This Article Figures Only Full Text Full Text (PDF) Data Supplement Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Hermanstyne, T.O. Articles by Gold, M.S. Search for Related Content PubMed PubMed Citation Articles by Hermanstyne, T.O. Articles by Gold, M.S. Social Bookmarking                         What's this?

Mechanotransducers in Rat Pulpal Afferents

¹ Program in Neuroscience, University of Maryland, Baltimore, MD 21201, USA;
² Department of Oral Biology, New Jersey Dental School, University of Medicine and Dentistry of New Jersey, 185 South Orange Ave, Newark, NJ 07103, USA; and
³ Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh, 3500 Terrace Street, Rm E1440 BST, Pittsburgh, PA 15213, USA

Correspondence: ^* corresponding author, goldm{at}dom.pitt.edu

The hydrodynamic theory suggests that pain associated with stimulation of a sensitive tooth ultimately involves mechanotransduction as a consequence of fluid movement within exposed dentinal tubules. To determine whether putative mechanotransducers could underlie mechanotransduction in pulpal afferents, we used a single-cell PCR approach to screen retrogradely labeled pulpal afferents. The presence of mRNA encoding BNC-1, ASIC3, TRPV4, TRPA1, the , β, and subunits of ENaC, and the two pore K⁺ channels (TREK1, TREK2) and TRAAK were screened in pulpal neurons from rats with and without pulpal inflammation. ASIC3, TRPA1, TREK1, and TREK2 were present in ~67%, 64%, 14%, and 10% of pulpal neurons, respectively. There was no detectable influence of inflammation on the proportion of neurons expressing these mechanotransducers. Given that the majority of pulpal afferents express ASIC3 and TRPA1, our results raise the possibility that these channels may be novel targets for the treatment of dentin sensitivity.

Key Words: dentin hypersensitivity • single-cell PCR • retrograde labeling • primary afferent

Journal of Dental Research, Vol. 87, No. 9, 834-838 (2008)
DOI: 10.1177/154405910808700910


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?