Uncovering the contribution of enhanced central gain and altered cortical oscillations to tinnitus generation.

Various theories and their associated mechanisms have been proposed as the neural basis of phantom sound perception (tinnitus), including central gain enhancement and altered cortical oscillations. However, it remains unknown whether these cortical changes directly cause tinnitus, or simply coexist with the phantom percept. Using chronically-implanted electrodes and drug delivery cannulae in rats, we examined whether enhanced central gain and cortical oscillations are consistent across different tinnitus induction methods (noise exposure; salicylate), and if directly-inducing enhanced central gain or altered cortical oscillations via pharmacologic manipulation of inhibition along the auditory pathway would cause behavioral evidence of tinnitus. We show that, while there appeared to be no clear link between tinnitus and the presence of enhanced sound-evoked cortical activity or altered spontaneous cortical oscillations, pharmacologic impairment of GABAergic neurotransmission in the auditory cortex was sufficient to cause tinnitus; collective findings which further advance our understanding of the neural basis of tinnitus.