Document Type

Honors Project On-Campus Access Only


Pain is a cardinal component of inflammation. Mast cells are granule-filled white blood cells, know for their functions in inflammation, tissue remodeling and host defense. A number of investigations performed in rats suggest that mast cells could also be involved in the initiation of inflammatory pain mechanisms. For example, degranulation of dural mast cells produces an extended excitation of meningeal nociceptors, underlying a possible mechanism for the initiation of migraine headaches. On the other hand, thermal hyperalgesia is produced by allergen-evoked inflammation, suggesting the important role of mast cell activation and mast cell products for the induction of this response. Therefore, this study aimed to establish murine models of pain where the potentially critical role(s) of mast cells could be examined. Here we are presenting evidence that suggests we may have two novel models useful for the study of mast cells as critical initiators of inflammatory pain. The first is a model of thermal hypernociception in mice following intraplantar administration of compound 48/80 (c48/80) - a chemical inducer of mast cell degranulation - and blockade of c48/80-induced hypernociception using sodium cromolyn (SCG) - a known mast cell stabilizer. In a second mast cell-specific model of thermal hypernociception, we show that sensitization with anti-dinitrophenyl (DNP)-Immunoglobulin E followed by antigen challenge with DNP also elicits a pain response to thermal stimuli in mice. We are currently using these models to characterize the precise roles of mast cells in the inflammatory pain response.



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