Brenda L. Lonsbury-Martin - US grants

The Proposed studies are a continuation of a long-term program of research designed to study the physiological bases of the transition from temporary to permanent noise-induced hearing loss (NIHL). Earlier studies in our laboratory demonstrated that measures of electrical activity from single cochlear nucleus neurons were extremely sensitive indicators of both the temporary and permanent aspect of sound-inducing hearing loss. Additionally, when challenged in a intraunit-exposure paradigm, neurons developed abnormalities related to a number of common symptoms of NIHL. Most recently, single nerve fiber studies showed that postexposure alterations displaying decrements in firing rates for cochlear nucleus cells can be understood in terms of corresponding changes at the periphery. Moreover, central changes associated with increased postexposure firing to high level stimuli may also be partially explained at the receptor-cell level. The present experiments are designed to determine if sound- induced changes in cochlear nonlinearity can account for augmentations in discharge rate observed for single nerve fibers. Following exposure to selected stimuli, nerve-fiber properties will be related to corresponding characteristics of acoustic distortion products (DPs) in what may be a promising new means of assessing the early stages of NIHL. For these studies, relatively short- duration, pure-tone or octave-band noise exposures will be utilized. Once basic nerve-fiber changes are categorized under these particular exposure conditions, our intraunit paradigm will be superimposed to determine if various stages of damage influence the incidence of increased nerve-fiber responsiveness. Other experiments making use of well-established behavioral testing techniques will assess the sound-induced deficits in threshold-dection according to frequency-place principles so that similarly induced alterations in unit and DP activity can be appropriately interpreted with respect to the underlying histopathology. These studies will extend our knowledge of the transitional stages of NIHL and provide useful insights into how sensory encoding is altered in the noise-damaged ear.

The Proposed studies are a continuation of a long-term program of research designed to study the physiological bases of the transition from temporary to permanent noise-induced hearing loss (NIHL). Earlier studies in our laboratory demonstrated that measures of electrical activity from single cochlear nucleus neurons were extremely sensitive indicators of both the temporary and permanent aspect of sound-inducing hearing loss. Additionally, when challenged in a intraunit-exposure paradigm, neurons developed abnormalities related to a number of common symptoms of NIHL. Most recently, single nerve fiber studies showed that postexposure alterations displaying decrements in firing rates for cochlear nucleus cells can be understood in terms of corresponding changes at the periphery. Moreover, central changes associated with increased postexposure firing to high level stimuli may also be partially explained at the receptor-cell level. The present experiments are designed to determine if sound- induced changes in cochlear nonlinearity can account for augmentations in discharge rate observed for single nerve fibers. Following exposure to selected stimuli, nerve-fiber properties will be related to corresponding characteristics of acoustic distortion products (DPs) in what may be a promising new means of assessing the early stages of NIHL. For these studies, relatively short- duration, pure-tone or octave-band noise exposures will be utilized. Once basic nerve-fiber changes are categorized under these particular exposure conditions, our intraunit paradigm will be superimposed to determine if various stages of damage influence the incidence of increased nerve-fiber responsiveness. Other experiments making use of well-established behavioral testing techniques will assess the sound-induced deficits in threshold-dection according to frequency-place principles so that similarly induced alterations in unit and DP activity can be appropriately interpreted with respect to the underlying histopathology. These studies will extend our knowledge of the transitional stages of NIHL and provide useful insights into how sensory encoding is altered in the noise-damaged ear.