Elizabeth Hardy, John Crespo, Nathan T. Fried (faculty)
Monosodium Glutamate (MSG), a flavor enhancer commonly used as a commercial food additive, has anecdotally been associated with increased pain and migraine symptomatology. Recently, this was tested in a mouse model where 21 days of MSG exposure induced hyperalgesia, potentially due to an increase in nitric oxide within the brain. However, the mechanism is still unclear with the potential for increased glutamate release, increased glutamate receptor expression occurring (NMDA and AMPA), or modified Ca2+/calmodulin signaling being the root cause. MSG is known to stimulate glutamate receptors, triggering umami, known as our fifth sense, further causing behavioral and afferent nerve responses. Studies have also demonstrated that glutamate receptor activation is key to the development of chronic pain and an increase in afferent nerve activity. Drosophila Melanogaster are an excellent model system to identify this mechanism because behavioral pain assays are readily accessible and they share several genetic components with humans, including glutamate receptor signaling. To explore the mechanism behind how MSG affects pain processing, we must first determine if similar to mice and humans, MSG induces increased nociception in Drosophila. Thus, we hypothesize that MSG will increase pain sensitivity in Drosophila due to systemically increased levels of glutamate causing nerve cell to overexcitation. We will test this by using a chemical, thermal, and mechanical nociception assay in Drosophila Melanogaster larvae where animals are exposed to noxious stimuli following MSG exposure and measuring the latency to a canonical pain–associated rolling behavior. Our pilot data reveals that wild–type Drosophila larvae respond in 4.54 +/– 2.95 seconds to 10% hydrochloric acid. Using this baseline, we can then test whether the latency of rolling decreases (indicating greater chemical nociception) following exposure to a range of concentrations of MSG. We will then test whether this exposure changes their thermal and mechanical sensitivity under both acute and chronic pain conditions. Follow-up studies will explore whether stimulation of glutamate receptors are a key component to the mechanism behind this phenomenon, essentially increasing sensitivity and leading to chronic pain. Further research on this mechanism, will allow us to understand why some patients differentiate in sensitivity to the effects of dietary MSG.
Preview this research