Age-related increases in calcium-binding protein immunoreactivity in the cochlear nucleus of hearing impaired C57BL/6J mice.

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Age-Factors, Aging, Animals, Calcium-Binding-Protein-Vitamin-D-Dependent, Calcium-Binding-Proteins, Cell-Count, Cell-Survival, Cochlear-Nucleus, Female, Hearing-Loss-Central, Heredodegenerative-Disorders-Nervous, Immunohistochemistry, Male, Mice, Mice-Inbred-C57BL, Neuronal-Plasticity, Neurons, Parvalbumins, Research-Support-Non-U, S, -Gov't, Research-Support-U, S, -Gov't-P, H, S, Species-Specificity, Up-Regulation

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Neurobiol Aging 2004 Sep; 25(8):1085-93.


Aging C57BL/6J (C57) mice (1-30 months old), were used to study calcium-binding protein immunoreactivity (parvalbumin, calbindin and calretinin) in the cochlear nucleus. A quantitative stereological method, the optical fractionator was used to determine the total number of neurons, and the total number of immunostained neurons in the posteroventral- and dorsal cochlear nuclei (PVCN and DCN). A statistically significant age-related decrease of the total number of neurons was found in the PVCN and DCN using Nissl staining. In the DCN, an age-related increase in the total number of parvalbumin-positive neurons was found, while no changes in the total number of calbindin or calretinin positive neurons were demonstrated. In the PVCN, the total number of parvalbumin, calbindin, or calretinin positive neurons remained stable with increasing age. The percentage of parvalbumin, calbindin, and calretinin positive neurons significantly increased in the DCN, and the percentage of parvalbumin and calbindin-positive neurons increased in the PVCN. These findings imply that there is a relative up-regulation of calcium-binding proteins in neurons that had not previously expressed these proteins. This plastic response in the profoundly hearing impaired C57 mouse may be a survival strategy for cochlear nucleus neurons.