INTRINSIC INHIBITION IN THE COCHLEAR NUCLEAR COMPLEX

University Of Illinois Urbana-Champaign, Champaign IL

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Abstract

Understanding how auditory information is processed in the cochlear complex is essential for developing diagnostic tools to evaluate the ascending auditory system and for determining what information must be provided by cochlear prosthesis. The cochlear nuclear complex is the first locus of auditory information processing after sound is transduced in the cochlea, and in the cochlear nuclei information carried by auditory nerve fibers is divided into parallel ascending pathways. A number of psychoacoustic experiments have pointed to the cochlear nuclei as the site of a process that reduces the information available for sound localization shortly after the onset of a sound and contributes to the precedence effect. In vitro studies have suggested that tuberculoventral neurons, which project from the dorsal (DCN) to the ventral cochlear nucleus (VCN), contribute to the reduction in information. Recently, in vivo findings showed that the tuberculoventral neurons mediate both a rapid and a slower inhibition. The rapid inhibition significantly decreased the response at the onset of a sound and the slower inhibition reduced the availability of information just after the onset. Although the rapid inhibition can suppress onset transients and the slower inhibition can contribute to the precedence effect, the precise functions of these two inhibitory inputs are unknown. Determining the functions of this intrinsic circuitry is central to understanding the processing of information in the ventral cochlear nucleus. The specific aims of this study are to determine how the rapid and the slower inhibitory inputs modulate the responses of VCN neurons to stimuli used in psychoacoustic studies on sound localization, to identify precisely the neural circuits that provide and control both the rapid and the slower inhibition, to characterize physiologically the tuberculoventral neurons, and to begin investigating the pharmacology that underlies the two changes in response. The specific aims will be accomplished using extracellular, single unit recordings in ketamine- anesthetized chinchillas. The recordings from VCN neurons will be made before and after injections of lidocaine are made at various locations and depths within the DCN to inactivate different components of the neural circuits projecting to the VCN. Tuberculoventral neurons will be identified by electrical stimulation of the tuberculoventral tract, and their responses to tones, clicks and noise will be characterized.