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Auditory-nerve rate responses are inconsistent with common hypotheses for the neural correlates of loudness recruitment.

ABSTRACT: A number of perceptual phenomena related to normal and impaired level coding can be accounted for by the degree of compression in the basilar-membrane (BM) magnitude response. However, the narrow dynamic ranges of auditory-nerve (AN) fibers complicate these arguments. Because the AN serves as an information bottleneck, an improved understanding of the neural coding of level may clarify some of the limitations of current hearing aids. Here three hypotheses for the neural correlate of loudness recruitment were evaluated based on AN responses from normal-hearing cats and from cats with a noise-induced hearing loss (NIHL). Auditory-nerve fiber rate-level functions for tones were analyzed to test the following hypotheses: Loudness recruitment results from steeper AN rate functions after impairment. This hypothesis was not supported; AN rate functions were not steeper than normal following NIHL, despite steeper estimated BM responses based on the AN data. Loudness is based on the total AN discharge count, and recruitment results from an abnormally rapid spread of excitation after impairment. Whereas abnormal spread of excitation can be observed, steeper growth of total AN rate is not seen over the range of sound levels where recruitment is observed in human listeners. Loudness of a narrowband stimulus is based on AN responses in a narrow BF region, and recruitment results from compression of the AN-fiber threshold distribution after impairment. This hypothesis was not supported because there was no evidence that impaired AN threshold distributions were compressed and the growth of AN activity summed across BFs near the stimulus frequency was shallower than normal.Overall, these results suggest that loudness recruitment cannot be accounted for based on summed AN rate responses and may depend on neural mechanisms involved in the central representation of intensity.

SUBMITTER: Heinz MG

PROVIDER: S-EPMC2538332 | biostudies-other | 2005 Jun

REPOSITORIES: biostudies-other

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Project description:Spiral ganglion neurons (SGNs) and the associated components of the auditory nerve are primary carriers of auditory information from hair cells to the brain. Loss of SGNs occurs with many pathological conditions, resulting in permanent sensorineural hearing loss. Neural stem/progenitors (NSPs) have been well-characterized in several locations of adult brain and retina. However, it is unclear whether NSPs are present in the adult auditory nerve. Here we examined the self-renewal potential of the adult auditory nerve using ouabain application as a well-established mouse model of acute SGN injury. The observed increase in cell proliferation, alteration in enchromatin/heterochromatin ratio and down-regulation of histone deacetylase expression in glial cells suggest that the quiescent glial cells convert to an activated state after SGN degeneration. This was further confirmed by global gene expression analysis of injured auditory nerves, which showed up-regulation of numerous neurogenesis- and/or development-associated genes shortly after ouabain exposure. These genes include molecular markers commonly used for the identification of NSPs. Under a strict culture regimen, auditory nerve-derived cells of adult mouse ears gave rise to neurospheres, suggesting that multipotent NSPs are present in adult cochlear nerve. Neurosphere assays on Sox2 transgenic mice revealed that Sox2+ glial cells are the source for NSPs. Our data also showed that acute injury or hypoxia enhances neurosphere formation. Taken together, our study revealed that glial cells of adult cochlea exhibit several NSP characteristics, and hence these mature non-neuronal cells may be important targets for promoting self-repair of degenerative auditory nerves. Auditory nerves were removed from the temporal bones of adult CBA/CaJ mice, aged 8 to 12 weeks. Tissues were either collected and used directly as the tissue samples or dissociated and used for the cell culture samples. Dissociated auditory nerve cells were propagated and grown to full confluency (5-7 days), constituting the cultured cell samples. For neurosphere samples, growth medium was changed to neurosphere formation medium and the cells were cultured for an additional 12 days. All samples were prepared in triplicate (n=3).

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Auditory-nerve rate responses are inconsistent with common hypotheses for the neural correlates of loudness recruitment.

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