This research will use an appropriate animal model to define the behavioral, physiological, and cellular changes that correlate with deficits in auditory temporal processing. We will test the hypothesis that one type of early insult (exposure to low levels of lead) but not another (exposure to loud sound) causes a deficit in hearing rapid changes in sound. Four observations from the literature predict that lead toxicity is a reasonable manipulation for investigating auditory temporal processing deficit. First, lead poisoning causes dyslexia. Second, children with dyslexia have auditory temporal and phonological processing deficits. Third, early exposure to low levels of lead in these animals causes an auditory temporal processing disorder. Fourth, the development of hearing in humans and these animals is remarkably parallel in many aspects, including auditory temporal processing. Signal detection analyses of unconditioned delays in the subjects' vocalizations will quantify the early development of forward, backward, and simultaneous masking, discrimination of speech and speech-like stimuli containing voice- and tone-onset-time cues. Several non-temporal controls (absolute thresholds, frequency and intensity discrimination) will prove the deficits are unique to rapidly changing sounds. Physiological recordings and immuno-histochemistry of cells of the central auditory system will define possible mechanisms of the behavioral deficits. According to an important current hypothesis, difficulty processing the basic elements of language (phonemes) is due to a deficit in the perception of rapidly changing sounds. Basic questions about the early development of auditory temporal processing and the insults that can cause a decrement in these important abilities remain unanswered. This basic information will help us understand the effects of common environmental insults and perhaps the etiology of phonological processing deficits (associated with dyslexia in children) that affect between 5 percent and 17 percent of our children.

Agency
National Institute of Health (NIH)
Institute
National Institute on Deafness and Other Communication Disorders (NIDCD)
Type
Research Project (R01)
Project #
5R01DC004303-02
Application #
6523512
Study Section
Special Emphasis Panel (ZRG1-IFCN-6 (01))
Program Officer
Donahue, Amy
Project Start
2001-09-30
Project End
2005-08-31
Budget Start
2002-09-01
Budget End
2003-08-31
Support Year
2
Fiscal Year
2002
Total Cost
$166,871
Indirect Cost
Name
University of Texas Health Science Center Houston
Department
Otolaryngology
Type
Schools of Medicine
DUNS #
City
Houston
State
TX
Country
United States
Zip Code
77225
Lurie, Diana I; Brooks, Diane M; Gray, Lincoln C (2006) The effect of lead on the avian auditory brainstem. Neurotoxicology 27:108-17