Title:  Residual inhibition: from the mechanism to tinnitus treatment 

Abstract: Neurons in various sensory systems show some level of spontaneous firing in the absence of sensory stimuli. In the auditory system spontaneous firing has been shown at all levels of the auditory pathway from spiral ganglion neurons in the cochlea to neurons of the auditory cortex. This internal "noise" is normal for the system, and it does not interfere with our ability to perceive silence or analyze sounds. However, this internal noise can be elevated under pathological conditions. After cochlear insult the input to the central auditory system becomes markedly reduced. To compensate for this loss, the central gain enhancement (or neural amplification) increases neuronal sensitivity which gives rise to hyperactivity. Such hyperactivity has been hypothesized to cause phantom sound perception or tinnitus. This implies that suppression of this hyperactivity should reduce/eliminate tinnitus. Research from our laboratory has been devoted to identifying the mechanism underlying residual inhibition of tinnitus, a brief suppression of tinnitus following a sound stimulus. We found that during this suppression spontaneous firing of auditory neurons is greatly reduced and it is mediated by metabotropic glutamate receptors (mGluRs). The key mechanisms that govern neural suppression in animals closely resemble clinical psychoacoustic findings of residual inhibition observed in tinnitus patients. We also demonstrated that drugs targeting mGluRs suppress spontaneous activity in auditory neurons and reduce/eliminate behavioral signs of tinnitus in mice for several hours. Thus, these drugs are therapeutically relevant for tinnitus suppression in humans.

 This year’s SHRP schedule is available here: https://purdue.edu/TPAN/hearing/shrp_schedule 

Titles and abstracts of all SHRP talks are here: https://purdue.edu/TPAN/hearing/shrp_abstracts

The seminar is hosted by the Department of Speech, Language and Hearing Sciences.