The transient receptor potential melastatin 8 (TRPM8) receptor is activated by the chemicals menthol and icilin and mediates innocuous and noxious cold. The role of TRPM8 in mediating noxious cold pain in pulpal neurons was assessed in this study. We used immunohistochemistry to evaluate the expression of TRPM8 in mice molars mediating noxious cold. In order to characterize the neuronal population expressing TRPM8, we used a retrograde tracer, Fos to identify pulpal neurons in the trigeminal ganglion. This method combined with multiple label immunohistochemistry identified the neurochemical properties of pulpal afferents that express TRPM8. The results in this study demonstrated that Fos expression in the transition zone neurons in the trigeminal ganglion increases significantly upon noxious cold stimulation in normal pulp of the experimental mouse. This finding suggests that a noxious cold stimulus increases neural activity in relevant brainstem neurons. In the presence of dental pulp injury (i.e., pulpal inflammation), a reduction of Fos expression in the transition zone neurons is observed compared to normal pulp, although not statistically significant. Degeneration of nerve fibers may be the reason why a reduction was seen in our study. The finding that the absence of TRPM8 does not effect cold-evoked Fos expression significantly indicates that TRPM8 is likely not the only receptor responsible for thermosensation in the dental pulp in mice.
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|Commitee:||Marshall, Grayson, Miller, Arthur|
|School:||University of California, San Francisco|
|Department:||Oral and Craniofacial Sciences|
|School Location:||United States -- California|
|Source:||MAI 50/05M, Masters Abstracts International|
|Keywords:||Cold, Pain, Pulpitis, Transient receptor potential melastatin 8|
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