GAD levels and muscimol binding in rat inferior colliculus following acoustic trauma

Abstract

Pharmacological studies of the inferior colliculus (IC) suggest that the inhibitory amino acid neurotransmitter γ-aminobutyric acid (GABA) plays an important role in shaping responses to simple and complex acoustic stimuli. Several models of auditory dysfunction, including age-related hearing loss, tinnitus, and peripheral deafferentation, suggest an alteration of normal GABA neurotransmission in central auditory pathways. The present study attempts to further characterize noise-induced changes in GABA markers in the IC. Four groups (unexposed control, 0 h post-exposure, 42 h post-exposure, and 30 days post-exposure) of 3-month-old male Fischer 344 rats were exposed to a high intensity sound (12 kHz, 106 dB) for 10 h. Observed hair cell damage was primarily confined to the basal half of the cochlea. There was a significant decrease in glutamic acid decarboxylase (GAD 65) immunoreactivity in the IC membrane fraction compared to controls ( P<0.05) at 0 h (−41%) and 42 h (−28%) post-exposure, with complete recovery by 30 days post-exposure ( P>0.98). Observed decreases in cytosolic levels of GAD 65 were not significant. Quantitative muscimol receptor binding revealed a significant increase (+20%) in IC 30 days after sound exposure ( P<0.05). These data suggest that changes in GABA neurotransmission occur in the IC of animals exposed to intense sound. Additional studies are needed to determine whether these changes are a result of protective/compensatory mechanisms or merely peripheral differentiation, as well as whether these changes preserve or diminish central auditory system function.