The purpose of this study was to characterize the impact of tooth injury on the distribution of tyrosine receptor kinase B (TrkB) among trigeminal ganglion neurons and assess the time course for tooth injury-induced TrkB distribution changes. In addition, we sought to further characterize the subpopulation of the afferents expressing TrkB receptors. Fifteen adult male Sprague-Dawley rats were studied. Pulpal inflammation was induced and ganglia were subsequently harvested and processed at different time points. Standard immunohistochemical fluorescence techniques were used to visualize TrkB-like immunoreactivity and isolectin B4 binding. Results indicate that full-length TrkB receptors are present in 36.6% of trigeminal ganglion neurons. This percentage decreases for the first 48 h and then increases to 41% by 7 days after tooth injury. Finally, TrkB appears to be present in a large percentage (54%) of isolectin B4+ neurons, suggesting that it is present in nociceptive afferents. These data highlight the fact that even mild injury results in sustained changes in nociceptive circuitry and raise the possibility that the brain-derived neurotrophic factor/TrkB system may contribute to persistent pain after tooth repair.