Impact of chorda tympani nerve injury on cell survival, axon maintenance, and morphology of the chorda tympani nerve terminal field in the nucleus of the solitary tract

Authors

  • Rebecca B. Reddaway,

    1. Department of Psychology, University of Virginia, Charlottesville, Virginia 22904
    Current affiliation:
    1. Department of Anatomy and Regenerative Biology, The George Washington University, 2300 I Street, NW, Ross Hall 431, Washington, DC 20037
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  • Andrew W. Davidow,

    1. Department of Psychology, University of Virginia, Charlottesville, Virginia 22904
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  • Sarah L. Deal,

    1. Department of Psychology, University of Virginia, Charlottesville, Virginia 22904
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  • David L. Hill

    Corresponding author
    1. Department of Psychology, University of Virginia, Charlottesville, Virginia 22904
    • Department of Psychology, University of Virginia, P.O. Box 400400, Charlottesville, VA 22904-4400
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Abstract

Chorda tympani nerve transection (CTX) has been useful to study the relationship between nerve and taste buds in fungiform papillae. This work demonstrated that the morphological integrity of taste buds depends on their innervation. Considerable research focused on the effects of CTX on peripheral gustatory structures, but much less research has focused on the central effects. Here, we explored how CTX affects ganglion cell survival, maintenance of injured peripheral axons, and the chorda tympani nerve terminal field organization in the nucleus of the solitary tract (NTS). After CTX in adult rats, the chorda tympani nerve was labeled with biotinylated dextran amine at 3, 7, 14, 30, and 60 days post-CTX to allow visualization of the terminal field associated with peripheral processes. There was a significant and persistent reduction of the labeled chorda tympani nerve terminal field volume and density in the NTS following CTX. Compared with controls, the volume of the labeled terminal field was not altered at 3 or 7 days post-CTX; however, it was significantly reduced by 44% and by 63% at 30 and 60 days post-CTX, respectively. Changes in the density of labeled terminal field in the NTS paralleled the terminal field volume results. The dramatic decrease in labeled terminal field size post-CTX cannot be explained by a loss of geniculate ganglion neurons or degeneration of central axons. Instead, the function and/or maintenance of the peripheral axonal process appear to be affected. These new results have implications for long-term functional and behavioral alterations. J. Comp. Neurol. 520:2395–2413, 2012. © 2012 Wiley Periodicals Inc.

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