TRP expression in the trigeminal system following tooth injury

Perceptions of pain and temperature are firstly dependent upon ion channels embedded in the membranes of primary afferent neurons. Following tissue inflammation, sensory neurons become hyperexcitable to sensory stimuli and respond more robustly to painful stimuli (hyperalgesia) and to previously non-painful stimuli (allodynia). One particular superfamily of ion channels, called transient receptor potential channels (TRP), has received particular attention as a potential contributor to post-inflammatory allodynia/hyperalgesia. Objectives: We aimed to determine the temporal pattern of expression of TRP channels in dental pulp and trigeminal ganglia (TG) of rats following pulp exposure. Methods: Right maxillary incisors or mandibular molars of rats were exposed and allowed to recover for 1, 3 or 7 days. Control rats were handled but received no dental injury. Following recovery, sections of TG and pulp were immunoreacted with antibodies directed against TRPV1 or TRPM8 channels and neurofilament protein (to visualize axons) and viewed with a confocal microscope. Levels of TRP immunoreactivity were calculated by using signal-to-noise ratio (SNRs) where experimental fluorescence was divided by control fluorescence (sections receiving no primary antibody). Results: SNRs of TRPV1-expressing TG neurons significantly increased 1 and 3 days following pulp exposure (Student's t-test; p<0.05) compared to TG neurons of uninjured animals. Interestingly, pulps analyzed from the same animals did not display similar changes in TRPV1 channel immunoreactivity. One week following exposure, TG TRPV1 SNRs were not significantly different from uninjured animals (p=0.08) demonstrating a return to baseline levels. Our preliminary data show that TRPM8 SNRs significantly increase in both the TG and pulp at all time points examined. Conclusion: We report that following dental injury, TRPV1 expression significantly increases in the TG, but not the pulp and TRPM8 immunoreactivity increases in both the TG and pulp. Antagonists directed against TRP channels may lead to new treatments for pain.