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Distribution of P75 neurotrophin receptor in adult human cochlea—an immunohistochemical study
Mechanisms underlying the unique survival property of human spiral neurons are yet to be explored. P75 (p75NTR) is a low affinity receptor for neurotrophins and is known to interact with Trk receptors to modulate ligand binding and signaling. Up-regulation of this receptor was found to be associated...
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Published in: | Cell and tissue research 2012-06, Vol.348 (3), p.407-415 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Mechanisms underlying the unique survival property of human spiral neurons are yet to be explored. P75 (p75NTR) is a low affinity receptor for neurotrophins and is known to interact with Trk receptors to modulate ligand binding and signaling. Up-regulation of this receptor was found to be associated with apoptosis as well as with cell proliferation. Its distribution and injury-induced change in expression pattern in the cochlea have been mainly studied in rodents. There is still no report concerning p75NTR in post-natal human inner ear. We analyzed, for the first time, p75NTR expression in five freshly fixed human cochleae by using immunohistochemistry techniques, including myelin basic protein (MBP) as a myelin sheath marker and TrkB as the human spiral neuron marker, and by using thin optical sectioning of laser confocal microscopy. The inner ear specimens were obtained from adult patients who had normal pure tone thresholds before the surgical procedures, via a trans-cochlear approach for removal of giant posterior cranial fossa meningioma. The expression of p75NTR was investigated and localized in the glial cells, including Schwann cells and satellite glial cells in the Rosenthal canal, in the central nerve bundles within the modiolus, and in the osseous spiral lamina of the human cochleae. The biological significance of p75NTR in human cochlea is discussed. |
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ISSN: | 0302-766X 1432-0878 1432-0878 |
DOI: | 10.1007/s00441-012-1395-7 |