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Visceral Pain

The Role of Brain-Gut Signaling

An article published in the American Journal of Physiology Gastrointestinal and Liver Physiology discussed a study of visceral pain, the goal of which was to “test the hypothesis that the microglia in the central nucleus of amygdala contribute to chronic stress-induced visceral hypersensitivity via complement C1q/C3-CR3 signaling-mediated synaptic remodeling.” The central nucleus of amygdala in rats were implanted with micropellets of corticosterone or cholesterol. Rats of both sexes injected with corticosterone showed hypersensitivity and an increased number of abdominal contractions. Simplified, stress hormones led to the development of visceral pain.

The study concluded that an “increase of corticosterone level in the central nucleus of amygdala was sufficient to prime microglia and induce microglia-modulated synaptic remodeling, which contributed to the development to visceral hypersensitivity. The increased synaptic engulfment was associated with classical complement cascade that was initiated by the increased microglial expression of C1q. Blocking the C1q/C3-CR3 cascade by applying CR3 antagonist, NIF, was sufficient to attenuate CORT-induced synaptic remodeling in the CeA and the consequential visceral hypersensitivity. These data raised the possibility of targeting microglia-synapse signaling to develop novel therapeutic treatments for IBS. These findings uncover a role of microglia-synapse signaling in the brain-gut regulation and support a future therapeutic target to treat visceral pain."

 

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