Tracking the expression of GABAA receptor subunit a1, Glutamic-Acid Decarboxylase-67, N-Methyl-D-Aspartate receptor subunit 2A in rat auditory pathway following noise-induced hearing loss

Excessive exposure to loud noise or a mechanical insult results in damage to the cochlea, which can lead to a range of neuronal changes in key nuclei in the auditory pathway. Neuronal changes that have been observed include plasticity of tonotopic organisation, changes in the pattern of spontaneous activity and in the balance of excitatory and inhibitory transmitter systems. Moreover, a cochlear hearing loss is strongly associated with tinnitus in humans. This suggests that one or more of these neuronal changes may be involved in generating tinnitus, although the mechanisms and site remain unknown. In an attempt to determine which area(s) may be involved in the generation of tinnitus, we are investigating neuronal changes at a number of levels of the auditory pathway (auditory cortex (AC), inferior colliculus (IC) and dorsal cochlear nucleus (DCN)), primarily focusing on the balance of excitatory and inhibitory transmitter systems. In this study we examined the time-course of changes in the expression of the GABAA receptor subunit a1(GABAARa1), Glutamic-Acid Decarboxylase-67 (GAD-67), N-Methyl-D-Aspartate receptor subunit 2A (NMDAR2A) in AC, IC and DCN up to 32 days following exposure to a 16kHz band pass (1/10th octave noise (115 dB SPL))