Abstract
The American Tinnitus Association has estimated that over 50 million Americans experience tinnitus. Currently the only known effective treatment is the use of biofeedback techniques. Because tinnitus is thought to be perpetuated via a hyperexcitation of the amygdalo-auditory cortex circuits, biofeedback therapy may act to increase GABAergic inhibition of these circuits. Previous experiments in our laboratory have shown that GABAergic neurons are disproportionately damaged during blast-exposure. We hypothesize that flooding the amygdalo-auditory cortex circuit with GABA prior to the blast trauma may decrease the excitation in these circuits and increase the threshold of activity necessary for tinnitus formation. To test this hypothesis, animals were tested for tinnitus using acoustic startle responses (i.e., startle, pre-pulse, and gap detection tests). They were then exposed to blast sounds (90 dB SPL; 1 hour/day). During this sound exposure, animals became accustomed to the sounds and started to sleep during the exposures. After 2 weeks of sound exposure, animals were exposed to a 20 psi blast pressure wave, and then subsequently tested for tinnitus twice per week post-blast-exposure. The incidence of tinnitus was then compared in the sound-exposed group of animals versus blasted non-sound-exposed animals. The incidence of tinnitus with soundexposure (i.e., biofeedback treatment) was substantially decreased when compared to similar animals that did not receive the biofeedback treatment. We hypothesize that biofeedback therapy may be a simple and cost-effective prophylactic treatment for individuals that are at risk for blast-exposure.