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Altered localization of Ca v 1.2 (L‐type) calcium channels in nerve fibers, Schwann cells, odontoblasts, and fibroblasts of tooth pulp after tooth injury
Author(s) -
Westenbroek R.E.,
Anderson N.L.,
Byers M.R.
Publication year - 2003
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10863
Subject(s) - odontoblast , schwann cell , anatomy , immunostaining , pulp (tooth) , nerve injury , chemistry , microbiology and biotechnology , pathology , biology , medicine , neuroscience , immunohistochemistry
We have determined the localization of Ca v 1.2 (L‐Type) Ca 2+ channels in the cells and nerve fibers in molars of normal or injured rats. We observed high levels of immunostaining of L‐type Ca 2+ channels in odontoblast cell bodies and their processes, in fibroblast cell bodies and in Schwann cells. Many Ca v 1.2‐containing unmyelinated and myelinated axons were also present in root nerves and proximal branches in coronal pulp, but were usually missing from nerve fibers in dentin. Labeling in the larger fibers was present along the axonal membrane, localized in axonal vesicles, and in nodal regions. After focal tooth injury, there is a marked loss of Ca v 1.2 channels in injured teeth. Immunostaining of Ca v 1.2 channels was lost selectively in nerve fibers and local cells of the tooth pulp within 10 min of the lesion, without loss of other Ca v channel or pulpal labels. By 60 min, Ca v 1.2 channels in odontoblasts were detected again but at levels below controls, whereas fibroblasts were labeled well above control levels, similar to upregulation of Ca v 1.2 channels in astrocytes after injury. By 3 days after the injury, Ca v 1.2 channels were again detected in nerve fibers and immunostaining of fibroblasts and odontoblasts had returned to control levels. These findings provide new insight into the localization of Ca v 1.2 channels in dental pulp and sensory fibers, and demonstrate unexpected plasticity of channel distribution in response to nerve injury. © 2003 Wiley‐Liss, Inc.