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Chronic CO exposure impairs the developing auditory system

Institution: University of California, Los Angeles
Investigator(s): Douglas Webber, Ph.D.
Award Cycle: 2004 (Cycle 13) Grant #: 13FT-0150 Award: $75,000
Subject Area: General Biomedical Science
Award Type: Postdoctoral Fellowship Awards

Initial Award Abstract
The development of hearing can be affected by components found in cigarette smoke. Several years ago, a research team found prenatal exposure to cigarette smoke caused infants to have a decreased auditory arousal when compared to infants that had not been prenatally exposed to cigarette smoke. One of the most concentrated chemicals in cigarette smoke is carbon monoxide (CO). My objective is to determine the lowest CO exposure that will cause deficits in the developing auditory system. My approach is to compare the response of the auditory system in CO exposed and non-CO exposed animals to sound using pure tone stimulation. The animal model is the developing rat.

The object of this study is to test the hypothesis that “chronic exposure to carbon monoxide causes permanent auditory”. The auditory deficit begins in the neurons of the spiral ganglion and lead to a potential dysfunction in sound processing in higher auditory regions. The spiral ganglion neurons connect the sound sensory cell (hair cell) to the brain. In our studies to date, CO exposures have been at concentrations above the EPA guidelines of 9.5 ppm as an 8 hour average. We want to determine if the spiral ganglion and the inferior colliculus (IC) are damaged from chronic CO exposure at 6 ppm, by examining the cells of the spiral ganglion using histology and immunocytochemistry and examining the status of the neuronal activation marker c-Fos in the inferior colliculus. The results we obtain will be compared and contrasted to information we have already published. Six parts per million CO exposure is in the range that can be detected occurring from secondhand smoke in a poorly ventilated room. Next, it is our objective to determine if there is a problem with pattern formation. Patterning is a process by which neurons are activated in a specific manner from a common stimulus, i.e. the same brain regions are always activated by the same sound. By using single and broadband frequency sound stimulation paradigms, we will able to determine if the CO exposed animals have a decreased tonotopic c-Fos expression when compared to non-CO exposed controls, and if these band patterns are located in the proper area. The central nucleus of the inferior colliculus (CIC) is organized in the normal tone/sound specific manner. This ‘tonotopic’ organization of the CIC is associated with the laminar organization of the disc-shaped neurons and their dendritic fields. A change in laminar pattern and c-Fos expression can occur with sound deprivation during the onset of hearing. We believe that reduction in cellular activity caused by CO exposure is similar to a sound deprivation.

Our work is relevant to second hand-smoke exposure, in particular the effects it might have on the developing auditory system. It is worth determining, if CO is contributing to the auditory deficits associated with cigarette smoke. We have reported that chronic mild CO exposure (12 to 50ppm) can cause developmental auditory deficits. We want to determine the lowest concentration that causes auditory deficits, and also how do these deficits affect the pattern formation associated with different sounds. A change in pattern formation suggests a change in overall handling of auditory information by the brain. This could cause problems in understanding auditory information.