAARα1 expression. In auditory cortex these changes were evident from 4 days to 32 days where we saw a progressive increase in GABAARα1 up to twofold by 32 days. These increases may reflect an attempt to balance excitatory transmission, which is known to increase following noiseinduced hearing loss.