Using an appetitive operant conditioning paradigm to screen rats for tinnitus induced by intense sound exposure: Experimental considerations and interpretation.

In an effort to help elucidate the neural mechanisms underlying tinnitus in humans, researchers have often relied on animal models; a preclinical approach which ultimately required that behavioral paradigms be designed to reliably screen animals for tinnitus. Previously, we developed a two-alternative forced-choice (2AFC) paradigm for rats that allowed for the simultaneous recording of neural activity at the very moments when they were reporting the presence/absence of tinnitus. Because we first validated our paradigm in rats experiencing transient tinnitus following a high-dose of sodium salicylate, the present study now sought to evaluate its utility to screen for tinnitus caused by intense sound exposure; a common tinnitus-inducer in humans.

Variability in the Estimated Amplitude of Vowel-Evoked Envelope Following Responses Caused by Assumed Neurophysiologic Processing Delays.

Vowel-evoked envelope following responses (EFRs) reflect neural encoding of the fundamental frequency of voice (f). Accurate analysis of EFRs elicited by natural vowels requires the use of methods like the Fourier analyzer (FA) to consider the production-related f changes. The FA's accuracy in estimating EFRs is, however, dependent on the assumed neurophysiological processing delay needed to time-align the f time course and the recorded electroencephalogram (EEG).

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.