Injury to tooth pulp often results in extensive sprouting of sensory nerve fibers at the site of wound repair due to local increases in nerve growth factor (NGF) concentration. NGF interacts with high-affinity binding sites, termed trk A receptors, located on the cell membranes of responsive neurons. If NGF induces wound repair and/or nociceptive responses in tooth pulp, then changes in expression of NGF receptors (trk A receptors) in response to dentin injury would be expected. To characterize the role of trk A receptors in mediating NGF-induced signals to sensory neurons, trigeminal ganglia from adult male rats were examined for changes in expression of trk A as a function of time after injury to maxillary molar dentin. In situ hybridization was performed with 35S-labeled riboprobes encoding the sense or antisense trk A sequences, and grain densities quantified over maxillary neurons. As early as 12 h after tooth injury, grain density counts increased by 71% above control level, indicating an increase in trk A receptor mRNA expression. Grain densities obtained from ganglia harvested at all time points through 168 h after injury remained elevated. At 336 h (14 days) after injury, trk A receptor expression had decreased such that grain density counts were not different from preinjury levels. Thus our results suggest that NGF may be mediating repair and pain responses by the sustained upregulation of its cell surface receptor, trk A, in neurons of the trigeminal ganglia.
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