Projections of the second cervical dorsal root ganglion to the cochlear nucleus in rats

Physiological, anatomical, and clinical data have demonstrated interactions between somatosensory and auditory brainstem structures. Spinal nerve projections influence auditory responses, although the nature of the pathway(s) is not known. To address this issue, we injected biotinylated dextran amin...

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Published inJournal of comparative neurology (1911) Vol. 496; no. 3; pp. 335 - 348
Main Authors Zhan, Xiping, Pongstaporn, Tan, Ryugo, David K.
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 20.05.2006
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Summary:Physiological, anatomical, and clinical data have demonstrated interactions between somatosensory and auditory brainstem structures. Spinal nerve projections influence auditory responses, although the nature of the pathway(s) is not known. To address this issue, we injected biotinylated dextran amine into the cochlear nucleus or dorsal root ganglion (DRG) at the second cervical segment (C2). Cochlear nucleus injections retrogradely labeled small ganglion cells in C2 DRG. C2 DRG injections produced anterograde labeling in the external cuneate nucleus, cuneate nucleus, nucleus X, central cervical nucleus, dorsal horn of upper cervical spinal segments, and cochlear nucleus. The terminal field in the cochlear nucleus was concentrated in the subpeduncular corner and lamina of the granule cell domain, where endings of various size and shapes appeared. Examination under an electron microscope revealed that the C2 DRG terminals contained numerous round synaptic vesicles and formed asymmetric synapses, implying depolarizing influences on the target cell. Labeled endings synapsed with the stalk of the primary dendrite of unipolar brush cells, distal dendrites of presumptive granule cells, and endings containing pleomorphic synaptic vesicles. These primary somatosensory projections contribute to circuits that are hypothesized to mediate integrative functions of hearing. J. Comp. Neurol. 496:335–348, 2006. © 2006 Wiley‐Liss, Inc.
Bibliography:National Institutes of Health - No. RO1 DC04395
ArticleID:CNE20917
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SourceType-Scholarly Journals-1
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content type line 23
Associate Editor: Gert Holstege
ISSN:0021-9967
1096-9861
DOI:10.1002/cne.20917